Summary: In this lecture, Dr. Lansing, Dr. McFarland and Dr. McCay discuss the physical and psychological issues associated with aging.
WNYC archives id: 67568
(Automatic transcript - may present inaccuracies)
>> Meeting will please come to order. Members of the Graduate Fortnight, as president of the New York Academy of Medicine, it is my great pleasure to extend the most cordial welcome to you at this, the opening meeting of our 28th Graduate Fortnight. For the benefit of those who are with us for the first time this evening, I would like--I would--What's the matter with this thing? For the benefit of those who are with us for the first time this evening--Can you hear that?
[ Inaudible Discussion ]
Is this any better? For the benefit of those who are with us for the first time this evening, I would like to review briefly the origin of the Graduate Fortnight and call your attention to certain important features of the program. Can you hear now, right there?
[ Inaudible Remark ]
It's dead I think.
[ Pause ]
Don't seem to be able to get any help here. All right. Sebastian, is it all right now? These are all dead apparently.
[ Inaudible Remark ]
They're all right?
[ Pause ]
All right?
[ Pause ]
All right. The Graduate Fortnight was actually started at the suggestion of Dr. Ludwig Kast in 1927. He was then professor of medicine at Post-Graduate Hospital and Medical School and had been interested for many years in graduate training of physicians. The plan of having a two-week seminar on various subjects in post-graduate fields in medicine and surgery was greeted with great enthusiasm. Some of the most distinguished names in medicine and in its allied sciences have participated in these meetings since their inception in 1928. And they have now become an integral part of the academy's activities reaching large audiences who look forward to them each year. The title of this year's program, "Problems of the Aging" is surely one of the most of the timely and just extremely interesting to note that this was also the title and the subject of the first night, Fortnight held in 1928. It is now an established fact, we have a growing proportion of our populus living beyond the age of 65 years. And as their numbers increase, there is bound to be a corresponding rise in the incidents of chronic disease and a relative need for more major surgery in these older patients. The problems of the aging are too numerous for us to mention here. But the program committee has gone into this topic in great detail and we will hear much more about it at the various discussions and the clinics during this Fortnight. The program as you will notice now includes three very important memorial lectures. That is the Ludwig Kast, the Wesley M. Carpenter and then Harlow Brooks. There is little doubt that you will all realize as you scan this year's program, that its arrangement was a stupendous task which started last December. I would like to take this opportunity to thank all those who helped us make it possible. Dr. Irving Wright, chairman of the Committee on Medical Education, Dr. Robert Craig, executive secretary of that committee, and all the members of that committee. Dr. Clarence de la Chapelle, chairman of the Subcommittee on Graduate Fortnight and the 16 members of his committee deserve great praise for spending many hours of hard work in arranging this program. I would like also to thank Dr. Charles Wilkinson, Jr., chairman of the Committee on Panel Meetings and the nine members of his committee, as well as the directors of the scientific exhibit, Dr. Alfred Angrist and Dr. Norman Higginbotham. Please do not miss seeing this interesting exhibit. We are very grateful to Dr. Carl Muschenheim, chairman of the Committee on Hospital Clinics and the members of his committee, whoever arranged this splendid group of clinics. These are held in the various hospitals each afternoon and I urge you all to visit them as you will find them very much worth your while. I am confident that the work and effort put into the arrangement of this program will bring rich rewards. And I hope that you will all enjoy this Graduate Fortnight meeting. It is now my pleasure to turn the meeting over to Dr. Clarence de la Chapelle, chairman of the Committee on Graduate Fortnight and associate dean of the Post-Graduate Medical College. Dr. de la Chapelle.
[ Applause ]
>> Mr. President, ladies and gentlemen, the first speaker of the evening, Dr. Albert Lansing, professor of anatomy Emory School of Medicine in Atlanta, Georgia. Dr. Lansing was formerly at the Washington University in Saint Louis where he was an associate of Dr. Cowdry, known to all of you for his work in the field of arteriosclerosis and also in aging and author of two of the finest monographs in these two subjects. Dr. Lansing began his career as a gerontologist with Dr. Cowdry in 1941, although he admits that his interest in gerontology goes back to his high school days. Although Dr. Lansing is an anatomist, he was trained as a zoologist and most of his work has been done on cell physiology. His activities in the problems of aging had quite naturally spread over all three fields. This evening, Dr. Lansing will introduce the subject of the Fortnight namely aging by presenting the Ludwig Kast lecture. His presentation has the provocative title, "What is Aging?" Dr. Lansing.
[ Applause ]
>> Thank you for your kind introduction. Let me say by way of opening that although it's not my usual practice to work from a written text, tonight I will do so. I found this time goes along but I have a tendency to say things in haste and repent them at leisure. I want to avoid that tonight. So that if I say anything that is gauche that is to be taken exception to, you can say Lansing said it with premeditation. I'll read my text. To be called upon to deliver this lecture honoring Dr. Ludwig Kast is of particular significance to me personally. Dr. Kast was a forward thinking man, who through the Josiah Macy, Jr. Foundation did much to further the development of research on aging in the United States. This is a matter of record. It's also a matter of record that my first postdoctoral post in 1941 at Washington University School of Medicine was financed by a grant for research on aging from the same Josiah Macy, Jr. Foundation. One might assume from the title of my talk that a firm definition of aging will be offered before I close. The assumption, however, would not be valid. According to my desk dictionary, "to define" is first, to mark the limits or boundaries of, to make distinct or fix an outline or character. Second, to describe, expound or interpret, to explain, hence to determine the precise significance of, to discover and set forth the meaning of as a word. And third, to set apart in a class by identifying marks, to distinguish. Now, any number of maladies of man or beast can be defined in accord with the preceding criteria, diphtheria, poliomyelitis, erythroblastosis fetalis and so forth. Diphtheria for example is defined in my medical dictionary as an acute infectious disease or toxicosis due to the presence of Corynebacterium diphtheriae. The disease may be attended with patches of false membrane in the throat or on other mucus surfaces, and the resulting absorption of diphtheria toxin. The disease is attended with swelling of the larynx and pharynx, consequent dyspnea, aphonia, and dysphagia. The general symptoms are fever, heart weakness, anemia and great prostration. Diphtheria continues from a few days to one or two weeks frequently ending fatally. It is extremely contagious. End of quote. This is a definition. The disease is delimited and set apart by identifying marks, a specific causative agent is indicated, the symptoms are listed, as is the time course and prognosis. But how can we do this for aging? What is the causative agent? When does a condition begin? What are the changes that occur in aging? What is the time course of the disease? If indeed we can call aging a disease. The only point that we can make with assurance is that aging invariably results in death of the organism. From a less academic viewpoint, the situation is even further confused by a lack of resolution between concerned with aging and concerned for the aged. The last 10 years, I've seen a phenomenal growth of interest in problems of the aged. Thousands literally are professionally concerned with the welfare of the elderly and the senile. With the tremendous increase in life expectancy that we are enjoying today and as much rooming steadily, our entire population structure stands the [inaudible] sharply. Thanks to the conquest of infectious diseases, more of us are living long enough to experience cardiovascular disease, malignancies and senile decay. Medicine is increasingly concerned with problems attending care of the aged patients. Further, with more of us living long enough to enter into post-compulsory retirement life, there is ever growing concern by social scientists and economists in annuities, retirement schemes and