The complete exclusion of applied nutrition and basic physiology from clinical obstetrics in the United States continues unabated. There remains absolutely no significant recognition of the role of prenatal malnutrition, especially of protein-calorie (p-c) deficiency, in the etiology and pathogenesis of metabolic toxemia
of late pregnancy. Karen R. (not her real name), R.N., age 27, worked as a nurse in the neonatal intensive-care unit of the Staten Island Hospital during her first pregnancy which was terminated by C-Section at 35 weeks on February 3, 1979, because of “severe pre-eclampsia.” Her 5 pound baby girl developed respiratory distress syndrome and was treated in her own Neonatal I.C.U. and survived.
She and her husband had attended Lamaze classes and she wanted a natural childbirth with her husband present, without drugs; she wanted to be “bonded” to the baby and breastfeed right after delivery. Instead, she had an emergency C-Section with her husband not present; she didn’t see the baby until 52 hours after birth. She tried to breastfeed, but failed.
On March 2, 1979 Karen called on our “TOXEMIA HOT LINE” wanting to know ‘What happened to me and my baby?” As I elicited a history it was clear that she had suffered protein-calorie deficiency severe enough to cause metabolic toxemia of late pregnancy (MTLP). On March 5, 1979 she wrote a letter at my request describing her pregnancy and diet:
“During my pregnancy my focus was directed toward labor and delivery, and breastfeeding, so most of the books I read were related to these specific areas. Maybe if I had paid more attention to my diet, and nutritional aspects of pregnancy, labor and delivery would have been a reality. Instead I ended up with a surgical birth, premature baby, and much disappointment.
“July through November 26 (1978) I was working the night shift. During the first 15 weeks I was nauseated almost continually, and vomiting fairly often - had ZERO appetite. I was eating one meal a day, usually:
- off work - 8 a.m.
- home to bed
- awakened 3 - 4 p.m., had toast, sometimes cereal
- dinner at 6130 to 7130 P-m.t Milk$, potato or pasta, no appetite for meat, but would usually eat a small portion: ½ hamburger…rarely ate dessert.
- evening - coffee
- work at 11 p.m. — 12 midnight, coffee; 3 a.m. coffee, soda & snack (usually cookies); 6:30 to 7 a.m. - usually some juice.
- home to bed at 8 a.m.
(She is 5 feet 4 inches and weighed 124 lbs. pre-pregnancy. She gained nothing the first 8 weeks — and by her 24th week in November, she had gained only 6 lbs. to 130.)
“From Nov. 26 to Jan. 25 I worked full-time day shift as an Inservice Instructor:
- 6 a.m. up
- 7:15 - at work
- 8:30 - breakfast … usually cereal with skim milk, coffee, sometimes orange juice or fruit
- 12-1 p.m. - lunch: usually soup with crackers,skim milk or diet soda, tuna or chicken salad (not a sandwich, i.e., no bread), fruit salad.
- 4 p.m. - home from work, usually had a diet soda or skim milk
- 6:30 to 7 p.m. - Dinner: lots of pasta-type dishes, spaghetti, macaroni, etc. sometimes with vegetables. Milk or soda. No dessert. No snacks.
- 10 p.m. bed
(No eggs, little meat, less than a quart of milk daily.)
“Then there was the episode of gastro-enteritis in January. I know I was dehydrated and depleted during that episode.” She told me on the phone that she had ketones in her urine for several days then and was worried about it, but her OB-GYN, who was kind enough to make a house call, told her not to worry as it wasn’t important.
On a visit January 2, 1979, Karen had BP of 140/80, first elevations and a “trace” of protein in urine. Her OB-GYN advised bed-rest on her left side, to restrict dietary salt and to force fluids (mostly water) and to return in 3 days. On January 5, her BP was back to 110/70, she had lost 3 lbs, 142 to 139, and had one-plus proteinuria she went back to work. On January 19, BP was 120/70, weight 142½ and one-plus proteinuria recorded again.
On Feb. 2, she had some ankle edema, had gained to 144½ lbs., some headaches and BP was up to 160/90 with one-plus proteinuria persisting. She was admitted to the hospital that day for ‘rest.’ The next day because of hyperactive reflexes and “involuntary tremors” of arms and legs, she was rushed to the O.R. for a C-Section.
At no time during her training to become a registered nurse, during her Lamaze childbirth classes, nor during her prenatal visits with her OB-GYN (whom she considered gave her very good prenatal care), did Karen get any idea that protein-calorie deficiency could cause MTLP or a low birth weight baby. She daily took a prenatal vitamin-mineral tablet, Filibon, was careful to avoid salt as much as possible, and tried not to gain too much weight (i.e., diet soda, skim milk, no bread, etc.).
| Her weight just before delivery was 144 lbs., from 124 lbs., for a total gain of 20 lbs.; however most of this was water weight as on the 4th postpartum day, after delivery of a 5 lb. baby, she was back to 124! This is concrete evidence of a protein-calorie deficiency. |
It is a fact that nobody knows why Karen developed MTLP; not a soul in her own hospital. They could only chide her: “Why Karen, you had one of the worst cases of pre-eclampsia we’ve seen in this hospital in months.” And her baby ended up with RDS, a patient in her own neonatal intensive care unit!
What will it take to bring light into this darkness of USA obstetrics? The role of protein-calorie deficiency in etiology of MTLP was clearly recognized by Ross at Duke and Strauss at Harvard in 1935. Yet U.S.A. obstetrical and nutrition scientists rigidly reject this thesis in favor of the “NOTHING IS KNOWN’ position. We must let the people know!
Tom Brewer, M.D.
Croton-on-Hudson, NY