Everybody "knows" the difference between food and poison.

But some poisons are subtle. And on an alien world ...

 

by CARL A. LARSON

 

Strong Poison 2

 

 

None of us is likely to be among the migrants leaving the confines of our planetary system, though they will carry faithful copies of our genes, fulfill our dreams. They will be called Jane and Ivan, Alma and Tom, Tamara and Martin—unless our tribe is doomed to change in its early extraterrestrial settlements, los­ing the drive that once made us mas­ters of this planet. If we count on only one "human" trait being pre­served, that of exponential popu­lation growth, our descendants will be forced to leave this solar system in quest of living space. Sooner or later our species will meet entirely new poison hazards; as threats to in­dividuals in the case of planned and well prepared reconnaissance; as a menace to an already changing, not quite human species, in the case of an exodus forced upon breeds which have sold their birthright for a mess of pottage.

The key word will, in both cases, be selection. Sooner or later, with or without intention and plan, trans-mundane populations will adjust to entirely novel surroundings. To a marvelous extent human beings can measure up to dour environments, but when a population, or a species, adapts to conditions of near-ex­tinction through pest and poison it will invariably be through sacrifice of individual lives. In the long run it simply will not be a matter of sur­vival of the sufficiently fit; a goal-di­rected species will have to redefine its fitness estimates with changing conditions.

Predictions about the forging and molding effects on a human, or hu­man-derived, species by virtually ex­terminating poisons of worlds with alien suns would at first blush look like extravagant guesses. As a matter of course we have sparse data about the main hazards that will meet mi­grant populations beyond the realm of Sol, and none about organic poi­sons likely to threaten our descendants. But we know some principles, sometimes sketchy, of human popu­lation changes under grim environ­mental conditions. We possess a growing, if crude, knowledge about ways and means of living beings to handle poisons; and we may have, as a forthcoming species, been through similar hazards in jungle and rain forests.

In the crucible of starvation a pop­ulation may suffer predictable losses among children and old people, its mass will contract, only to expand again, given time and good harvests. Selective forces at work through such catastrophes will be subtle as to their effects. Radically different results can be observed in epidemics killing the feeble, the elderly, but also a high proportion of people under thirty, including healthy young men and women. Those above thirty are survivors of an earlier epidemic. Im­munity, or increased resistance, is the short answer to a riddle with a few subtleties of its own.

Poison hazards, however, as they meet tribes which are forced to change their staple diets, could add some not so subtle patterns of selec­tion to the increased jeopardy of feeble and unprepared individuals. It is a curious fact that recent events have provided a model of what may have happened to our primate fore­bears and also of analogous dangers that could meet our great-grand­children as fugitives on a guileful planet. When African and Asian stu­dents at European universities were observed not to drink milk com­ments were few, some European stu­dents don't drink much milk. But somebody asked why, and got such answers as: "But I do when I need a laxative," and "Milk invariably gives me collywobbles."

Proving milk to be a poison to some non-European students, or what? Just wait a little. Enzymolo­gists read up on the matter and found it had been "known" since 1954 that benevolent givers of dried milk to people in Africa were carry­ing on what by no means could be called chemical warfare against de­fenseless ethnic groups, but certainly was a less harmful model of such un­dertakings. To make a long but fairly monotonous story short: Caucasians have, over many generations, be­come adapted to a high intake of cow's milk—as far as we can see now, through selection. Fair dairy maids and farmers' daughters may have been a little less keen on founding families with wooers whose guts would ruefully rumble when exposed to milk. You wouldn't call this effect poisonous? Or not a result of strong toxic action? Right as far as the individual is concerned, but this is how selection works. People of European origin mostly belong to the minority of the world population tolerant to lactose, milk sugar, after infancy and early childhood. During the first year of life, or, decreasingly, in the first few years, Asian and Afri­can children have active lactase, the enzyme converting milk sugar, quite like Caucasian children. Then most children lose their intestinal lactase activity. As long as they don't come upon the idea of ingesting milk they know nothing about their "defi­ciency." A practical knowledge of the effects of milk in adults is preva­lent at least on Bali, where milk is taken as a laxative.