social security systems. Still others press for extension of retirement age or abolition of compulsory retirement. Entering into retirement usually signifies the beginning of a period of intense insecurity. Finances are inadequate, modern transport has spread families over hundreds and thousands of miles, so that the retired person with a very modest income or the couple cannot readily move in with the children. And even if the children did live nearby, modern housing is not designed to accommodate the presence of old folks under a single roof. The feeling of being unneeded and unwanted grows. It is into this bridge that the social workers attempt to step. All of these problems that I've been listening are real and severe but they are problems of the aged. When it comes to the problems of aging, the strategic rather than tactical problem, the academic issue, the questions of what is aging, why is aging, what are the changes that occur during aging. It is painful to note, at least for me, that there are less than a handful, literally less than a handful of serious, serious workers in United States in this field. There are probably a number of factors responsible for the pause of the [inaudible] scientist in [inaudible]. I hope that wasn't my voice. There are probably a number of factors responsible for the pause of the [inaudible] scientist in research on aging. Funds for research are more readily available for research on diseases of popular concern. But I do not believe that there's a serious shortage of funds for research on aging. More likely than not, the lack of clues that might direct research into specific avenues is primarily responsible. And appreciation of the apparent inevitability of aging, no doubt, displays many from doubling in this problem. I've already taken the view that a sound definition cannot be formulated now. It may also be noted that there is a surprising lack of variety in so far as theories of aging are concerned. Let us omit from our discussion that frankly irresponsible and the imaginative notions had cropped up from time to time, the [inaudible] fountain of youth sort of thing. Not much will be missed if in addition we omit from our discussion the theories of autointoxication resulting from intestinal putrefaction. Metchnikoff was seriously taken by this notion at the turn of the century. And although it faded more or less after Metchnikoff's death, every now and then a paper appears today urging that intesnical--I'm sorry, intestinal putrefaction is a cause of aging. Same objection that applies to the theories that aging results from failure of the cardiovascular system or failure of the nervous system or failure of any particular mammalian organs also applies to the intestinal intoxication theory. I have expressed repeatedly and will continue to express that aging is too fundamentally processed to be rationalized so simply. Aging is virtually universal. It occurs in plants as well as in animals. It occurs in animals without arteries, without large intestines and without complex nervous systems. Even in these relatively simple animals, without these complex systems, the process of aging follows a pattern much like that of man. The organism develops, goes through a brief adolescence, matures, enjoys a brief period of adult vigor, gradually declines and dies. To be taken seriously is the concept that senescence is due to the failure or deterioration with time of the protoplasmic colloid. Among the early proponents of this theory, Berdar [assumed spelling] and Marinesco, a parallel is often drawn between the in vitro aging of colloids as manifested by syneresis and the apparent loss of water from in vivo colloid system, protoplasm. Similar in principle but put more simply is the often expressed thought that aging is like the running down of a clock, the wearing out of an automobile part or a pair of shoes. The difficulty with this whole concept is that the living cell is not a clock, not an automobile motor, nor a pair of shoes. The latter are nonliving systems. They do not possess a self-synthetic mechanism. The living cell does. It distinguishes life from nonliving. A critical diagnostic feature of the living system is the capacity for self-renewal. It is an expression of this capacity for self-renewal that is measured and turned over studies with radioactive isotopes and similar techniques. Protoplasmic constituents are constantly being replaced or be it at varying rates. If in senescence there are old protoplasmic constituents present, it can only be due to inadequacy of the cell-synthetic mechanism. Indeed, it is not too far fetched to speculate that aging is primarily due to an insufficient rate of protoplasmic self-duplication. One last general group of theories on aging remains to be considered, although they vary in detail, all holding principle that in senescence, there is the progressive accumulation of toxic materials in the cell. These materials, whether they are held to be pigments, these so-called age pigments, crystals, insoluble compound or products of incomplete metabolism are supposed to interfere with vigorous cellular life. Some decades ago, Benedict refined this concept by proposing that in senescence, cellular permeability is decreased. More recently, I espoused this idea and elaborated still further by proposing that in senescence, the decrease in cell permeability is a product of an increase in the calcium content of the cell surface. Aside from the fact that there is very little evidence that cell permeability does decrease with age, these theories leave us in much the same quandary as we would be without them. Why should permeability of the cell membrane decrease with age? Or if calcium does increase with age, could decrease transport across the cell membrane, why should this happen? One is taken back to my earlier suggestion that aging may involve inadequate self-duplication, self--inadequate self-renewal, in this case, referring specifically to inadequate renewal of the cell surface. Now thus far, I have been emphasizing the things that we don't know. Perhaps, I've been too gloomy. There are a few observations that could well serve as takeoff points for further experimentation. First, I have in mind a relatively uncommon clinical situation known as progeria. In this disease of children, there is the appearance of many of the superficial characteristics of senility. Although the abnormal adrenal and anterior pituitary glands in the victims of progeria might point to an endocrine disturbance, the suggestion of premature senility is strong. As a matter of fact, many of these children die of coronary thrombosis before the age of 10 years. It may well be that the association between progeria and senility may be little more than a pigment of the imagination. On a long chance, it may also be that a profound metabolic disturbance does bring about premature senility in these unfortunate children. A comprehensive analysis of the clinical and histological changes in such individuals might be very rewarding. It hasn't been done as yet. Returning to tissues and cells, one comes very quickly to the liver, the happy hunting ground of biochemists and histologists. There have been a few studies of the nucleic acid content of young and old liver cells. One might expect a quantitative reduction in either or both the pentose and deoxypentose nucleic acids in old cells. Nucleic acids are thoroughly established to be associated with protein synthesis. Old tissue presumably is less capable of protein synthesis than young and hence should contain less of these materials associated with protein synthesis. However, Lowry and later Schultz [assumed spelling] found no significant change with age in the amount of either of the nucleic acids. Now, it may well be that the message employed were not sufficiently subtle to detect fine differences. That always is a possibility. Or it may also be that the physical structure of the nucleoproteins changed with age rather than their amount per cell. Certainly, the old liver cell is not as effective as a young liver cell. Mitotic activity in regenerating old liver is lower than that of young liver. Also, the radiophosphorus uptake of old liver after experimental hepatectomy is resumed. McKellar cytological analysis of rat liver is also interesting. During fetal life, there is of course a high level of mitotic activity in the cell. This means that both chromosomes and nucleus are dividing along with the cytoplasm to get synchronous cell division. Later, in the young animal, postnatally, one finds an increasing number of binucleate cells, cells with two normal occurring nuclei along with the products of normal mitosis. In this situation, it would appear that while the chromosomes and nuclei are dividing in synchrony, the cytoplasm is not. Still later, in middle life, [inaudible] cells increase in population density. Cells, appearing to be perfectly normal but its nuclei contains multiple sets of chromosomes. In this situation, it would appear