Developmental Malformation in Man and Other Animals: A Bibliography with Introduction

By Howard H. Hillemann, PhD

Summary: In the introduction to this bibliography of over 200 references, Dr. Howard Hillemann speaks of the evolution of humankind’s beliefs about disease and bodily defects, from early notions attributing such abnormalities to “divine visitation” to the idea, as of 1957, that such disorders are the result of a combination of genes and environment. Regarding the latter, Hilleman points out, “Proper nutrition is the most important single factor in the prevention of disease or in the recovery therefrom” and presents a list of references supporting this claim. While much of the content cited is no longer in print, merely perusing the categories and titles of the papers of the bibliography is “impressively educational in itself,” Hillemann writes. Published by the Lee Foundation for Nutritional Research, reprint 66C, circa 1957.

[The following is a transcription of the original Archives document. To view or download the original document, click here.]

Developmental Malformation in Man and Other Animals: A Bibliography with Introduction[spacer height=”20px”]

In the more primitive stages of man’s cultural origins, it was more generally believed than not that disease and structural malformation, congenital or of later appearance, represented forms of divine visitation—evidence in some instances of a supernatural curse and in others as marks of special preference or purification.

With the philosophically disturbing discovery in the late seventeenth century of a microscopic world of living organisms—whose existence hitherto had not been even so much as suspected—came novel interpretations of pathology based on material rather than on transcendental considerations, the former being amenable to rational testing. The activities of fermentation, putrefaction, and decay were soon laid at the door of microorganisms, and a simple step of the mind suspected rightly that disease processes may be of the order of such microorganismal functions, or at least related to and associated therewith.

In retrospect the seeds of thought relating to symbiotic virus of facultative pathogenesis were sown about 4000 B.C. by the Egyptian father of medicine, Imhotep, later identified as the Greek Aesculapius, when he spoke of “the intrusion of something from within, not coming from the outside.” In the nineteenth century, Pidoux stated that “disease is borne of us and in us.”

Thus, for the first time in history was born the first rational explanation of a disease condition or process. This principle represents nothing more than a realistic discovery of a principle laid down about 400 B.C., probably by Hippocrates II, in the Book on the Sacred Disease. This disease, considered in the light of modern knowledge, was very likely epilepsy. The book set forth the cardinal scientific method or principle of assuming natural explanations for all observable events. This principle was restated in the sixteenth century by Paracelsus in these words: “Ere the world perishes, many arts now ascribed to the work of the devil will become public, and we shall then see that the most of these effects depend upon natural forces.”

Joseph Lister (1827–1912) observed that carbolic acid solution sprayed in garbage cans would stop decay and the breeding of flies. Another simple mental transfer created the material chemotherapeutic approach to diseases that now, for the most part, are considered to be of microorganismal origin. Thus was born chemotherapeutics, which crystallized in two schools of thought, one centering about the virtues of the massive dose, the other championing the cause of the minimal, or homeopathic, dose.

Much energy soon became expended in the elaboration and application of divers and sundry chemicals and compounds designed to be effective specifically for this or that ailment, until some 30,000 or more drugs were created to cover a spectrum of some 20,000 or more classified human ailments.

The thought that yet other important factors or agencies might be causative in pathology was not born until the latter part of the eighteenth century, which saw the birth of heredity and genetics. One hastens to add, however, that the sixteenth century’s Paracelsus had emphasized hereditary factors in disease. The newer knowledge made it possible to explain the origin and perpetuation of certain types of disease—inborn errors of metabolism and malformations as manifestations of genic combination and mutation. This continues to be a fruitful area of active and profitable investigation.

Rational explanations of disease were appearing from other quarters also. In 1911 Casimir Funk discovered the beriberi-preventive vitamin, and from this humble beginning arose a gigantic literature, still on the increase, calling attention to and attesting to the fact that many diseases are purely diseases of malnutrition, and that, by and large, many other pathologies are in one way or another tied up with specialized metabolic deficiencies of nutritional origin.

The modern doctrine relating to health and disease emphasizes that pathology and malformation have their roots in either pure genic conditions and composition or in environmental factors operating from without—or, as many would have it, for nearly all instances not in either of these alone but in a combination of interacting genetic and environmental factors. It is self-evident that no matter how “perfect” genes may be, their “normal” effects cannot be made manifest in the absence of those material ingredients to be gleaned by the organism from its environment, just as a master mason would fail in building without suitable brick and mortar.

The subject of fetal malformation in man and other animals is of increasing interest and importance, especially since we now know some of the causes, remedies, and preventatives for these problems. It is in behalf of this area in modern biology and medicine that the attending bibliography is prepared. A bibliography such as this has a twofold function.

First, it calls attention to the fact that there are many environmental factors now recognized to be responsible for deviations from the normal and preferred state, not the least of which is inappropriate nutrition. Proper nutrition is the most important single factor in the prevention of disease or in the recovery therefrom.

To peruse the categories and titles of the papers in such a bibliography is impressively educational in itself. The second, more obvious function is to provide an immediate and ready reference for those who wish to begin a more intensive study of the literature, gaining thereby a basic and extensive understanding of the subject at hand.[spacer height=”20px”]

Table of Contents

  1. General References on Teratogenesis
  2. Genetic Defects
  3. Radiation Defects
  4. Hormonal Induction
  5. Chemical Induction
  6. Parasites and Congenital Defects
  7. Oxygen and Atmospheric Pressure
  8. RH Factor, Overripeness, Maternal Limitations, Toxemia, Physical Injury, Electroshock
  9. Nutritional Deficiency and Hyper States
  10. Vitamin Antagonists and Analogs[spacer height=”20px”]

I. General References on Teratogenesis

1. Duraiswami, P.K. (1952). “Experimental causation of congenital skeletal defects and its significance in orthopaedic surgery.” J. of Bone and Joint Surg. 34B(4):646–698.