We could, of course, envision a strange new world supplying poisoned manna to space migrants, se­lectively killing everybody above age four. The intensity of poisonous ac­tion—we shall return later on to what we could reasonably expect on the lines of true poisons—could, of course, vary greatly in parallel situ­ations, but let us try another model. A number of our forebears were constrained to feed on emergency comestibles which became their main victuals within a few genera­tions. Those who had, or readily developed, the chemical equipment necessary to digest, absorb and uti­lize the new food had big families and became prevalent. Those who could not adapt in this way—through sacrifice expressed as small family size and childlessness of some mem­bers as well as through chemical ad­justment in others—the makeshift food could be a genocidal poison by lowering the nutritional standard and fostering disease resistance. A genocidal poison need not be a dramatic killer of individuals.

Let us be very careful now before we agree on too much. A poison, un­qualified, can kill or change an indi­vidual; a substance, z, can kill or change a human, or humanlike, pop­ulation, so we may call z a poison—right? We certainly come up against an ambiguity at this point. Here time becomes a critical factor and not only with regard to terminology. We are more prone to call a swift dele­terious action poisonous than a slow effect. When human populations are concerned we have to count both types of injuries: those reducing population number and survival chances over a few generations and, conversely, unobtrusive changes sapping the life force of a numerous population through a considerable length of time. In both cases our in­terest is centered on the survivors. How will they differ from the goners? By possessing a little more, or a little less, of an enzyme some­where in the alimentary canal or ac­tive in the intermediary metabolism? Perhaps the emerging tribe will look and act quite out of line with ances­tral generations?

A close-up of the spaceport at the time of the great skedaddle will show you men and women in mute despair, hollow-cheeked, tired, but not unlike the crowds at the railroad stations of European cities when THEY were closing in on their prey. A few Martian generations have not changed humanity very much; Dick and Clem, Claire and Margot have lost nothing of their ability to make a mess of things. Now time is out, the spaceship is leaving and the thin hope of survival under a remote sun is aboard.

Other crews have left ports drawn on to more well-defined goals, better armed materially and in a spirit of conquest, but great migrations have, since the dawn of history, been more or less manifestly compelled by the shove of trouble at home. A daring spirit has certainly been a better companion on a long and perilous voyage than bleak despondency. There is no need to tone down the importance of crew selection for the final outcome. But badly prepared migrations to well-nigh unknown planets will parallel the flight of hominid flocks from one deadly dan­ger into an entirely new set of haz­ards: among funkers and gallants there are few to survive.

On account of the smallness of such founder groups the populations emerging from them can differ from each other and also from the original population with regard to gene fre­quencies. This is a mechanism differ­ent from selection: genes without ap­parent advantage with respect to survival of the individual or the spe­cies can establish themselves. In ex­treme cases the partner gene can get lost; American Indians virtually lack the blood group gene B. If fifty per­cent of our Martian descendants have gene "heads" and the other fifty percent its partner gene, "tails," we can readily get a model of what could happen if just four persons be­came parents of the new population on the planet Guirid by flipping four coins. There is a chance of one in sixteen "tails" getting lost and the emerging population will be all "heads." There is safety in numbers, if there are two hundred founder parents faithfully representing the gene frequencies of the initial, Mar­tian population, the chance of losing "tails"—or "heads"—completely is only (1/2)200.

What has happened in the pre-hominid past, and what will happen again, is that relatively rare genes will be exposed to repeated risks of getting lost; that similarly other genes, rare or moderately common, will reduce or increase their relative frequencies in migrant populations, through no apparent adaptive value at all. But the strange new environ­ment will start playing with such populations, stunting them with ex­treme gravity fields, harassing them with unaccustomed magnetic forces, radiation, extreme temperatures, poison. Under some of these condi­tions "heads" might reveal a com­pletely unexpected advantage, an­other planet could offer "tails" a warmer welcome. Changes of this fortuitous kind are rapid; even with­out selection a single generation of reduction to a few individuals, plus a few generations of increase in num­ber, suffice to let a "new" population emerge.

But the profound, adaptive changes in a new surrounding are of another type. If we put together what evidence we have about poison haz­ards outside our planetary system, it is largely indirect, and some evidence of a fundamental nature is a little shaky. Before going into this problem complex we must shoot a cursory glance at the efficient type of Homo transmundanus adjustment as different from what can happen when "neutral," nonspecific genes become established by mere chance—through various kinds of what has been called "genetic drift." Remember, selection may give "tails" an edge over "heads," but this is by no means necessary for the chance supremacy of one gene over its partner gene. The invariably effi­cacious way to thrive in a new sur­rounding is to sacrifice the nonadap­tive gene and keep its adaptive, in the specific surrounding superior, partner gene. This is selection, in one way or the other it means that the species sacrifices some members to survive as a species.