that the chromosomes are multiplying but the nucleus and cytoplasm is lagging behind. This progressive failure of capacity for multiple patients may be taken as a measure of reduced growth potential. And this is my thesis, aging as a product of reduced growth potential. It is really a restatement of my earlier suggestion that aging must be a consequence of inhibited capacity for self-duplication. There is some evidence to support this view and nothing would please me more than to present the data in detail. But out of consideration for my audience, I will be or try to be very concise. Biologists studying aging are few, very few, and data are very slow and accumulating. One is compelled, as I have been, to cite the same work over and over and over. I don't want to confuse the audience. Chronologically now, Sonneborn's experiments in 1930 should be listed first. Although Sonneborn was not particularly interested in gerontology at the time, his observation on the flatworm Stenostomum incaudatum represents one of the major advances in the field. His experimental animal, this little flatworm called stenostomum, was presumably genetically homozygous and raised under standardized environmental condition. Reproducing age sexually, this flatworm multiplies by transverse fission. It give rise to anterior and posterior daughter organisms by simple transverse binary fission. Now these two daughters differ in one significant respect, the anterior product of division receives the head of the parent, the mother, and much of the trunk, and has only to regenerate the tail component to become a complete offspring. The posterior product, on the other hand, of this transverse fission, must regenerate a full head and much of the trunk. It carries from the mother only a small segment of the tail. Thus, the anterior daughter experiences very little cell multiple patient and growth while the converse is true for the posterior daughter. This is an important point. In the design of his experiment, Sonneborn segregated these fission products in isolation cultures and established two contrasting lines of purely anterior or purely posterior products through a long series of generation. Bearing in mind that all the lines were genetically uniform and nurtured under standardized environmental conditions, one might expect comparable lifespans for all of these lines. But this was not the case. The min lifespan in days for all of the anterior lines, those which had very little growth, was 35.0 plus or minus 1.1, while for posterior line, lines that regenerated most of the body, for these posterior lines had a min lifespan of 63 and a half days, to live 77 days, and the last two lines had lived 115 days at which time the lines were discarded. It would appear then that lack of active growth in the anterior line is coupled with the observed, reduced longevity. Several years ago, I made a comparable series of observations on a multicellular but microscopic freshwater organism, the rotifer. The rotifer's development is determinate. All of its cells are formed during embryonic life and hence are of the same age, the somatic cells as well as the germplasm. In addition, since its reproduction is parthenogenetic, all the reproductive products of an individual are genetically identical. Using a standardized culturing technique, I attempted to determine if the progeny of actively growing adolescent rotifers had different lifespans than progeny of full grown and elderly mother. As in Sonneborn's experiments, two types of divergent lines were established. One was composed of successive generations of firstborn rotifer. The other, consisted of successive generations of descendants of full grown for elderly mother. In the lines of rotifers derived from adult mothers, the min lifespan decreased in each successive generation until the line became extinct and the number of generations required to bring the line to its end depended upon the age of the mother. Lines derived from elderly mothers died out in four generations, from middle-aged mothers died out in eight generations, and from newly matured mothers, in 17 generations. Apparently, a capacity for reducing longevity is transmitted through the adult rotifer age. This does not occur in lines of rotifers from actively growing adolescent animal. Longevity of each successive generation in the adolescent lines is greater than that of the preceding so that in experiments carried some 54 generations, rotifers were developed whose longevity was at least four times greater than that of the original stock. The eggs of actively growing rotifers do not contain or at least do not express the capacity for reducing longevity. There were a number of interesting ramifications to these experiments but they are not essential to this discussion. One intriguing point does come up. How does one reconcile these observations with Weismann's concept of the immortality of the germplasm. If our observations are sound with the rotifers, it would appear that the germplasm of the adult of at least this one species is as mortal, just as mortal as a [inaudible]. Perhaps the concept should be modified to this extent. The germplasm of only the actively growing young individual is potentially immortal and perpetuates the species. It may even be that aging of the species results from conditions favoring breathing of adult and elderly individuals. We still have not defined aging but can we at least develop a reasonable description of the process. Aging certainly is not advantageous from the point of view of the individual. It always has a fatal outcome. Time is of the essence and last, aging occurs when growth slows down or stops. Aging then is a process of unfavorable progressive change usually correlated with the passage of time, becoming apparent after maturity and terminating invariably in death of the individual. That is a situation as I see it in 1955, of course, I may be wrong. However, it's interesting to turn the clock back, and if I may take just another moment or two, to quote Raymond Pearl in 1928, we'll go back almost 30 years. And I'll quote several observations, several generalizations he made. He poses two of the broad problems in the problems of aging. The two big issues to Pearl were. First, why do living things die? What is the meaning of death in the general philosophy of biology? Second, why do living things die when they do? What factors determine the duration of life in general and in particular? And what is the relative influence of each of these factors in producing the observed result? There are five generalizations according to Pearl that can be made with assurance that could be made in 1928. First, there is an enormous variation in the duration of life both intra and interracially. That is a sound observation we can all agree. Second, there is no generally valid orderly relationship between the average duration of life of the individuals composing of species and any other broad fact now known in their life history or their structure or their physiology. And by that, he is referring to the correlations that have been attempted between metabolic rate and longevity, the number of heartbeats and longevity and so forth. And I personally would endorse that statement. We have no generally valid orderly relationship between any known process and aging. Third, natural death as distinguished from accidental death is preceded by definite structural and functional changes in the body. For myself, I would say certainly there must be structural and functional changes but we haven't found them yet. Fourth, naturally death--natural death occurs normally and necessarily only in animals composed of many cells. This since has been shown to be not true. Protozoa, under many conditions, age and die just like metazoa. And last, life itself is a continuum. Natural death is a new thing which has appeared in the course of evolution. The somatic death of higher multicellular organisms is simply the price they pay for the privilege of enjoying those higher specializations of structure and function which have been added on as a sideline to the main business of living thing which is to pass on in unbroken continuity the never dimmed fire of life itself. That is Pearl and not Lansing. This was the status of affairs 30 years ago. It is remarkably unchanged. What I have tried to do this last 30 minutes is to draw a sharp line between the problems of the aged and problems of aging. Because of the rapid changes occurring in our population structure, we are urgently concerned with issues involving clinical management of the senile, social and economic ills of the elderly. The biology of aging, the studies of mechanism of aging is lagging seriously. Yet in the long run, I strongly suspect that much of what we can do in at least the clinical area concerning the aged will depend upon developments at the biological level. As Dr. Robert Moore has very actively said not too many years ago, "The biology of today is the medicine of tomorrow." Thank you.