2. Gruenwald, P. (1947). “Mechanisms of abnormal development.” Arch. Path. 44:398–436; 495–559, 648–664.

3. Willier, B.H., P.A. Weiss, and V. Hamburger. (1955). Analysis of development, Section XIV: Teratogenesis. Edgar Zwilling, pp. 699–719. W.B. Saunders Co., Philadelphia.[spacer height=”20px”]

II. Genetic Defects

4. American Medical Association. (1954). “Deformities in stillborn infant.” J.A.M.A. 156(8):804.

5. American Medical Association. (1956). “Genetically determined disorders of the renal tubules.” J.A.M.A. 160(3):190.

6. American Medical Association. (1956). “Agammaglobulinemia.” J.A.M.A. 160(10): 28.

7. Asmundson, V.S., and C.F. Pun. (1956). “Crooked neck dwarf in the turkey.” J. Exp. Zool. 131(3).

8. Auerbach, R. (1954). “Analysis of the developmental effects of a lethal mutation in the house mouse.” J. Exp. Zool. 127(2).

9. Beatty, R.A. (1951). “Animal breeding.” Abstr. 19:238.

10. Braden, A.W.H., and C.R. Austin. (1954). “The fertile life of mouse and rat eggs.” Science. 120:610–611.

11. Corner, George W., and George W. Bartelmez. (1954). “Early abnormal embryos of the rhesus monkey.” Carnegie Institute of Washington Pub. 231. Contributed to Embryol. 35:1–9.

12. Estborn, B. (1956). “Familial occurrence of multiple sclerosis.” Nord. Med. 54: 1665–1667. Abstr. J.A.M.A. 160(11):998.

13. Foote, C.H. (1955). “Urogenital abnormalities in the golden hamster.” Anat. Rec. 121(4): [page number omitted].

14. Gluecksohn-Waelsch, Salome. (1953). “Lethal factors in development.” Quart. Rev. Biol. 28(2):115–135.

15. Hertig, Arthur T., John Rock, Eleanor C. Adams, and William J. Mulligan. (1954). “On the preimplantation stages of the human ovum: a description of four normal and abnormal specimens ranging from the second to the fifth day of development.” Carnegie Institute of Washington Pub. 240. Contributed to Embryol. 35:199–220.

16. Hickey, M.F. (1953). “Genes and mermaids: causation of congenital abnormalities.” Med. J. of Australia, May. Abstr. J.A.M.A. 152(12):1131.

17. Hollander, Willard, John W. Gowen, and Janice Stadler. (1956). “A study of 25 gynandromorphic mice of the bagg albino strain.” Anat. Rec. 124(2): [page number omitted].

18. Landauer, Walter. (1956). “Hereditary and induced cross-beak of fowl. Experiments with ethyl carbamate.” J. Exp. Zool. 132(1): [page number omitted].

19. Michelson, Ann M., Elizabeth S. Russell, and Pinckney J. Harman. (1955). “Hereditary muscular dystrophy in mice.” Proceedings of the National Academy of Sciences. 123:367.

20. Rafferty-Machlis, Gertrude, and Carl Gottfried Hartman. (1953). “Early death of the ovum in the opossum with observations on moribund mouse eggs.” J. Morph. 92(3): [page number omitted].

21. Romanoff, A.L. (1949). “Critical periods and causes of death in avian embryonic development.” Auk. 66:264–270.

22. Silberberg, Martin, and Ruth Silberberg. (1956). “Faulty skeletal development in ‘yellow’ mice.” Anat. Rec. 124(2):129–143.

23. Theiler, Karl, and Salome Gluecksohn-Waelsch. (1956). “The morphological effects and the development of the fused mutation in the mouse.” Anat. Rec. 125(1): [page number omitted].

24. Went, F.W. (1952). “Gene action in connection with growth and development.” Science. 116:530.

25. Westergaard, M. (1955). “Mutations as cause of disease.” Ugeskr. Laeger. 117: 1593–1599. Abstr. J.A.M.A. 160(15):1371.[spacer height=”20px”]

III. Radiation Defects

26. Alper, Tikvah, and M. Ebert. (1954). “Influence of hydrogen ion concentration on radiation effects.” Science. 120:608–609.

27. American Medical Association. (1955). “Response of human beings accidentally exposed to significant fall-out radiation.” J.A.M.A. 159(5):430–434.

28. Bagg, H.J. (1920). “Pathological changes accompanying injections of an active deposit of radium emanation.” J. Cancer Research. 5:1.

29. Bagg, H.J. (1920). “The response of the animal organism to repeated injections of an active deposit of radium emanation.” J. Cancer Research. 5:301.

30. Bagg, H.J., and C.C. Little. (1924). “Hereditary structural defects in the descendants of mice exposed to roentgen ray irradiation.” Am. J. Anat. 33:119.

31. Biology Division, Oak Ridge National Laboratory. (1953). “Symposium on the effects of radiation and other deleterious agents on embryonic development.” Oak Ridge, Tennessee, April 20–21, 1953. Reprinted from J. Cell. and Comp. Physiol. 43(Suppl. 1): May, 1954.

32. Bishop, D.W. (1950). “Anaerobic pickup of P32 by seminal bull sperm.” Anat. Rec. 108:573.

33. Bishop, D.W., and I. Weinstock. (1948). “Uptake of radioactive phosphorus by bull spermatozoa.” Anat. Rec. 101:731.

34. Blair, Henry A., Ed. (1954). Biological Effects of External Radiation. McGraw-Hill: 330 W. 42nd. Street, New York 36, NY, 530 pp. $7.00.