In principle, this sacrifice could occur simply by poisoning everybody who does not carry the advan­tageous gene. Would the less suc­cessful partner gene disappear then? It could well happen, swiftly and completely, but again the number of individuals is the joker in the sur­vival game. Let a fairly large crew arrive safely on planet Haljo only to be poisoned right away with an un­foreseen bane. The survival gene S could be relatively rare, and the crew correspondingly reduced, or it could be the standard gene, with a few fa­talities, limited to those carrying only the nonsurvival partner gene, s. In both instances crew members wouldmost likely be SS, Ss and ss, with only ss—majority or minority—going to the wall. This is because each or­dinary gene and its partner—allele ­have two sites: in the paternally and maternally inherited chromosome of each pair. And so Ss, the hetero­zygotes, will survive and new ss will crop out to be killed in the next gen­eration. From an initially high fre­quency complete elimination of all ss will, in a few generations, reduce the s frequency to a low percentage; if s is low at the first poison exposure a small and very slowly decreasing number of casualties, of ss individ­uals, is likely to occur in every sub­sequent generation until a bottom level of s frequency is reached. The preservation of this detrimental gene may, as we shall see, mean survival in the next galactic abode.

At this point we may well ask about evidence. Outside our planetary system thought may be bent on escaping rather than worrying hard, and sometimes very unpalatable, re­alities. Can we really know anything about the effect on migrating human populations of trans-solar poisons? We shall take a look first at the poi­sons, then at the distribution of hu­man genes enabling our descendants to cope with them.

In a troubled world there are men and women who can tell you: "We kissed the soil when we had passed the border." Something like that would be less likely to happen on an unknown planet, under a pale foreign sun. After a long voyage, would anybody be careless enough to breathe the poisonous atmosphere of the haven attained? Though various kinds of inorganic poison can be taken for granted, wherever we go within the galaxy, we will be pro­tected against them. It is something else again that protective devices can be fatiguing to the extreme and leave space travelers little resistance and vigilance to bear up against more in­sidious poisons.

To this latter class we would refer stuff interfering with specific chem­ical processes involved in the main­tenance of life. Keeping close to what we really know, we would guess at organic poisons laming en­zymes known today to occur in vari­ant molecular forms in some per­sons. Mineral poisons inactivate an enzyme in all mammals. Arsenic in­hibits sulfhydryl enzyme systems es­sential to living cells, to mention one case in point. But it is easier to think of organic poisons as fitting nicely into the locks of human life processes, impairing only one molecular form of a specific enzyme. There is fairly good reason to think of carbon compounds as present throughout the universe.

True enough, messages from space reaching our planet as meteorites may not permit far-reaching con­clusions about the composition of in­terstellar matter. On the other hand our sun is a rather common G star, meaning that about fifteen percent of the stars in our galaxy belong to the same spectral category, with a temperature of some 6,000° C. Astro­metric investigations have demon­strated perturbations of stars that fit the idea of unseen planets—with our present equipment Earth would be unseen from one of them. It would not be too rash an assumption to think that meteorites may tell us a rather common story about galactic conditions.

One of these messengers ap­peared, with light and thunder, at Orgueil in southern France on May 14, 1864. Some twenty fragments, fist- to head-sized, were collected and studied. They were carbonaceous chondrites, a term applied to carbon-containing meteoric stones with chon­drules, or rounded granules of mineral embedded in their mass. We get many such dispatches from the asteroid belt circling between Mars and Jupiter, so we know there is carbon, but not all of them are read as carefully as the Or­gueil stones.

The gist of many refined labora­tory studies of these stones is that their hydrocarbons resemble those produced by living organisms, but the porosity of carbonaceous chon­drites has made people question the cosmic origin of such hydrocarbons. Terrestrial contamination is a tricky thing to exclude.

Recently NASA exobiologists got hold of uncontaminated material, from a stone dropping down near Murchison, Australia, on September 28, 1969. When they examined large fragments with gas chromatography and mass spectrometry the NASA scientists found five amino acids known from living organisms, in­cluding human beings. They found other amino acids, too, and dextro­rotatory isomers of the terrestrial type amino acids: glycine, alanine, valine, proline and glutamic acid.