[ Applause ]
>> Thank you, Dr. Lansing. Next speaker is Associate Professor of Industrial Hygiene of the Harvard School of Public Health. He has specialized in the problems of industrial psychology, physiology and medicine. He has published many papers on the effects of oxygen want on the central nervous system and also in the field of aging. Dr. McFarland studies combined extensive laboratory investigations as well as field observations in all parts of the world. In 1935, he was a member of the International High Altitude Expedition to Chile where studies were made of miners who lived at an altitude of 18 to 20,000 feet, or rather they lived at 18,000 feet and worked at 20,000 feet. As a consultant, he organized the medical program, one of the largest airway systems of the world, and directed the flight fatigue studies on the air cruise and opening the initial flights both across the Atlantic as well as the Pacific. Incidentally speaking during this evening when I asked him when he first became interested in problem of aging, it was about at that time with his contact with the pilots and these so called fatigue study. Well, many of you know Dr. McFarland because of his two recent books on aviation medicine, the first one written primarily for engineers entitled "Human Factors in Air Transport Design" and the other for industrial physicians or for the public in general as well as physicians, "Human Factors in Air Transportation". Dr. McFarland, this evening, will discuss the psychological aspects of aging. Dr. McFarland.
[ Applause ]
>> That's a good one.
[ Inaudible Remark ]
>> Thank you. Thank you very much, Mr. Chairman. My topic this evening is the psychological aspects of aging. It is interesting to point out by way of introduction that the current medical literature emphasizes disease and disabilities of the older person. The current physiological studies stress the gradual impairment of various organic functions or loss of capacities. In current experimental psychology literature, the interesting fact is brought out that many abilities are maintained longer than previously expected and in fact, some of them are advanced beyond what we had originally believed. And my objective this evening is to review some of this experimental literature for the physician and to point out areas of overlap and to try to give a general orientation of the psychological point of view toward this problem. Before doing this, I would like to outline briefly three or four basic premises upon which my remarks ought to be based. In the first place, psychologists, as I'm sure many of you do, recognize that it is important to consider the functional ability of a person to do a job rather than merely his chronological age. It is also important not to take too seriously group means in this area when one understands the spread that exists within each age group. Therefore, it is important to consider the range of abilities, and I submit that the only true way we can understand about aging is to [inaudible] the individual longitudinally and to judge him on the basis of his individual characteristics rather than to try to attach him to an age group. And I think that it is important to point out that age by itself or in itself is not detrimental. Therefore, I am submitting that this person should be studied as an individual for his job in relation to the age that he is and as he grows older. The second basic consideration relates to the fact that the average increase in longevity and its implications for vocational adjustment implies that a person must be continually studied and that we must not consider averages alone. Changes in skill and mental adjustment should therefore be related to employability. And I think most of our group averages for ages are wrong because of the change in the nature of the age composition of the population. Not long ago, Dr. Paul White brought to one of our classes one of his prized patients who is 104 years of age. And he asked this man, Mr. Terry [assumed spelling], what he thought was the most--something about his past history and he said, "Well, Dr. White, the most interesting thing about my history is that I had pneumonia just 100 years ago."
[ Laughter ]
I hope he's as successful with his presentation. Now I think the important thing to point out is that these older people are changing the nature, the general nature of the population, and that we have to look at the individual throughout his growth period rather than to try to attach into age range. Therefore, the physician should aid in the continual reevaluation of an individual as he grows older. The third basic consideration relates to motivation and interest. All the evidence from psychological study shows that the older person, if he wishes to learn and wants to learn can learn. And if he maintains a variety of interests and adapts to changes and participates in community activities, he is able to make a successful judgment into his later years. Now the role of the physician it seems to me on this process, to anticipate at age 45 and 50 years of age the problems that might arise at 70, just as an engineer should anticipate the defects in the use of equipment and defects in the design to prevent errors so the physician should attempt to anticipate if possible the anomalies at a younger age which might be of importance later. I've had an opportunity to follow a group of 240 problem medical cases with physicians and a group of airline pilots. And actually, only 10 percent of them were permanently grounded and it was possible to demonstrate very clearly that the longitudinal study was very revealing. Now, I want to give brief examples in the field of sensation, psychomotor skills, mental and emotional studies, the results of investigations to try to point out and verify some of these generalizations which I have made. First, let us look at the question of aging in the field of sensations. All of our sensations manifest changes to some degree and to some extent but the important question is, what is its significance in the areas of smell, and taste, and vibration, and pain, the changes are probably of little significance. In the field of vision, we could take examples such as demonstrated here on this chart of the changes in the range of accommodation with age plotted against years and for our visual acuity plotted against years and we have a fairly definite types of curves. But the loss of elasticity of the lens and the narrowing in the range of accommodation, we do have methods of correction and it is important to see that by understanding these changes and using the proper age, it is not difficult to adjust the person to various types of jobs. I want to mention briefly an experiment that we have carried out in the field of night vision, which has a high correlation with age. We found that if we carried out a night vision test, we had 200 subjects and this top part of the curve relates to the cone adaptation, the last part the rod adaptation. And if you put a bright light on the subject side and then follow their ability to see at low levels of illumination under carefully controlled situation, you get a curve of this sort. We took the best point in the curve, the best final rod adaptation--cone, rod adaptation and correlated it with the age and is brought out in the next slide. We obtained a very interesting and a very high correlation. Actually, it was about 0.85 between age and the final point of rod adaptation. For each 13 years, the intensity of the dim light had to be doubled to be just perceptible. Now this is of considerable interest in regard to putting tinted windshields in front of an older person who is driving at night. The tinted windshield is like putting an optical wedge which cuts out about 30 percent of the light. And then if you add to that the change with aging, it is important. Now, if you were considering this from the point of view of a truck driver, say, who is driving at night, he would experience difficulty and maybe at 50 years of age would have to be grounded or taken from the job. While if he was carefully studied and put on a daylight job, his active life could be below. So that it is possible to take the data and consider its significance in these different fields, and I submit that if these differences are carefully followed, you can aid in prolonging the useful life of the worker. Now, just for a moment let's look at the field of hearing. The decline in the higher frequencies, the well known fact in the field of hearing, the deaf old man, is a problem not because he can't hear but because he won't wear his--wear his hearing aid. I have an English friend who's very hard of hearing and he introduces you to Herbert, and Herbert is his hearing aid and that's a part of the man. And you would expect that in his makeup from the way he acts and it doesn't destroy anything. And in the relationship with the man, it makes it more interesting and amusing. And he doesn't--be able to hear a thing. Now, if you take such a slide as this, you would see that out beyond about a thousand cycles per second, there is a greater spread because there were a large number of older subjects in this group. Now, if you were showing this to an acoustical engineer, you would say that the engineer don't put a signal out here, at a 4000 cycles per second because you will penalize the older man. And if you are looking at this in relation to say any vocational aptitude as possibly inclined, this happens to be studies of pilot, you would want to know the significance of this decline. And a regulation was going to be passed to say that a pilot whose hearing would drop below about 30 decibels at this range would have to be grounded. This would have grounded about 300 men. So we challenged this and said that it was important to test the men in the presence of noise because the older pilots had said, we do hear everything we have to hear and it seems unfair. So we pointed out the fact that is brought out in the next slide that in the presence of noise, the person who is hard of hearing actually heard almost as well as the normal subject because of the recruitment phenomenon. And you'll note here on sound intensity at the bottom, it is plotted