Will the Baby Be Normal?

Deformed, unfinished, sent before my time Into this breathing world, scarce half made up, And that so lamely and unfashionable That dogs bark at me as I halt by them . . .

--Shakespeare (Richard III} Every day, hundreds of thousands of U.S. women have in the back of their minds the nagging question, "Will my baby be normal?'' Each year, for most of the 4,250,000 newly delivered mothers, it becomes, "Is the baby all right?" For more than 4,000,000 of them the answer is yes, to sighs of vast relief. But to the remainder, doctors and nurses try to postpone breaking the news that the baby is in some way malformed. If the child lives, he may later join "Richard the Crouchback" in railing against his fate, and with better reason.*

Last week, to improve the proportion of favorable answers for mothers the world over, 480 experts (from 26 nations) in medicine and a dozen related sciences met in London's Church House in the world's first international conference on congenital malformations.

Twilight Genes. Said Montreal's Dr. F. Clarke Fraser: probably no more than 10% of birth defects are caused by defective genes. If both parents have an abnormal dominant gene, the child is sure to carry the defect. But there are many twilight-zone genes, which some individuals carry without showing ill effects but may pass on, in crippling form, to their offspring. Then there are recessive genes, which may be so elusive that the experts cannot hope to trace cause and effect.

The most remarkable case of a congenital malformation traceable to one gene, noted the Rockefeller Institute's Dr.

George W. Corner, is that of the Dionne quintuplets. Developed from a single fertilized ovum, which then repeatedly sub divided, all the girls had the defect. Fortunately, it was minor : nothing more than a slight webbing between the second and third toes of each foot.

The vast majority of inborn defects are now recognized as due to something that goes wrong in the environment of the fetus -- in the womb. In most cases, the underlying cause is unknown. In a few cases, the direct cause is now clear, thanks to an Australian ophthalmologist.

A dozen conferees paid tribute to Sir Norman McAlister Gregg, 68, the Sydney ophthalmic surgeon who saw a local epidemic of cataracts in the newborn in 1941. By detective work he found that in all but ten of 78 cases the mothers had had German measles (rubella) in the first four months of pregnancy. Around the world, Gregg's findings were soon confirmed. Thus a common infection, almost invariably mild in children but which may be severe in adults, was convicted as a crippler and killer of the unborn.

Apparently the rubella virus inflicts its severest damage on whichever tissues happen to be developing fastest when the infection strikes. Toronto's Dr. Andrew J. Rhodes gave this timetable: rubella causes cataracts in the sixth week, deafness by infection in the ninth, heart defects fifth to tenth weeks, dental deformities sixth to ninth weeks.

As soon as Gregg's epochal discovery was confirmed, researchers began to hunt for a protective vaccine and for proof that abnormalities might be caused by other virus diseases infecting the mother. So far they have had little luck. Mumps, said Dr. Rhodes, is next in line as a crippier and killer in utero. Influenza has been indicted in some jurisdictions, but the evidence is not so clear.

Exception to Innocence. Whenever a woman bears a malformed child, she tortures herself with the questions, "Is it my fault? What did I do wrong?" In most cases, nothing. The one clear exception to the rule of maternal innocence is syphilis. Its spirochetes do not attack the fetus until relatively late in its development. If syphilis is diagnosed early in pregnancy, intensive treatment with penicillin can give the mother's unborn child almost sure protection.

Burden of the London conference was that while much remains to be done, far more has been accomplished in the last quarter-century than in the previous 2,500 years. Except for specialized and usually local deficiencies in the diet, such as iodine, malnutrition is now known not to be a major cause of malformations. Stress and strain on the mother play a role in some birth defects (they have been blamed for harelip and cleft palate), but just what is far from clear.

If, despite all reasonable precautions, the baby is defective, today's surgery and medicine offer far more hope of alleviating the condition than before World War II. Many severe abnormalities in and around the heart, once crippling and eventually fatal, are now corrected by daring surgery. "Water on the brain" (hydrocephalus) can be drained away by ingenious valves and tubes.

Man may soon be tinkering with his chromosomes and the genes they contain. Mongolism has recently been shown to be associated with a supernumerary chromosome: victims have 47 instead of the normal 46. Some cases of intersex abnormalities have one or even two extra female (X) chromosomes. Within the chromosomes, a defective gene may fail in its function because a single fraction of its nucleic acid molecule is aberrant and inutile. The time may come, suggested the Rockefeller Institute's Geneticist Edward L. Tatum, when medical men will be able to replace a defective gene with a specially tailored nucleic acid molecule, or to boost a patient's deficient supply of functioning molecules with an injection of the right kind. If that day comes, man will be close to controlling the fashioning of his offspring before they are conceived.

* Best evidence now is that Richard III, though puny and below average height (whereas eldest brother Edward IV was a muscular giant of 6 ft. 4 in.), was not visibly deformed. "Crouch-back" probably referred to a shoulder slope induced by vigorous practice which overdeveloped the muscles of his sword arm. Shakespeare, truckling to the Tudor court, made Plantagenet Richard a monster.

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