This is a point where one should stop, look and listen. Amino acids occur in two different forms or opti­cal isomers, their asymmetrical crys­talline structures twisting the plane of polarization of light to the right, D form; or to the left, L or levorotatory form. Amino acids entering as build­ing blocks into our enzymes and structural proteins are L isomers, and so are the amino acids of organisms eating us and being eaten by us. Why shouldn't proteins on so far unseen planets—and G type stars might have one or two planets, on the average, where life has taken hold—be com­posed mainly of D amino acids? If so, meat on a dextro planet won't ex­actly poison the terrestrial consumer, but such proteins would be rather in­adequate for growth and tissue re­pair. And food could be very pala­table indeed without containing arginine and histidine, but both these amino acids are, together with eight others, indispensable for normal growth. If our great-grand­children try a diet where one or a few essential amino acids are sub­stituted, and there are alternatives to think of, this diet could act as a true genocidal poison. It could be useful to think of the Murchison message as a reminder of such possibilities.

There is, however, another type of conclusion to be drawn from obser­vational facts as secured and inter­preted by the NASA exobiologists. An electric discharge, when repeated in a mixture of hydrogen, methane, ammonia and water, will produce various kinds of amino acids, D and L, in proportions resembling those of the Murchison stone. When the cos­mic amino acids are considered abiotic, originating in the absence of life, they are by no means off our present subject.

In the first place, the mixture pro­ducing amino acids under laboratory conditions is present in the cloudy masses of Jupiter's cold exosphere; someday you may be able to go to Io and have a close look. Then you will see what our planet once looked like, under life-generating conditions that were certainly more conducive to the origin of life as we know it. But there is nothing telling us that life in other forms is not being generated in the lower and temperate cloud layers of Jupiter. Our next concern will be with life factories in interstellar space.

There strong poison, by any defi­nition, is indeed met with though it is of no great interest as such. Inter­stellar gas clouds seem to contain hydrocyanic acid, methyl alcohol, formaldehyde, formic acid and cy­anoacetylene. Nobody will go there unprotected; of interest, in our present context, is that such gas clouds represent virtual pilot plants for prebiotic organic compounds, in­cluding amino acids.

Again we meet conditions resem­bling those of our own planet when early self-replicative molecules arise. This is about what scanty knowledge we have today. But by reasonable in­ference we may assume that it is at least possible that some of the bil­lions of extrasolar planets have passed stages of prebiotic chemical evolution similar to those on Earth and that a launching of various life forms has followed. Our descendants may well meet the bewildering abundance of foodstuffs and poisons that our forebears encountered when ousted from their arboreal Eden.

Given an infinite number of life-sustaining orbs any number of poisons could occur, from the deadly gas oxygen, nipping life in its bud, to elaborate poisoners successfully sur­viving the attempts of highly in­telligent beings to eradicate them. Among space migrants rapid selec­tion may occur against those who won't accept the challenge of the en­tirely unknown.

As for life processes exposed to cosmic poisons, and the selective events mediated through more or less severe disturbances of such pro­cesses, we may depart from our knowledge of metabolic cycles in man and mammals. Briefly, chemical processes occurring in some cosmic formations and industrial plants at high pressure and elevated tempera­ture can take place at body tempera­ture in the presence of catalysts. In the course of evolution plants and animals have come to be increas­ingly dependent upon biocatalysts, enzymes, which further various links in long chains of chemical events. At any level two links can be separated by inactivating the enzyme that keeps them together. Inactivation can be brought about by, for in­stance, a plant poison, or through failure of the gene controlling the production of the enzyme. Scores of such genes are known just because defective variants of them have been observed, mostly in persons carrying both substandard genes.

So far we have seen a lot of detri­mental effects of such enzyme inactivating genes and barely enough advantage to build models of what could take place. Generally speak­ing, a human population would be better off in an entirely new sur­rounding, with unknown poisons, if it carries a number of variant genes. Going back to the pattern already mentioned, it would be fine for an individual to have both normal genes, that is being an SS homo­zygote, as long as he stays here, or on Mars. A population of only SS indi­viduals leaving for the great un­known could succeed—or they could be all killed. Crews composed of SS, Ss and ss individuals have a better chance, one of the three keys could fit the new ecologic lock.