against loudness level and the noise decibels that in this subject, that the recruitment phenomenon thought is hearing back to that of a more normal range in the presence of about 70 decibels. And those of you who are hard of hearing probably have recognized this fact. So the point I'm paving is that we must understand and know this phenomenon and relate the defect to the requirements of the job and try to prolong the useful life of each worker and to understand these changes that is possible to do that. When a union heard about this and found that we had prevented about 300 of them from being grounded, they asked now what other subjects can we study. We had wonderful collaboration and cooperation from that. We did not compromise anything in regard to safety here. I'm sure that it was worth our [inaudible] to all concerned. Incidentally, flying was originally to be a young man's vocation. I would to point out at present there are 1000 private pilots over 60 years of age who hold medical certificates. There are about 300 airline pilots over 50 years of age and about 50 approximately 60 years of age. The important point here is that we must know when does compensation no longer--when does it no longer overcome the declining functions with age. If compensation is present, there may be a defect in certain areas but the subject is able to make a successful adaptation, and this holds true in any vocational skill. Now, what about psychomotor functions and skill? We recognized that there is a gradual rise in youth as brought out in this slide and it is followed by a slow decline in the maturity. I think driving an automobile is an interesting skill to consider and we recognize that older people are able to make this adjustment quite successfully. The older person requires stronger signals and more time to relate new data to relevant material in past experience. And if allowed more time, he will not get muddled. Well, in industry, the important thing then is to replace the man and have him do work where complicated material does not have to be carried out against limited time intervals. And if he is allowed adequate time, he can do the work successfully. So why put a man in a position when he gets beyond certain age ranges where he must do the work so fast that it's possible to use his judgment and experience and place him--continuously replace him on the new job in relation to these abilities. Well, what about mental functions? Mental ability, which might include memory, learning, imagination, and thinking is a more complicated type of thing that we have recognized that it can be measured through mental test. The slide shows the results of a large number of subjects, three different studies and getting somewhat the same result. You will note that the peak is around 20 years of age and if one goes out to measure test of abilities, we just saw it, that they tend to come to a peak there and gradually decline. But I would like to point out here again that it is based upon speed and time limits and other types of judgments might fare quite differently. For instance, in a vocabulary test, in one study it was shown that there was an improvement up to 60 or 70 years of age with older individuals and when they were compared with the aged in institutions who did not have a chance to use vocabulary, they were much poor in their scores. And it would appear that the brain is a function [inaudible] an argument, that it has to be used the same as any other organ of the body. And if you cannot keep actively engaged in some sort of mental activity, the organ will change as apparently in other organs of the body. Some years ago a very elaborate study was made at Columbia University in adult learning by Professor Thorndike. And all of the tests showed that no one under 45 should hesitate to learn new jobs or to carry out new task. And I would submit that this probably could be extended to about 55 years now. Well, let us take a mental function such as memory, immediate memory. Any older person will recognize some change, memories scores are poor at 65 than at 50 years, but we don t know how much poor. And meanings and judgments and standards of excellence are not so much enclosed in the latter, that case. It's very interesting nowadays to obtain the list of professors who are retired from universities of 65 years of age. They get on a list and they find a job in a [inaudible] distinguished institution and they carry out their jobs quite as successfully and efficiently. And I think possibly our whole concept of retirement will have to be changed, certainly if my definition is going to be carried out, if you judge a man in relation to what he can perform or do and not on the basis of his chronological age. Now, I believe that these functions are tied up. The underlying mechanisms dealing with such a thing as memory are related to an interference of oxidation, either delivery or utilization or some interference in this process. And I want to just briefly mention two studies in this area. Here is a slide which shows what happened to immediate memory as we went to a higher altitude in the Andes. We could not remember as well, it is well known, just as you drink a lot of alcohol, your immediate memory is not so good because somewhat the same end result is taking place. There's an impairment of oxidation. Well, I took college students and put them in the altitude chamber and I found that their memory function dropped to 12 or 14,000 feet about the same as their professors when they were about 60 years of age. So, that you can take a younger person in a function of this sort and demonstrate the change. The same thing can be demonstrated as shown in the next slide in regard to light sensitivity. Here are the results of a diminution and light sensitivity plotted against altitude. And you can see a fairly regular curve here. As the altitude goes up here at--the first effect is around 4 or 6000 feet which is one of the most sensitive tests we have in this field. And here at 18 or 20,000 feet, there's an increase in the threshold of about 200 percent. So I would suggest that the older person's decline in this function, memory or light sensitivity, is due to the influence of lowered oxygen due to changes in volume radar diffusion or some other factor. Well now, if there was time, I could develop the thesis that our concepts about the older worker in industry have been false in the past. Certainly the last war demonstrated very clearly that the older workers could come back and do a job successfully. They have--There's a lower labor turnover for the older worker, there are fewer accidents, there's less cost to retrain new employees. The output is about the same, there isn't a marked difference in output unless this time factor that I mentioned is brought in or unless something involved in physical lifting or physical work is involved. There's less breakage or spoilage and they're loyal and stable. And I think there has been a shift. One very interesting thing about it relates to the accident rate. I could demonstrate with 15 or 20 slides from different studies to show that older workers were safer. If you watch them on a production line, a younger man may let his hand get out of sight but not an older worker, he'll watch his hand. Moving pictures have demonstrated this type of response in many others to show that the older worker can do his job. This next slide brings out a very interesting point, I think, in regard to accidents in general. You know here that in this country, the accidents from 1 to 24 ranked first. This is based on the bureau of the census study in 1946. And accidents ranked second, the heart disease between 25 and 44. And recent data would suggest that this age range shifted over and that actually accidents ranked first from about 1 to 40 years of age. So that we have here a behavioral factor that--or factor that is of great significance, and it's the younger person who gets into trouble on the highway. It's the younger person who has the higher accident rate in industry. So here I can point out that our ideas about this type of performance was changing and it has changed. And it is advantageous to the older person. Well, what about personal and social adjustments? We need more studies in this area. We need longitudinal studies and not cross-sectional ones. A group of 20-year-olds differ from a group of 50-year-olds but this doesn't tell us what current 20-year-olds will be 30 years from now. The emotions and interest and attitudes undergo changes with age but no formula is available. It is often said that the older person has fewer interest or that they are less adjustable to social demands or that they have difficulties of adjusting. But this is difficult to show in terms of group averages and actually it is necessary to watch the individuals for a period of time to get a fair understanding of this aging process. And we emphasize speed in our mental test, we emphasize speed in our work, we have speed and youth as a part of our social doctrine. But I suggest that this might be only a part of our emotional immaturity, that it isn't necessarily a basic concept that we have to follow. And I suggest therefore that if we are to understand the aging process, it is necessary to consider the individual throughout a lifetime and not pay too much attention to these averages by group decades. I suggest further that it's functionally what a man can do on the job that is important, and to analyze these changes in relation to the profession or the job. And I think we have many stereotypes in this field that current psychological research is tending to break down. And we also note that with more complex mental functions, the older person is more resistant to change. And I think that there are many points that can be developed in industry to show the place of the older worker in industry and also in many of the professions. So I suggest that the physician, in dealing with older people, if he can aid in keeping his patient with a broad and wide variety of interest, if he can get him to accept personal and social change and if he can participate in community activities, he will do much to prolong the useful life of the individual.