35. Brailsford, J.F. (1948). The Radiology of Bones and Joints, 4th ed., J. and A. Churchill, Ltd., London.

36. Brunst, Victor Victorovich. (1954). “The effect of local X-ray irradiation upon the development of the anterior part of the head of the axolotl.” J. Morph. 95(2): [page number omitted].

37. Byrnes, V.A., D.V.L. Brown, H.W. Rose, and P.A. Cibis. (1955). “Retinal burns—new hazard of the atomic bomb.” J.A.M.A. 157:21–22.

38. Chapman, Arthur O. (1954). “The effects of varying dosage of radioactive phosphorous (P32) in the early chick embryo.” J. Morph. 95(3): [page number omitted].

39. Chapman, Arthur O., and John S. Latta. (1956). “Abnormalities produced in the chick embryo by radioactive phosphorous (P32 ).” Anat. Rec. 124(2):452, D52.

40. Cheng, Amber Lieng-Shan, Roslyn Berniece Alfin-Slater, and Harry James Deuel. (1954). “The effect of fat level of the diet on general nutrition. XIII. The effect in increasing doses of X-irradiation on the protective action of fat on radiation injury.” Nutr. 54(2): [page number omitted].

41. Cook and Duncan. (1952). Modern Radiochemical Practice. Oxford Press.

42. Dent, James Norman, and Ernest L. Hunt. (1954). “Radiotracer techniques in embryological research.” J. Cell. and Comp. Physiol. 43(Suppl.1): Symposium (opere citato).

43. Duraiswami, P.K. (1952). “Experimental causation of congenital skeletal defects and its significance in orthopaedic surgery.” J. Bone and Joint Surg. 34B(4):646–698.

44. Hicks, Samuel Pendleton. (1954) “The effects of ionizing radiation, certain hormones, and radiomimetic drugs on the developing nervous system.” J. Cell. and Comp. Physiol. 43(Suppl. 1):151–178. Symposium (opere citato).

45. Hobbs, Jr., A.A. (1950). “Fetal tolerance to roentgen rays.” Radiology. 54:242–246.

46. Hollaender, Alexander, Ed. (1953). Radiation Biology, Vol. I: High Energy Radiations. McGraw-Hill: 330 West 42nd St., New York 36, NY,1201 pp. $17.50.

47. Hollaender, Alexander, Ed. (1954). Radiation Biology, Vol. II: Ultraviolet and Related Radiations. McGraw-Hill: 330 W. 42nd Street, New York 36, NY.

48. Hollaender, Alexander, Ed. [1954]. Radiation Biology, Vol. III: Visible Light. McGraw-Hill: 330 W. 42nd Street, New York 36, NY.

49. Kamen, M.D. (1951). Radioactive Tracers in Biology. Academic Press.

50. Kimeldorf, D.J., and S.J. Baum. (1954). “Alterations in organ and body growth of rats following daily exhaustive exercise, X-irradiation, and post-irradiation exercise.” Growth. 18(2):79–96.

51. Levy, B.M., et al. (1953). “The effect of a single sub-acute X-ray exposure to the fetus on skeletal growth; a quantitative study.” J. Morph. 93(3):561–571.

52. Moloney, W.C., and Marvin Kastenbaum. (1955). “Leukemogenic effects of ionizing radiation on atomic bomb survivors in Hiroshima.” Science. 121:191–192. (Note on forthcoming article.)

53. Neel, J.V., et al. (1953). “The effect of exposure to the atomic bombs on pregnancy termination in Hiroshima and Nagasaki: preliminary report.” Science. 118:537–541.

54. Pecher, C., and Jacqueline Pecher. (1941). “Radio-calcium and radio-strontium metabolism in pregnant mice.” Proc. Soc. Exp. Biol. and Med. 46:91–94.

55. Plummer, G. (1952). “Anomalies occurring in children exposed in utero to atomic bomb in Hiroshima.” Pediatrics. Springfield, Ill., 10:687–693. Abstr. J.A.M.A. 151(14):1235.

56. Rugh, Roberts. (1954). “The effect of ionizing radiations on amphibian development.” J. Cell. and Comp. Physiol. 43(Suppl. 1):39–75. Symposium (opere citato).

57. Russell, Liane Brauch. (1956). “X-ray-induced developmental abnormalities in the mouse and their use in the analysis of embryological patterns. II. Abnormalities of the vertebral column and thorax.” J. Exp. Zool. 131(3): [page number omitted.]

58. Russell, Liane Brauch, and William Lawson Russell. (1954). “An analysis of the changing radiation response of the developing mouse embryo.” J. Cell. and Comp. Physiol. 43(Suppl. 1):103–149. Symposium (opere citato).

59. Sacks, Jacob. (1953). Isotopic Tracers in Biochemistry and Physiology. McGraw-Hill: 330 W. 42nd Street, New York 36, NY, 383 pp. $8.50.

60. Spear, Frederick Gordon. (1953). Radiations and Living Cells. John Ailey and Sons, Inc.: 440 Fourth Ave., New York 16, NY, 222 pp. $3.50.

61. U.S. Atomic Energy Commission. (1950). Medical Aspects of Atomic Weapons. U.S. Govt. Print. Office, Washington, DC, 24 pp.

62. Wasserman II, R., and B.F. Trum. (1955). “Effect of feeding dogs the flesh of lethally irradiated cows and sheep.” Science. 121:894–896.

63. Weiss, Paul. (1954). “Summarizing remarks.” J. Cell. and Comp. Physiol. 43(Suppl 1):329–331. Symposium (opere citato).

64. Willier, B.H. (1954). “Phases in embryonic development.” J. Cell. and Comp. Physiol. 43(Suppl. 1):307–317. Symposium (opere citato).

65. Wilson, J.G. (1954). “Differentiation and the reaction of rat embryos to radiation.” J. Cell. and Comp. Physiol. 43(Suppl. 1):11–38. Symposium (opere citato).