What we have seen in somewhat parallel situations here is Ss individuals being favored, in taxing sur­roundings, at the cost of both SS and ss individuals. It is very likely that foreign planets will offer situations where ss persons rarely reproduce, SS individuals often though not al­ways, are poisoned to death before having a family and Ss heterozygotes prevail. To complete such simple patterns we may think of the scores of different genes known to occur in a rare, substandard variant respon­sible for an inactive enzyme, while the normal variant produces full ac­tivity of this specific enzyme in homozygotes—AA, BB, CC et ce­tera—and about fifty percent enzyme activity in heterozygotes. Then we should add a few hundred similar genes so far not observed.

But selective processes of a more subtle kind have been, and are, at work here right now. Basically, it is the same pattern with the modi­fication that no homozygotes are rare and neither EE or ee, say, are obvi­ously handicapped. In some in­stances differences in enzyme activ­ity are concerned, but these differences need not be at all critical. As a matter of fact the apparent health of the four percent of the To­ronto population revealing a sev­enty-five percent activity of serum cholinesterase fits the pattern of sev­eral other enzyme variants; we can get along quite well with far less than the highest enzyme activity as observed in, for instance, EE homozygotes.

In such instances selective forces of a mostly obscured nature are at work, otherwise seventy-five-per­centers in the case just mentioned would be much rarer. Though the enzyme variants were detected through abnormal reactions to muscle relaxant drugs, it is not a question of selection in fervently drug-consuming populations. Selec­tion may well act upon qualitative differences, crudely observed in the laboratory by means of elec­trophoretic technique, which we know to be inherited in a reasonably simple way. But what kind of selec­tive forces could conceivably be at work in modern Western popu­lations?

Perhaps this question puts the saddle on the wrong horse. Should we ask, instead, for selective forces operative until quite recently?

Though questions of this kind may be of crucial importance to rapidly growing human populations here and now they are sadly hard to an­swer. We know about teeth and skulls of our hominid ancestors, and such evidence may have conveyed the impression of evolution as a slow process, but we know nothing about the distribution of enzyme variants a hundred years ago. When fairly common gene variants are involved, we have to count both with the possi­bility of selection at work—for and against a variant gene with a definite advantage in some respects only—and with the relaxed selection against other genes which are now increasing their relative frequency.

They still will need a few genera­tions, in the latter instance, to outrival their relatively rare partner gene or genes.

As far as heritable variants of se­rum cholinesterase are concerned we may have some clues. Under rather specific circumstances the gene de­termining a less active enzyme vari­ant may convey a distinct advantage. Some African tribes have used the calabar bean for trial by ordeal. The suspect had to swallow a few rather innocent looking, big beans. If he was innocent, he vomited; if guilty, he died from respiratory paralysis. There was a third possibility: he could be guilty and still survive—be­cause he carried a gene for an atypi­cal cholinesterase not lamed by the bean poison.

Miscarriage of justice on account of an atypical gene in the defendant may have interesting sociologic as­pects, but we have to leave them and ponder the question of enzyme in­hibitors distributed in food plants. They are not as violently poisonous as that occurring in calabar beans, but many common vegetables have been observed to contain enzyme in­hibitors which can, under untoward circumstances, cause disease and even death. We have little precise knowledge about the selective effects of such agents and we might be in­clined to think that the inability of Homo sapiens to avoid poisonous vegetables would belong to pre­history. If so, we would be mistaken.

In the 1830's crops failed in some districts in India, the seed of Lathyrus sativus was consumed as a substitute food and “the younger part of the population. . .from the age of thirty downwards, began to be deprived of the use of their limbs be­low the waist. . ." The same thing happened to about sixty thousand persons in one Indian district in 1922; similar outbreaks of paralysis were observed in 1945 in India; even Spain, France, Italy and Syria have had epidemics of "lathyrism." We may keep the possibility open that plant poisons, strong, weak and con­ditional, have until recently balanced some human enzyme genes at a level comparable to that of blood group genes.

Upon such systems of relatively frequent gene variants with distinct selective advantages and dis­advantages biogenic poisons may act on new planets. The result could well be rapid selection for genes deter­mining specific enzyme variants. This type of adaptation will occur at the cost of individual reproduction or even individual lives, but part of this cost has been paid in the long past when originally "substandard" genes became established at high-frequency levels.

What if entirely new genes, en­gaged in enzyme production, arise because of the rather intense cosmic radiation on Mars? We have to count with mutations which are not new and untried, but rather occurring at a somewhat higher rate than here. One side of this increased rate of muta­tions which have been weighed in the balance and found wanting is a somewhat increased rate of death and infertility until the mutant genes have reached their new level of equi­librium. Would that be the worst thing that could happen?

