Science in Christian Perspective
Walter R. Hearn, Ph.D.
From: JASA 11 (September 1959): 10-12.
Probably many A.S.A. members were attracted to George Wald's article in Science, 128, 1481 (12 December, 1958), "The Significance of Vertebrate Metamorphosis," by its unusual introduction-a quotation f rom the third chapter of the Gospel of John! The author used Nicodemus' question about the nature of a second birth to draw attention to the fact that all living things have a life cycle, beginning with birth and ending with preparation for a second physical birth, this time of their offspring. Wald makes a convincing case for "metamorphosis" as a phenomenon common to the whole vertebrate stock including man, a process by which the animal is prepared to leave its natal environment; in order to reproduce, the animal must eventually return, thus completing its life cycle. To return, a second metamorphosis may be necessary which may be almost a direct reversal of the first one. In his closing paragraph, Wald says:
"Our history as vertebrates is not dust to dust but water to water. From this point of view Nicodemus' great question can be given a broad and positive biological answer. Every animal can and must return to the 'womb'-not, indeed, to be born again; but to bear the next generation. For a catadromous fish, the 'womb' is the sea; for anadromous fishes and amphibia, a pond or stream; for land vertebrates, a uterus or egg."Professor Wald, eminent biologist of Harvard and Woods Hole, is best known for his work on the visual systems of vertebrates (which he says led him to this thesis), but he presents evidence for changes in many other biochemical systems during vertebrate metamorphosis. His paper amounts to a reaffirmation of the principle of "recapitulation"-but this time on a biochemical basis. For instance, he points out that the eye pigment of certain eurylialine fishes (those which can live in water of widely varying salt concentration) changes during their life cycle: If the fish lives in salt water but goes upstream to spawn, as in the case of salmon, the adult pigment will be the "salt-water type" based on retinene (from vitamin A,), but before the adult returns to its natal environment the pigment changes to the "fresh-water type" based on dehydroretinene (from vitamin A2). The reverse situation applies to certain fresh-water eels which spawn in salt water. In the familiar metamorphosis of tadpoles, the change from a fresh-water environment to a dryland environment is accompanied by changes in the type of visual pigment, the type of hemoglobin in the erythrocytes, the nature of the plasma proteins, and the mechanism of excretion of nitrogenous compounds.
Of course, as in the case of anatomical "recapitulation" these observations in themselves do not necessarily strengthen the case for phylogenetic evolution' but Wald interprets them in this way, postulating that the ancestral vertebrates arose in fresh water and possessed visual systems based on vitamin A2. The most speculative part of his thesis is probably the suggestion that puberty represents the vestigial remains of the second or reverse metamorphosis in the case of the land vertebrates. "To be sure, this does not prepare a land vertebrate to migrate, for the natal environment is now segregated, and puberty prepares the animal only to mate. Here only one representative cell-the spermatozoan-completes the return to the natal environment; and this, of course, undergoes a profound metamorphosis before being launched upon a migration as formidable, relative to its size, as that of any salmon." It is well established that the human fetus manufactures a different molecular species of hemoglobin from that of the adult and that the shift to the adult type comes after birth, so the term metamorphosis can legitimately be applied to the human species. Webster gives the zoological definition of metamorphosis as "a marked and more or less abrupt change in the form or structure of an animal during postembryonic development."Here of course we are dealing with changes in structure at the molecular level, changes in metabolism rather than in gross porphology. As I have pointed out ("Biochemical Complexity and its Significance in Evolution," JASA, June, 1955), this will surely be the predominant theme in future considera tions of the extent and precise mechanisms of evolution. The evidence from comparative biochemistry and chemical embryology presented in Wald's article certainly does not "prove" that biochemical evolution has occurred, any more than Darwin's assembled evidence "proved" that morphological evolution had occurred. However, in reading this paper I think I felt the kind of excitement that some of Darwin's contemporaries must have felt over his writings: here is a theory that suggests new things to look for and brings together many kinds of evidence into a unified concept! The theory may not be true, of course, but meanwhile it is useful because it is exciting and challenging. And some day, if biochemists are sufficiently clever and diligent, we may be able to find out if the theory is true.