66. Wilson, J.G., and J.W. Karr. (1950). “Differences in the effects of X-irradiation in rat embryos of different ages.” Anat. Rec. 106:259–260.

67. Yamazaki, James N., Stanley W. Wrigh,t and Phyllis M. Wright. (1954). “A study of the outcome of pregnancy in women exposed to the atomic bomb blast in Nagasaki.” J. Cell. and Comp. Physiol. 43(Suppl. 1): [page number omitted]. Symposium (opere citato).

68. Zirkle, Raymond E., Ed. (1954). Biological Effects of External X and Gamma Radiation, Part I. McGraw-Hill: 330 W. 42nd Street, New York 36, NY, 530 pp. $7.25.[spacer height=”20px”]

IV. Hormonal Induction

69. American Medical Association. (1951). “Circulatory disturbances in the genesis of congenital malformation.” J.A.M.A. 147(2):180.

70. American Medical Association. (1952). “Experimental production of congenital anomalies with cortisone.” J.A.M.A. 148(3):206.

71. American Medical Association. (1955). “Pregnancy and cortisone.” J.A.M.A. 159(3):212.

72. Brown, E.E. (1954). “Pathogenesis of mongolism following maternal illness: role of adrenals.” Arch. Pediat. 71:47–53.

73. Fraser, Frank Clarke, Harold Kalter, Bruce E. Walker, and T.D. Fainstat. (1954). “The experimental production of cleft palate with cortisone and other hormones.” J. Cell. and Comp. Physiol. 43(1): [page number omitted].

74. Greenwald, Gilbert S. (1956). “Estrogen injury to the pregnant rabbit.” Anat. Rec. 124(2):404.

75. Hoffman, F., C. Overzier, and G. Uhde. (1955). “Question of hormonal production of fetal hermaphroditism in human beings.” Geburtsh. u. Frauenh. 15:1061–1070. Abstr. J.A.M.A. 160(17):1535.

76. Kalter, Harold. (1956). “Modification of teratogenic action of cortisone in mice by maternal age, maternal weight, and little size.” Am. J. Physiol. 185(1):65–68.

77. Kalter, Harold, and F.C. Fraser. (1953). “The modification of the teratogenic action of cortisone by parity.” Science. 118:625–626.

78. Nelson, Marjorie M., and H.M. Evans. (1954). “Maintenance of pregnancy in the absence of dietary protein with estrone and progesterone.” Endocrinology. 55(5):545–549.

79. Smithberg, Morris. (1956). “Congenital deformity in the mouse induced by insulin.” Anat. Rec. 124(2):441.[spacer height=”20px”]

V. Chemical Induction

80. American Medical Association. (1954). “Smoking and drinking in pregnancy.” J.A.M.A. 154(2):186.

81. American Medical Association. (1956). “Effect of reserpine in the newborn.” J.A.M.A. 160(3):209.

82. Ancel, P. (1955). “Malformations determinees par des injections de substances chimiques localisees a la tete d embryons de poule.” J. Embryol. and Exp. Morph. 3(4):335–354.

83. Bieber, Samuel, and George H. Hitchings. (1955). “The developing pig embryo and growth inhibitors.” Cancer Research. (Suppl. 3): 80–82.

84. Bodenstein, Dietrich. (1954). “Effects of radiomimetic substances on embryonic development, with special reference to nitrogen mustards.” J. Cell. and Comp. Physiol. 43(Suppl. 1): [page number omitted].

85. Dagg, C.P., and David A. Karnofsky. (1955). “Teratogenic effects of azaserine on the chick embryo.” J. Exp. Zool. 130(3):555–572.

86. Driscoll, William T., and R.M. Eakin. (1955). “The effects of sucrose on amphibian development with special reference to the pituitary body.” J. Morph. 129(1):149–175.

87. Ferm, Vergil H. (1956). “Teratogenicity and placental permeability of trypan blue in the rabbit.” Anat. Rec. 124(2): Abstract 180.

88. Ferm, Vergil H. (1956). “Permeability of the rabbit blastocyst to trypan blue.” Anat. Rec. 125(4): [page number omitted].

89. Fox, M.H., and C.M. Goss. (1956). “Experimental production of a syndrome of congenital cardiovascular defects in rats.” Anat. Rec. 124(2):189–207.

90. Friar, Wayne F., and Gilbert L. Woodside. (1956). “Effects of 8-azaguanine on early chick embryos grown in vitro.” Growth. 20(1):9–18.

91. Hamburgh, Max. (1954). “The embryology of trypan blue induced abnormalities in mice.” Anat. Rec. 119(4):409–427.

92. Karnofsky, David A. (1955). “Assay of chemotherapeutic agents on the developing chick embryo.” Cancer Research. (Suppl. 3):83–85.

93. Landauer, Walter. (1954). “On the chemical production of developmental abnormalities and of phenocopies in chicken embryos.” J. Cell. and Comp. Physiol. 43(Suppl. 1): [page number omitted].

94 Landauer, Walter. (1956). “The teratogenic activity of pilocarpine, pilocarpidine and their isomers, with special reference to the importance of steric configuration.” J. Exp. Zool. 132(1): [page numbers omitted].

95. Liedke, K.B., et al. (1954). “The selective response of amphibian embryos to benzimidazole and benzotriazole derivatives.” J. Exp. Zool. 127(2): [page numbers omitted].

96. Sakula, A. (1954). “Streptomycin and the foetus.” Brit. J. Tuberc. 48:69–72. Abstr. J.A.M.A. 154(7):1468.

97. Scott, F.M. (1954). “Metamorphic differentiation in Amaroucium constellatum treated with nitrogen mustard.” J. Exp. Zool. 127(2): [page number omitted].