[ Applause ]
>> Thank you, Dr. McFarland, especially for your very encouraging remarks, at least very encouraging to those of us who are possibly half century long. The third and last speaker of the evening, a professor of nutrition at Cornell University. Besides being a biochemist, he is also a scholar in the field of aging. I might say that his interest in aging was stimulated more than a quarter of a century ago when he was a research fellow at Yale under Professor Mendel, who is a pioneer as you all know in the field of nutrition and metabolic disorders. On one occasion, he asked Dr. Mendel if retarded rats would have a longer span of life. The reply was, "You are young, try it." And so, for the next quarter of a century or more, Dr. McCay has been trying it. Dr. McCay will tell us about some of his experiences with experimental prolongation of the lifespan. Dr. McCay.
[ Applause ]
[ Inaudible Remark ]
>> President Donovan, Chairman de la Chapelle, guests and members. In the year of about 1200, Roger Bacon said that man had unique opportunities, that he had many lower animals that live relatively short periods, that man himself live relatively long. Therefore that man had the opportunity to study aging. About 700 years have passed since Roger Bacon wrote his Opus Majus and still we've made relatively little use of either our domestic animals or of man himself in the study of aging, at least experimentally. And before going into the subject of animals, I may say that I myself, I'm often appalled at our waste of opportunities with human material. We have thousands of people in our mental hospitals that we are boarding, that we are keeping from youth until they die in old age, are feeble-minded. We have equally large numbers of life terms and we're making practically no use of them. There's a vast reservoir of useful material there that would be--It should be easily used with an asset for research and as a--and a pleasure to those with whom the experiments are made. That was driven home to me a few years ago when we were developing a new diet for these fast--feeble-minded up at--New York. And we were working in the female ward with about 200 patients there. I was constantly interested as the--we worked week after week at the interest and the new life that came into that ward as a result of the experiments that were going on, how much interesting work we had and how it seemed to--what new life even into a group of low-grade spastic feeble-minded. And I think this was called to our attention many years ago by [inaudible] the famous biochemist at Harvard, when he said we were missing these great opportunities and we're missing them today. Among the people that seem to be making some news of such material are the dentists and perhaps it's easier to do dental work under such conditions than any other type of nutritional work. There have been recently some very interesting studies from Sweden where the dentist have used such material. A few years back, we did succeed in starting at Sampson, New York. We do out of the mental hospitals 8 or 900 undisturbed patients or relatively undisturbed. They were concentrated there at Sampson and then unfortunately Commissioner [inaudible] had to leave and the air force took the hospital back again. Well, the patients had to go back into the wards that are safe. That was our prayer there. Again, before entering upon the subject of animals, I was looking at the old book collection today that the librarian and Fred Zeman [assumed spelling] have gotten together up there. It's a very interesting book collection. I wondered why they didn't include the work of James Bennet up on nutrition written in 1876. The last chapter in that book which went through three or four editions, Bennet's nutrition book, deals with why do physicians die prematurely. And we solved that problem today. He said even at that date, 75 or 80 years ago it wasn't due to coming back with contagious diseases. That was common theory then. That really we doesn't know. And I've often wished that some of the class such as the one that used to write in occasionally from PNS, the class of 1900s, was trying to study itself and do what it could to increase the active life of that class, the class of 1900. What would it mean if we could increase the active life of our physicians even five percent? And how can we do it better than careful study? I have been interested in recent years in noting newer types of leadership and perhaps that is going into--in that same direction of getting at this question of why the early death of many physicians. And I noticed while I was abroad the last couple of years both in Switzerland and Germany that there's quite a movement for better food, better living, and overall picture and using that movement as being spearheaded by physicians. I noticed it was in Switzerland. So--and I believe the same thing is happening here. Now, to come back briefly to animals, and I must review for a few a minutes our work of the past 25 or 30 years, I hope it doesn't bore the veteran gerontologists that I see in this audience such as Ali Randal [assumed spelling] and Henry Simms [assumed spelling] and Dr. Lansing. But I thought it might be well to lay a basis and in the last part of the discussion this evening, I'm going to present totally new work that's never been presented before. And I suppose there's quite a hazard in that too in presenting a new research for the first time. Now as--We've worked with animals for more than a quarter of the century. We have often challenged the philosophy of Metchnikoff that Dr. Lansing mentioned this evening. In one sense, Metchnikoff believed that there was natural death in old age. You remember that Metchnikoff said the insects get through a cycle and die in old age. Interviewed quite a few people or very old, he said that many of them are dying naturally. They want--as natural as going to sleep. I am certain in our work that we have come to feel that we never see any natural death in old age that is not complicated by disease and in our animal work. And I'm sure that has modified our thinking. Now in nutrition, a few of the large basic problems that have--That we've often neglected in the past and are still neglecting to a certain extent, I think first concerns adaptation. And we could cite just a few examples of adaptation and nutrition in regard to old age. A few years ago, we were studying the problem of oxalates and we in nutrition have for long thought that rhubarb at high levels was dangerous, and spinach because too much could be eaten and wasting calcium. Well, we started studying animals and pretty soon we found that in very early life, there was a way to get calcium from oxalate, but just keep up that feeding and pretty soon the animal adjusted to it and it was able to use calcium in presence of oxalate just as effectively as it could without the oxalate indicating that the animal body has tremendous powers of adapting itself. And that's come into the calcium work the same way in nutrition in recent years. More and more we've come to realize that if an animal is kept upon a low calcium diet for much of its life, it can [inaudible] to old age and not lose calcium as readily as if it's been up on a high calcium diet from [inaudible]. And that's all the riddle of many of the people through the world that live upon perhaps two-tenths of a gram of calcium a day, whereas we try to have a gram of calcium per day. Another--That is a problem of adaptability to a specific diet. A second problem of tremendous neglect is the problem of imbalance. The literature from time to time reports many case of imbalance, imbalance among vitamins. Too much of one vitamin throws off another vitamin. Imbalance among trace elements and you remember some years ago the work of Fisher. He shifted the trace elements--I can't remember whether it's the copper or the manganese--in