Probably not. This is a tricky point, I for one am not sure we could, in any reasonably Martian-like environment, by practical, work­able devices, substantially reduce our "natural" mutation rate. If we, or our grandchildren, could bring about such protection, it might be a little worse than a high mutation rate, but not the worst bane that could poison our future space.

A fairly high mutation rate in­creases the survival potential of a species striving to conquer new worlds. But it is by far not the sole factor of survival. For a species to keep alive, it must keep genes that make individuals die. But even with a moderate rate of mutation we can keep such genes concealed through scores of generations. They are bal­anced and made temporarily in­nocent, not only by "good" partner genes—the situation Aa—but also by some of the billions . . . repeat: bil­lions . . . of other gene combina­tions in which they are, have been, and will be tried in human beings. Even if we overprotect ourselves against mutations we will have a chance, perhaps somewhat reduced, in new planetary homes.

New and unsuspected poisons may cause mutations in the somatic cells, as distinct from sex cells, of transsolar migrants. The toxin of As­pergillus flavus, a mold, which killed the economy of tropical countries ex­porting peanuts, has a potent cancer producing effect on mammalian, in­cluding human, cells, especially those of the liver. There are regions in Central Africa and South East Asia with a prevalence of liver can­cer about one hundred times that of regions protected against the mold poison, aflatoxin. Such fungal paral­lels of bacterial, botulin type toxins, may constitute worse dangers than radiation in entirely new surround­ings. They may produce mutations not limited to somatic cells. Still, there may be poisons in another sense, genocidal toxins stymieing hu­man conquest of the galaxy.

In every situation our species has so far encountered we have had gene reserves empowering us to survive in desert and tundra. Could there be some complex gene manifestation, stimulated and selected for by hard­ship, which has in the long past en­dowed humankind with a general adaptability? Intelligence seems to be an emotionally loaded word, and sometimes a rather ambiguous term, but, if there is something remotely like a capacity to acquire and apply knowledge with a biologic founda­tion, it could be suspected of having had, long ago, a positive selection value. In entirely new and unex­pected situations, where the appropriate tools and weapons could not be brought, with habitual behavior patterns spelling certain extinction, it was the cunning improviser who pre­vailed. If Sek and Ghel concluded there was no need for them to try the berries that killed Ud, they stood a better chance of survival than those who had to taste the nice fruits for themselves. And it was Sek and Ghel who became patriarchs.

Perhaps we should not draw too far-reaching conclusions from this. High intelligence invariably may not, in every social setting, confer a higher survival value—a substantially increased chance of handing down certain gene complexes. Tapeworms are not highly intelligent, though they are perfectly adjusted and highly reproductive. Yet our Martian great-grandchildren are likely to pick their crews for space pioneering among men and women possessing a high general intelligence. Such crews have, when odds are uncertain, a better chance of survival in un­handled situations. Selection for stu­pidity might become truly genocidal.

Though we know of a number of poisons which reduce available in­telligence, some morbid imagination would be needed to construct a situ­ation where a complex faculty like general intelligence would be se­lected against. The agent would not be a poison in its general sense.

It is another thing again that a number of genes for profound intelligence defect offer metabolic al­ternatives which may prove useful in highly specific, toxic surroundings. Every growing, new population would buy its survival by doing with­out complete protection against the poison hazard and keeping its in­telligence.

Human populations can do such things; blind selective forces are not the sole agents forming our fate be­yond the solar system. To speak of our kind as a goal-directed species could be grossly illogical—we really don't know where we are going. But we are the animals who know that we, as persons, shall certainly die. Many of us have an insight into re­production and its relationship with its preambles. Homo sapiens is the animal who can tell himself: "There's food I'll eat, but not right now. I have other things to do, first."

And as soon as humans have felt very strongly this or that "other thing," they have acted quite differ­ently from their mammalian cousins. Perhaps the goal was not worth­while, as we can see it from a remote and dignified standpoint. The sword that gleamed in the sun, pointing to Damascus; the rallying around the flag—they made men and multitudes aware of powers never released by the better-spent effort of filling the greatest number of bellies, to the greatest distension, in the shortest time.

Could be that our kind needs a far-off goal to unfold its truly human capabilities. A venom would be fatal to our profoundest drives if it dim­med that distant goal.