98. Wilson, James G. (1954). “Malformations caused by azo dyes.” Anat. Rec. 118(2):439.

99. Wilson, James G. (1955). “Teratogenic activity of several azo dyes chemically related to trypan blue.” Anat. Rec. 123(3): [page number omitted].[spacer height=”20px”]

VI. Parasites and Congenital Defects

100. Adams, J.M., H.D. Heath, D.T. Imagawa, et al. (1956). “Viral infections in the embryo.” A.M.A. J. Dis. Child. 92:109–114. Abstr. J.A.M.A. 162(10):1011–1012.

101. American Medical Association. (1953). “Etiology of congenital malformations.” J.A.M.A. 152(14):21–25.

102. American Medical Association. (1954). “Polio virus crosses the placenta.” J.A.M.A. 156(15):1460.

103. American Medical Association. (1955). “Microcephaly.” J.A.M.A. 158(14):1329.

104. American Medical Association. (1955). “Congenital malformations and rubella during gestation.” J.A.M.A. 159(10):1067–1068.

105. American Medical Association. (1955). “Maternal rubella in pregnant women.” J.A.M.A. 159(12):1245.

106. American Medical Association. (1956). “Infectious embryopathies.” J.A.M.A. 162(1):56.

107. Andreas, H. (1954). “Toxoplasmosis and malformations.” Zentral. L. Gynak. 75(43):1700–1709. Abstr. J.A.M.A. 155(1):79.

108. Bosatra, A. (1954). “Rubella embryopathy: Its importance as cause of congenital deafness.” Minerva Otorinolaring. 4:6–12. Abstr. J.A.M.A. 155(14):1290.

109. Robertson, G. Gordon, et al. (1955). “A study of abnormalities in early chick embryos inoculated with Newcastle disease virus.” J. Exp. Zool. 129:5–43.

110. Kleine, H.C. (1956). “Toxoplasmosis as cause of mongolism.” Ztschr. Geburtsh. u Gynak. 147(1):13–27. (1956). Abstr. J.A.M.A. 162(14):1342.[spacer height=”20px”]

VII. Oxygen and Atmospheric Pressure

111. American Medical Association. (1953). “Amniotic fluid embolism.” J.A.M.A. 151(11):943.

112. American Medical Association. (1953). “Mongolism: Some newer developments.” J.A.M.A. 152(14):21–25.

113. American Medical Association. (1954). “Prevention of oxygen toxicity.” J.A.M.A. 155(10):28.

114. American Medical Association. (1955). “Pulmonary hyaline membrane.” J.A.M.A. 159(15):1491.

115. American Medical Association. (1956). “Maternal oxygen and fetal distress.” J.A.M.A. 162(9):938.

116. Ashton, N., and C. Cook. (1954). “Direct observation of the effect of oxygen on developing vessels: Preliminary report.” Brit. J. Opth. 38:433–440. Abstr. J.A.M.A. 156(7):747.

117. Cook, Sherburne F., and Alvin A. Krum. (1955). “Deterioration of mouse strains exposed for long periods to low atmospheric pressure.” J. Exp. Zool. 128(3):561–572.

118. Ferner, H., and W. Runge. (1955). “Synthalin A as selective mitotic poison acting on a-cells of the islets of Langerhans.” Science. [Volume omitted]:122–420.

119. Meier, Gilbert W., and Emil W. Menzel. (1955). “Prenatal oxygen deprivation and subsequent specific behavior dysfunctions.” Science. 122:419–420.

120. Nelsen, Olin E. (1955). “The effects of increased atmospheric pressures upon early chick development.” J. Morph. 92(2):359-379.

121. Patz, A., A. Eastham, D. H. Higginbotham, and T. Kieh. (1953). “Oxygen studies in retrolental fibroplasia: II. Production of microscopic changes of retrolental fibroplasia in experimental animals.” Amer. J. Ophthalmology. 36:1497–1653. Abstr. J.A.M.A. 154(11):945.

122. Taylor, H.C. (1953). “Unrecognized intrauterine anoxia as cause of fetal death during labor.” Yale J. Biol. Med. 25:525. Abstr. J.A.M.A. 153(5):522.[spacer height=”20px”]

VIII. Rh-Factor, Overripeness, Maternal Limitations, Toxemia, Physical Injury, Electroshock

123. Allison, John E. (1955). “Growth of transplanted tissues derived from normal and overripe frog’s eggs.” Anat. Rec. 122(4):561–579.

124. American Medical Association (1954). “Endometrial chemistry and fertility.” J.A.M.A. 155(4):28.

125. Brenner, M. (1954). “Case of Rh incompatibility and deformities in successive infants.” Geburtsh. u. Frauenh. 14:150–153. Abstr. J.A.M.A. 155(10):939.

126. Briones, H., and R.A. Beatty. (1954). “Interspecific transfers of rodent eggs.” J. Exp. Zool. 125(1): [page number omitted].

127. Bromberg, Y.M., M. Salzberger, and A. Abrahamov. (1956). “Transplacental transmission of fetal erythrocytes with demonstration of fetal hemoglobin in maternal circulation.” Obst. and Gynec. 7:672–674.

128. Hess, Arthur. (1954). “Reactions of mammalian fetal tissues to injury. II. Skin.” Anat. Rec. 119(4):435–447.

129. Hess, Arthur. (1954). “Reactions of mammalian fetal tissues to injury. III. Skeletal muscle.” Anat. Rec. 120(3): [page number omitted].

130. Ingalls, T.H., and J.E. Gordon. (1947). “Epidemiologic implications of developmental arrests.” Am. J. Med. Sci. 214:322.

131. Runner, Meredith N. (1951). “Differentiation of intrinsic and maternal factors governing intrauterine survival of mammalian young.” J. Exp. Zool. 116(1): [page number omitted].