the diet of his mice and he found that he shifted the diseases of old age in his mice. By just a shift of very small amount in a mineral element, he changed the category of diseases, as the terminal diseases in his mice. So we have then a problem that's been very little study, the question of imbalance and the literature is little known because it doesn't help solve vitamins in trace elements. Well, the literature is more or less obscure. Many people in studying old animals forget that the animals they are studying are often suffering from many diverse diseases of old age. A week ago, we sent two elderly rats to Harvard. They phoned around over the country, the endocrinologist hunting some rats that were a thousand days old for males and they couldn't find anything at all. That's equivalent to phoning around over the country and hunting some old people to study that are 100 years old. They're phoning around for thousand day old male rats. But they finally phoned us and we said yes, we will intensify you with a couple of thousand day old male rats. But as we told them--as we did that, we told them certainly you must remember that those rats are probably heavily diseased. They probably have tumors, they have [inaudible] certainly. They're not just old, they are also diseased. A few years ago, I attended a conference right here in this hall in regard to reproduction in old age and the effects upon the quality of offspring. I heard the usual work upon mongolism in the human being. And then I heard a number of reports on mice. They were largely by geneticists, and not a single geneticist that day mentioned the possibility that this old mice might have been diseased at that the time of reproduction and that might have had a rather profound influence upon the young. So I think we constantly need to be thinking we're dealing with both disease and old age at the same time. I'm sure you all think that way. Now, to come down to specific work as your chairman mentioned and the--regarding retarded growth. And we've been studying retarded growth for about 25 years. So, we have come to believe that probably the best way we can find to produce very old animals is by the retarded growth method. Give an animal superb diet but never give it enough and keep it from growing throughout long periods of its life. With that I'm going to shift over to a few of the slides and the--I first just want to show one basic fact that always comes out in any rat work before going into the retarded growth [inaudible]. The first place we actually always see the sex difference with just occasional reversals. The female rat like a human being tend to outlive the male. This is just some--a random data sheet that I picked out here and you'll notice with one exception. But occasionally we get these reverses in our studies not always gives us hope that someday we males can learn the secret of the females because once in a while we'll get a reverse like that down there in the [inaudible] group where the males win. Using, however, in all our experiments with rats where we start with large mixed groups, we always end with a population of females. The next slide. And again, I want to call attention to a difference between the sexes that are consistent in our data. You'll notice the difference in bone density there, that the female usually have the denser bones. And again, one more fact, you can modify the conditions of the bones in old age. You'll note there that--and we repeated this experiment a number of times. We used diets that contain large amounts of milk throughout the whole of life. The animal ends life with denser bones. One experiment upon adaptability that I mentioned earlier is that concerning oxalates. And if you look at that chart at first, the animal suffered from loss of calcium in the presence of oxalate in its diet. Then it adapted and when the rat was about 80 days of age it began to assimilate oxalates, time it had gotten over to be 100 days later equal a 10-year-old child is doing about as well with oxalate in a diet as it was without it. Now I've taken one of the pictures of some years ago. A retarded growth picture and that you'll see readily the difference between these rats. These rats are both equal to people 96 years of age, approximately. They started life at the same time. The rat on the right was the rat that was retarded in growth. The rat on the left is a typical normal old rat. We could have reversed that picture very easily, in other words, man has it within his power to predetermine the aging of an experimental animal and that's what Roger Bacon wanted him to do which is just as readily have reversed that whole picture and has the aging in the other rat and the young rat on this side. That experiment would be then repeated in several times. Our laboratory, it takes about 5 years to do a total experiment of that sort. We've repeated it three times. And this is hope. Now what would this do, it shows that we can throwback the terminal diseases.
[ Pause ]
The reason this rat is young over on the right is for some reason or other the terminal diseases have been kept and that animal is staying young. That means we have it in our power to control this matter of aging. A similar experiment where they were kept back in growth for various periods and this group of rats at this time was equal to man about 70 years of age. The rat on the extreme right had never grown up yet. The rat in the--that 700 days of age equal to man 70 years old has just grown up. The rats over here on the extreme left grew normally, they have grown old. The rats on the right will go to the funeral of the rats on the left. Now when rats do grow up under such condition what happens to their size, and we can take any of the bones, we can take one of the long bones. And here's a tibia. You'll see that the rat never gets quite as large. It is always slightly smaller but not greatly smaller. It all--It can attain growth even when it's retarded until it's equivalent a thousand days, is equal to a man about a hundred years of age, before you allow it to grow up. It does a pretty good job of growing up even then. In the--A retarded rat you do not see tumors. The retarded rat behaves a lot like you and I would like to live. It lives a very long life. It has youth. It has apparently good health then after it does grow up, it terminates its life really quickly, usually from lung disease. In a retarded rat we do not see tumors such as this. In our normal rats we see about 12 percent of tumors of this type in other words among the terminal diseases that are checked are the growth of tumors. Now that was first observed by Moreschi [assumed spelling] about 1906 in Ehrlich's laboratory. He found that if that time that he could not transplant tumors into partially fasted mice, the tumors couldn't take. Now this is an experiment of similar nature, and again one that's--has been repeated by a number of times and by others. In growth retardation something happens that one no longer can get the tumors. The question of reproduction comes up and in the course of 25 years we've studied the effect of early sterility in both sexes compared to having fertility continue as long as possible. Now this female rat here is equal to a woman about 75 years old. And it is the oldest--It's a champion normal animal in our laboratory in reproduction. What happens to reproduction in retarded rats that are going to live much longer? It usually ceases somewhat earlier. They're usually sterile. The oldest litter we'd have in a retarded rat is a 17-month litter equal to a female--to a human about 50 years of age. In other words, you may have sterility in the female but it doesn't influence the length of life. We've done the same with the males by putting them up on diets marginal in vitamin E. The rats may grow, become sterile very early but it does not influence the span of life.