In subsequent issues of Science a number of correspondents complained that Wald's poetic imagination had carried him too f ar, which may be true. There was also a letter complaining that "twisting" the passage froill John to make it refer to physical rebirth was inexcusable, and suggesting that the editors consult theologians as referees to prevent such misuse of Biblical quotations. On thinking back over many sermons I have heard, I decided that Wald's use of this verse out of context was no more serious than much of the "poetic license" with Scripture so common in Christian preaching. And usually my objection to it there is not that it is done, but that it is disguised as logic and not honestly presented as poetic illustration. To go back to the ideas presented in this column last time, I think a Christian who does scientific work (or one who preaches!) should be able to look at what he is doing poetically as well as logically, if his life in Christ is to be really "abundant." Darwin, many of you will recall, complained eventually of losing his taste for beauty in literature, music, and art because of his engrossment in mechanistic thought. Should not those of us who have been born again spiritually have a richer life than that"
A third area of significance in evolutionary considerations to which I called attention in my 1955 paper (besides comparative biochemistry and biochemical embryology) is that of biochemical genetics. An excellent review of the status of human biochemical genetics is provided by Laurence H. Snyder in "Fifty Years of Medical Genetics," Science, 129, 7 (2 January, 1959). This paper, Dr. Snyder's 1958 AAAS Presidential Address, is as exciting and challenging as the one by Wald referred to above. There are now inany well established cases in which inherited diseases, known to be controlled by a single gene, can be pinned down to a single abnormality in a specific metabelie pathway. For example, Vernon Ingram of Cambridge (Nature, 180, 326 (1957).) showed that in the pathological hemoglobin of sickle cell anemia, only one of the nearly 300 amino acids of the protein's structure differs from that of normal hemoglobin, a glutamic acid being replaced by a valine; it is remarkable that such a slight alteration in a single macromolecule in the body should prove fatal to individuals with only the sickle hemoglobin- (The disease gets its name from the fact that at low oxygen tension the abnormal hemoglobin crystallizes from solution and the erythrocyte membrane then collapses to a shape resembling a sickle under the microscope.)
Here again we are getting down to the level of molecular morphology, but it is also possible in at least one case to relate a gross structural anomaly to a specific metabolic disfunction. This is the case of hereditary spherocytosis, in which the erythrocytes develop as spheres rather than as biconcave disks. If you have seen the Moody Science Film, "Red River of Life," you will remember the sequence showing that the biconcave disk gives the theoretically optimum combination of rapid diffusion and mechanical strength. In the presence of a specific dominant gene possessed by those suffering from spherocytosis, apparently one of the enzymes of glycolysis, enolase, is inhibited or for some other reason fails to function properly. Glycolysis is the pathway by which carbohydrate is anaerobically converted to lactic acid; enolase catalyzes the specific step in which 2-phosphoglyceric acid is converted to 2-phosphoenolpyruvic acid. This latter compound ordinarily loses its phosphate in the next step to a molecule of adenosine diphosphate (ADP), producing a molecule of adenosine triphosphate (ATP) which can provide energy to drive a variety of biochemical reactions. The erythrocytes, having no mitochondrial enzymes for oxidative metabolism, are more dependent on glycolysis for energy than are other cells of the body, and in the diseased condition have insufficient ATP to maintain the normal cell shape. The cell membrane is mechanically weaker and ruptured erythrocytes accumulate in the spleen in the disease.
There is also much interest at present in relating mental disorders to specific biochemical abnormalities, and in several cases a single gene-enzyme disfunction has been implicated. In one severe type of mental disease the amino acid phenylalanine cannot be oxidized to tyrosine because the enzyme catalyzing this step is missing or not functioning properly; as a result the phenylalanine accumulates and is de-aminated via an alternate pathway to phenylpyruvic acid, excretion of which in the urine is characteristic of the disease (oligophrenia phenylpyruvica). Greatly reduced pigmentation is also noticed in individuals suffering from this disease; the excess phenylalanine apparently inhibits the enzyme tyrosinase and thus diminishes the conversion of tyrosine to melanin. But perhaps the most fascinating, and most hopeful, fact about this disease is that it has been found possible to identify by a chemical test those apparently normal persons who are heterozygous carriers of the recessive gene for the disease: phenylalanine tolerance tests show that carriers of the gene have only about half as much active phenylalanine-oxidizing enzyme as persons- who do not possess the gene.