132. Torpin, Richard. (1956). “Variations in depth of implantation of the human ovum correlated with placental anomalies, spontaneous abortion, and premature separation.” Anat. Rec. 124(2):373.

133. Trasler, D.G., B.E. Walker, and F.C. Fraser. (1956). “Congenital malformations produced by amniotic-sac puncture.” Science. 124:439.

134. Witschi, E. (1952). “Overripeness of egg as cause of twinning and teratogenesis.” Cancer Research. 12:763–846. Abstr. J.A.M.A. 151(10):858.

135. Yamamoto, J., E.M. Hammes, and E.M. Hammes Jr. (1953). “Mental deficiency in child whose mother was given electric convulsive therapy during gestation: Case report.” Minnesota Med. St. Paul, 36:1260–1310. Abstr. J.A.M.A. 154(13):1132.

136. Oster, J. (1956). “The causes of mongolism.” Dan Med Bull. 3(5):158–164 (in English); Copenhagen, Denmark. Abstr. J.A.M.A. 162(14):1342.[spacer height=”20px”]

IX. Nutritional Deficiency and Hyper States

137. American Medical Association. (1951). “Vitamin E and abortion.” J.A.M.A. 146(15):1457.

138. American Medical Association. (1951). “Fetal malformation.” J.A.M.A. 147(2):180.

139 American Medical Association. (1951). “Seriousness for the fetus of unapparent disease of the mother.” J.A.M.A. 147(2):180.

140. American Medical Association. (1951). “Vitamin E and fertility.” J.A.M.A. 147(2):207.

141. American Medical Association. (1953). “Research on vitamins.” J.A.M.A. 151(10):854.

142. American Medical Association. (1953). “Azoospermia.” J.A.M.A. 152(12):118.

143. American Medical Association. (1953). “Calcium for uterine inertia.” J.A.M.A. 153(12):1141.

144. American Medical Association. (1953). “Excess vitamin A and congenital defects.” J.A.M.A. 153(13):1176.

145. American Medical Association. (1954). “Experimentally induced congenital defects in mammals.” J.A.M.A. 154(13):1115–1116.

146. American Medical Association. (1954). “Effect of ascorbic acid on anti-Rh agglutinins.” J.A.M.A. 156(11):28. Pfizer Spectrum.

147. American Medical Association. (1954). “Influence of vitamins on seminal fluid.” J.A.M.A. 156(13):1289.

148. American Medical Association. (1955). “Congenital hydrocephalus due to experimental hypovitaminosis A.” J.A.M.A. 157(3):298–299.

149. American Medical Association. (1955). “Infertility.” J.A.M.A. 158(7):620.

150. American Medical Association. (1956). “Vitamin E.” J.A.M.A. 160(2):133–134.

151. American Medical Association. (1956). “Robin’s syndrome (micrognathia and glossoptosis): Case report.” J.A.M.A. 160(9):811.

152. Asling, C. Willet, M.M. Nelson, H.V. Wright, and H.M. Evans. (1955). “Congenital skeletal abnormalities in fetal rats resulting from maternal pteroylglutamic acid deficiency during gestation.” Anat. Rec. 121(4):775–800.

153. Atkinsen, R.L., et al. (1955). “Vitamin E and reproduction in turkeys.” J.Nutr. 55:387–397.

154. Barbieri, L., and P.L. Esposti. (1954). “Modifications of islands of Langerhans following vitamin E therapy.” Minerva Med. 45:1324–1326. Abstr. J.A.M.A. 156(5):568.

155. Biskind, Leonard H., and Morton S. Biskind. (1944). “Accelerated postpartum involution of the uterus with vitamin B complex therapy.” Western J. Surg., Obst. and Gynec. 52:266–270; Bull. of N.Y. Acad. Med. 20(7):422.

156. Biskind, Morton S. (1947). “The relation of nutritional deficiency to impaired libido and potency in the male.” J. Gerontology. 2(4):303–314.

157. Blandau, R.J., Hans Kuanitz, and C.A. Slanetz. (1949). “Ovulation, fertilization, and transport of ova in old, vitamin E deficient rats.” J. Nutr. 38(1): [page number omitted].

158, Bo, Walter J. (1956). “Histochemical observations on the uterus of the rat following vitamin A deficiency. I. Glycogen and PAS positive substances.” Anat. Rec. 124(2):389–390.

159. de Reynier, J.P. (1956). Deaf-mutism. J.AM.A. 160(11):995.

160. Deuel II., J., et al. (1955). “XVI. Linoleate and linolenate in satisfying essential fatty acid requirement for pregnancy and lactation.” J. Nutr. 57(2):297–302.

161. Deuel Jr., Harry J., Charlotte R. Martin, and Roslyn B. Alfin-Slater. (1954). “The effect of fat level of the diet on general nutrition. XII. The requirement of essential fatty acid for pregnancy and lactation.” J. Nutr. 54(2): [page number omitted].

162. Deuschle, Frederick M., and Josef Warkany. (1956). “Congenital nasal malformations induced in rats by maternal riboflavin deficiency.” Anat. Rec. 124(2):398.

163. Dinning, James S., et al. (1955). “A biochemical basis for the interrelationship of pantothenic acid and methionine.” J. Nutr. 65(3):431–435.

164. Emmel, Victor M. (1956). “Influence of tocopherol administration on renal autolysis and body fat in vitamin E-deficient rats.” Anat. Rec. 124(2):399.

165. Everson, G. (1954). “Effect of varying the intake of calcium pantothenate of rats during pregnancy. I. Chemical findings in the young at birth.” J.Nutr. 53(3):341–350.

166. Everson, Gladys, Lois Northrop, Nam Y. Chung, and Robart Getty. (1954). “Effect of ascorbic acid on rats deprived of pantothenic acid during pregnancy.” J. Nutr. 54(2): [page number omitted].