[ Pause ]
Now, to go to new experiments that we have just started in the laboratory, they again are extension of some earlier ones and you can form your own judgment. About 1947, we started then studying calcium 45 in rats diets because we wished to use it as a tracer with old people. We're trying to determine the level at which we have obtained injury. We ultimately established that level, in that group of rats everyone died with bone tumors. Now a bone tumor is very rare in the normal colony of rats, I think in the course of about a quarter of a century and that we usually operate with about a thousand rats in our colony. We've seen two cases of bone tumors which is and our rats live about two years each. In a case of rats fed calcium 45, shortly after weaning for two weeks at a given level we see nothing that we can determine. We can't find any changes in the blood, no other changes but when that rat comes in the middle age then it develops bone tumors and every rat at a given level dies with the bone tumor. They come on the growing points of the bone. In other words, something happens during that two weeks immediately after weaning in relation to that calcium 45 that predetermines that that rat shall die with a bone tumor. Now below the crucial level we see no bone tumors in rats. And now during the past summer we've started these experiments, we have said to ourselves and that you can hazard a guess because we don't know. If a rat is retarded in growth what are we going to see in regard with the bone tumors? If it's retarded in growth and fed calcium 45 just as a normal, will those bone tumors become more prevalent and at lower levels of calcium 45 radioactive material because the rat's going to live longer and will get a chance for it to develop or can retarded growth defeat the bone tumor? We've set that up with both rats and with hamsters and we'll not have an answer of that for 2 or 3 years probably. But that's a question of retarded growth and we set it up not only with the rats this time but we've also set it up with hamsters. We've asked our beagles the same questions, our dogs. We've fed them the same level of radioactive calcium at the same--for the same length of time after weaning and we've had no bone tumors, I think they're now in the second or third year. Long after the rat would normally develop the bone tumor, the dogs haven't done so. All that we got with them, the shafts of the long bones thinned down. We had some fractures which we detected with our x-ray but no other changes. In other words, is there are wide species difference between the development of tumors from radio active materials. That's another picture, there's the x-ray picture of one of those bone tumors. Now to come to the newer research that has not been reported before. About 3 years ago, we decided to determine if we could make use of the--of parabiosis in the study of aging. As you'll remember that's an old operation. In one of the reviews it said that it started about 1860 in Claude Bernard's laboratory that Paul Barrett the famous aviation physiologist of his time started this type of operation where you established capillary circulation with young littermate rats. And we asked ourselves first if you'll use this parabiosis, can you get those rats into old age if you form this union when they're young and this was the first pair of littermates that we did in the laboratory. These lived until they were 527 days of age, that's equal to people about 52 years old. Now these were littermates and most of the work in parabiosis has been done with littermates because you run into these skin reactions the same you do in human beings in a very difficult time in getting your incision to heal between the two rats. This did tell us though that parabiosis might have some use in old age studies. So we decided to extend that field of work. We made only one study of interest in this other than keeping these rats until they were at that age. We finally killed them because one developed a bladder infection. We knew it only could be a matter of time until we'd lose the pair. But Dr. Rachel White [assumed spelling] was in our laboratory from University of London, she's a bacteriologist and she was comparing the intestinal flora of old and young rats. And she had found that the variability is chiefly among the yeasts that she gets marked differences in old and young animals in the distribution of the yeast. She's going back to Metchnikoff work there again. But she made a number of studies of the distribution in the microflora of the intestinal tracts of these two animals which have been parabiosed since youth and found each carries a distinctive microflora. We didn't expect that because they've had the same food since they were youngsters. They've gone into old age in this condition. Now just a few more pictures, I put a few of the surgical pictures. This is Dr. Frank Pope [assumed spelling] working last summer and I just put a little of this in. He has done the surgery and I thought you might be slightly interested in this operation. It's not a difficult one and just another picture. These are the rats. Now he has found this in the--The anesthetic is very important and it must be carefully controlled as well as the surgery. Now this is a pair that was done last summer and you can see these are quite normal rats, these are live in the laboratory that day. If I could have stayed two weeks, I would have brought these down and we could have a live exhibit instead of photographs that I have downstairs. This is a pair of non-littermates. And you can do non-littermate in parabiosis but it's difficult. Now if we're ever to do aging work I think we've got to develop the techniques so that we can be successful with non-littermates. Now it comes the problem, can you parabiose rats of very different ages. And we decided we'd use a special technique to see if we could get around these skin reactions. We'd combined our earlier experiments of retarded growth and at the same time try to get the same genetics. So what we did was bred--had a series of litters from the same parents but had them at different stages, you can do that with rats. And so we finally had litters that were born at 240 days difference in interval, that would be about 24 years in the life of a man. So we then had available rats from the same mother and father but 240 days different in age. In other words, one was moving into middle age and one was shortly after weaning. Now can you parabiose two very different ages, established your capillary circulation and we succeeded in doing that. Those rats are alive today. We have a number of pairs of those now. That means we have been able to parabiose a rat equivalent to a person about 6 years of age with one equivalent to a person about 30 years of age. And you run--when you do that, you run into a number of very unique problems, you're running not only in a difference in anesthetic requirement for the two very different ages, you run into a difference of skins. And then you finally you run into a difference of temperaments. We also did hamsters. This is the first time it had been done in our laboratory and I'm not sure they've been done before because the hamster affords another very useful animal for old age study. And then the last--and in this picture, I want to show the--where you run into the difference of temperaments. They must be adjusted temperamentally. Often you--a number of times we've run into this and the older rats seems to be the aggressor, it seems to be much more irritable than the younger rat. So when you make a parabiotic pair there's a question of adjustment to each other. And I suppose we feel much the same. It's some warning, when we we're 30 years old we woke up or someday after an anesthetic, we woke up and found we were parabiosed to a 6-year-old child. We had already lived quite awhile and the 6 year old lived much less. I can well sympathize with the rat. What it starts doing is chewing the head off of its mate. I believe that's the last.
[ Inaudible Remark ]
Now I asked Dr. Pope who were working with this temperament much more. In closing, I just wanted to read a statement he made for me about some of his observations last summer. These older rats, in first place this is not the retarded but some older ones which he parabiosed, seem to accept and adjust themselves to the new creative process of parabiotic living. Much less acceptance to this new form of living is seen in younger rats and considerably less acceptance was observed in the union of the retarded with the young rats. In this latter group most of the fighting was done with the retarded rat, occasionally with the young rat and never by both of the same union. I might suppose that the retarded older rat is the one to become easily annoyed, easily angered, quicker to lose patience and also quicker to deal out punishment. Of greater interest to me was the observation of the occurrence of alopecia in parabiotic pairs of all categories.
[ Pause ]
This alopecia was first noticed nearly all of the cases from three to five weeks following union and was still in evidence when I left in summer. This alopecia reminds me of the neurodermatitis which is commonly seen in frustrated, nervous and neurotic human. If this explanation is correct then we should be seeing a disappearance of the alopecia as the rats become more stable following acceptance to this twin mode of living. I might further say that the surgical technique was changed to bring each member of the union into greater proximity with each other and the more frustration and anger in fighting was observed. It seems that the pairs which were loosely attached had greater freedom of movement and appeared happier and more satisfied. Well, this evening I've briefly tried to point out some of the opportunities that we have in research with animals and I believe that animals can teach us much. Thank you very much.
[ Applause ]
>> Thank you Dr. McCay. I'm sure we all agree we've had the privilege of really stimulating presentations regarding the problem and all of the problems of aging. With your permission, I like to extend the thanks to the New York Academy of Medicine, especially its program committed to our three honored guests of the evening, Dr. Lansing, Dr. McFarland and Dr. McCay. Thank you very much.
[ Applause ]