167. Ferguson, T.M., and J.R. Couch. (1954). “Further gross observations on the B12 deficient chick embryo.” J. Nutr. 54(3):361–379.

168. Firth, Jay, and Bruce Conner Johnson. (1956). “Quantitative relationships of tryptophan and nicotinic acid in the baby pig.” J. Nutr. 59(2): [page number omitted].

169. France, Beulah. (1956). “Vitamin C therapy prevents miscarriage.” The Corvallis, Oregon Gazette-Times. 47(119): [page number omitted].

170. Fraser, F. Clarke, and T.D. Fainstat. (1951). “Causes of congenital defects.” Am. J. Dis. of Children. Nov. Abstr. J.A.M.A. 147(15):1453.

171. French, C.E., R.H. Ingram, L.K. Knoebel, and R.W. Swift. (1952). “The influence of dietary fat and carbohydrate on reproduction and lactation in rats.” J. Nutr. 48(1): [page number omitted].

172. Giroud, A., J. Lefebvres, H. Prost, and R. Dupuis. (1955). “Malformations des membres dues a des lesions vasculaires chez foetus de fat deficient en acide pantothenique.” J. Embryol. and Exp. Morph. 3(1):1–12.

173. Grainger, R.B., Boyd O’Dell, and A. Hogan. (1954). “Congenital malformations as related to deficiencies of riboflavin and vitamin B12, source of protein, calcium to phosphorus ratio, and skeletal phosphorus metabolism.” J. Nutr. 54(1):46.

174. Hedin, P.A., and M.O. Schultze. (1955). “Maternal diet and other factors affecting the lipid content of livers of very young rats.” J. Nutr. 56(1): [page number omitted].

175. Ingalls, Theodore H. (1956). “Causes and prevention of developmental defects.” J.A.M.A. 161(11):1047.

176. Jacobs, W.M. (1956). “The use of the bioflavonoid compounds in the prevention or reduction in severity of erythroblastosis fetalis.” Surg. Gynec. and Obst. 103:233–236. Abstr. J.A.M.A. 162(8):840–841.

177. Kocen, B.P., and L.F. Cavazos. (1956). “Effects of avitaminosis C on the reproductive tract of the guinea pig.” Anat. Rec. 124(2):417.

178. Kummerow, F.A., H.P. Pan, and H. Hickman. (1952). “The effect of dietary fat on the reproductive performance and the mixed fatty acid composition of fat-deficient rats.” J. Nutr. 46:489–498.

179. Lamming, G.E., G.W. Salisbury, R.L. Hayes, and K.A. Kendall. (1954). “The effect of incipient vitamin A deficiency on reproduction in the rabbit. I. Decidua, ova and fertilization.” J. Nutr. 52(2):217–225.

180. Lamming, G.E., G.W. Salisbury, R.L. Hayes, and K.A. Kendall. (1954). “The effect of incipient vitamin A deficiency on reproduction in the rabbit. II. Embryonic and fetal development.” J. Nutr. 52(2):227–239.

181. Larrivoll, Gertrude P., and C.A. Elvehjen. (1954). “Studies in the nutritional requirements of chinchillas.” J. Nutr. 52(3): [page number omitted].

182. Lockard, Isabel, and Lois Adell Gillihan. (1956). “Neurologic dysfunctions and their relation to congenital abnormalities of the central nervous system in cats.” J. Comp. Neurol. 104(3): [page number omitted].

183. Machlin, L.J., and William Tuckey Shalkop. (1956). “Muscular degeneration in chickens fed diets low in vitamin E and sulfur.” J. Nutr. 60(1): [page number omitted].

184. Mastboom, J.L., and A. Sikkel. (1952). “Value of vitamin E in treatment of toxemia of late pregnancy.” Gynaecologia Basel. 134:361–420. Abstr. J.A.M.A. 151(17):1523.

185. Menshik, Z. (1953). “Relations between dietary fats and vitamin E during the development of connective tissues.” Anat. Rec. 115(2):347–348.

186. Menshik, Z.(1956). “The elastic fibres of the heart and vitamin E.” Anat. Rec. 124(2):333–334.

187. Miller, E.R., et al. (1955). “The thiamine requirement of the baby pig.” J. Nutr. 56(3):423–430.

188. Monie, I.W., et al. (1954). “Abnormalities of the urinary system of rat embryos resulting from maternal pteroylglutamic acid deficiency.” Anat. Rec. 120(1):119–135.

189. Nelson, Marjorie M., C.W. Asling, H.M. Evans. (1952). “Production of multiple congenital abnormalities in young by maternal pteroylglutamic acid deficiency during gestation.” J. Nutr. 48(1): [page number omitted].

190. Nelson, Marjorie, Catherine Baird, Howard V. Wright, and Herbert Evans. (1956). “Multiple congenital abnormalities in the rat resulting from riboflavin deficiency induced by the antimetabolite galactoflavin.” J. Nutr. 58(1): [page number omitted].

191. Nelson, Marjorie M., and Herbert M. Evans. (1953). “Protein deficiency and resorption.” J. Nutr. 51:71.

192. Nelson, Marjorie M., and Herbert M. Evans.(1956). “Diet found vital during pregnancy.” Spokane Chronicle, Jan. 3.

193. Nelson, Marjorie M., et al., (1955). “Multiple congenital abnormalities resulting from transitory deficiency of pteroylglutamic acid during gestation in the rat.” J. Nutr. 56(3):349–370.

194. Overholser, M.D., et al. (1954). “The ventricular system in hydrocephalic rat brains produced by a deficiency of vitamin B12 or of folic acid in the maternal diet.” Anat. Rec. 120(4): [page number omitted].

195. Panos, T.C., and J.C. Finerty. (1954). “Effects of a fat-free diet on growing male rats with special reference to the endocrine system.” J. Nutr. 54(3):315–331.

196. Pearmain, John. (1952). “Commercial fertilizer and sterility.” Normal Agriculture. 2(2):2; col. 3, para. 1; Aug.

197. Perdue, Henry S., and Paul H. Philips. (1954). “Failure of vitamin B12 to increase survival of progeny of rats fed on all plant diet.” J. Nutr. 53(2): [page number omitted].

198. Platt, B.S. (1955). “Infant feeding and diseases in later life.” Brit. M. J. 1:179. Abstr. J.A.M.A. 158:497.

199. Pratt, Jean Paul, et al. (1951). “Metabolism of women during the reproductive cycle. XVIII. The effect of multivitamin supplements on the secretion of B vitamins in human milk.” J. Nutr. 44(1): [page number omitted].

200. Ragen, B.M., et al. (1955). “Vitamin A metabolism in infection.” J. Morph. 57(2):277–286.

201. Robertson, W. Van Bogart, and V.F. Cross. (1954). “Collagen formation in vitamin A deficient rats.” J. Nutr. 54(1): [page number omitted].

202. Ross, Margaret L., and Ruth L. Pike. (1956). “The relationship of vitamin B12 to protein metabolism during pregnancy in the rat.” J. Nutr. 58(2): [page number omitted].

203. Ross, Margaret L., and Ruth L. Pike. (1956). “The relationship of vitamin B6 to serum protein and nonprotein nitrogen in the rat during pregnancy.” J. Nutr. 60(2):211–219.

204. Runner, Meredith N., and James R. Miller. (1956). “Congenital deformity in the mouse as a consequence of fasting.” Anat. Rec. 124(2):437.

205. Schultze, Max O. (1953). “Nutritional value of plant materials.” J. Nutr. 49(2):245–257.

206. Schultze, Max O. (1953). “Nutritional value of plant materials: VIII. Lactation failure of rats fed diets containing purified soybean proteins.” J. Nutr. 49(2):231–243.

207. Schultze, Max O. (1954). “Weight increments of suckling rats as affected by litter size and maternal diet.” J. Nutr. 54(3): [page number omitted].

208. Schultze, Max O. (1955). “Effects of malnutrition in early life and subsequent growth and reproduction of rats.” J. Nutr. 56(1): [page number omitted].

209. Scott, M.L., et al. (1955). “Studies on vitamin E in poultry nutrition.” J. Nutr. 56(3):387–402.

210. Silberberg, M., and R. Silberberg. (1955). “Diet and life span.” Physiol. Rev. 35:347–362. Abstr. J.A.M.A. 158(15):1402–1403.

211. Stothers, Stephen C., et al. (1955). “The pantothenic acid requirement of the baby pig.” J. Nutr. 57(1): [page number omitted].

212. Ullrey, D.E., et al. [Title of article omitted.] (1955). J. Nutr. 57(3): [page number omitted].

213. Walker, Donald, and Zolton T. Wirtschafter. (1956). “Estrogenic inhibition of fetal resorption in lathyrism.” J. Nutr. 58(2): [page number omitted].

214. Walker, Donald, and Zolton T. Wirtschafter. (1956). “Resorption of embryos in rats on lathyrus odoratus diet.” J. Nutr. 58(2): [page number omitted].

215. Warkany, Josef. (1945). “Manifestations of prenatal nutritional deficiency.” Vit. and Hormones. 3:73.

216. Warkany, Josef. (1947). “Etiology of congenital malformations.” Advances in Ped. 2:1.

217. Warkany, Josef. (1954). “Disturbance of embryonic development by maternal vitamin deficiencies.” J. Cell. and Comp. Physiol. 43(1): [page number omitted].

218. Welch, B.L. (1954). “The relation of vitamin B12 to egg yolk storage of folic acid.” J Nutr. 54(4):601–608.

219. Wilson, James G., Carolyn B. Roth, and Josef Warkany. (1953). “An analysis of the syndrome of malformations induced by maternal vitamin A deficiency. Effects of restoration of vitamin A at various times during gestation.” Am. J. Anat. 92(2): [page number omitted].

220. Wixom, R.L., et al. (1955). “Interrelationship of serine and glycine for chick growth.” J. Nutr. 56(3):409–422.[spacer height=”20px”]

X. Vitamin Antagonists and Analogs

221. Meltzer, Hyman J. (1956). “Congenital anomalies due to attempted abortion with 4-aminopterglutamic acid.” J.A.M.A. 161(13):1253.

222. Naber, E.C., et al. (1954). “Thiamine analogy on embryonic development and growth of the chick.” J. Nutr. 54(4):579–591.

223. Thiersch, J.B. (1952). “Therapeutic abortions with folic acid antagonist 4-aminopteroylglutamic acid (4-amino P.G.A.) administered by oral route.” Am. J. Obst. and Gynec. 63:1185–1420. Abstr. J.A.M.A. 150(7):718.

By Dr. Howard H. Hillemann, MA, PhD, School of Science, Oregon State College, Corvallis, Oregon. Original source unknown. Reprinted by the Lee Foundation for Nutritional Research, Reprint 66C, circa 1957.  

Lee Foundation for Nutritional Research
2023 West Wisconsin Ave.
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Reprint No. 66C
Price – 25 cents
Printed in U.S.A.

Note: Lee Foundation for Nutritional Research is a nonprofit, public-service institution, chartered to investigate and disseminate nutritional information. The attached publication is not literature or labeling for any product, nor shall it be employed as such by anyone. In accordance with the right of freedom of the press guaranteed to the Foundation by the First Amendment of the U.S. Constitution, the attached publication is issued and distributed for informational purposes.


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