The following is reprinted from What Every Pregnant Woman Should Know, by Gail Sforza Brewer [Krebs], with Tom Brewer, M.D. (1977)

"Metabolic Toxemia of Late Pregnancy", p. 42.

Toxemia of pregnancy, "the ancient enigma of obstetrics," has presented a grave danger to pregnant women throughout history. Hippocrates, the ancient Egyptians and the the Chinese were perplexed by it.

Later medical writers observed that pregnant women with toxemia swell dramatically in the last half of pregnancy, gain large amounts of weight suddenly, develop high blood pressure and experience blinding headaches. Protein appears in their urine. In the most severe cases, women fall over in convulsions, lapse into coma and die, often with their babies undelivered.

Nobody knew why, though many theories were advanced to explain the origin of this killer disease. Atmospheric conditions, emotional instability, a too-tight uterus in first pregnancies or twins, poisons from the breasts and fatty accumulations pressing on pelvic arteries have all been blamed at one time or another. Yet none of these theories has been able to account for all known cases.

Various treatments have been devised to combat the classic signs and symptoms known as the "toxemia syndrome." Low-salt diets and diuretics aimed at reducing swelling, low-protein diets aimed at stopping protein spills in the urine, low-calorie diets and amphetemines aimed at limiting weight gain, drugs aimed at lowering high blood pressure, drugs aimed at preventing convulsions and, as a last resort, delivery as soon as possible by inducing labor with synthetic hormones or by Caesarean section have all been tried. None of these therapies has successfully eliminated the disease because none has been directed at its underlying cause.

Today [1977], as a result of evidence gathered by researchers over the past forty years, we know conclusively why pregnant women get toxemia. Even better, we know there is an inexpensive way to prevent toxemia in every pregnant woman.

A demonstration toxemia prevention project was instituted in the prenatal clinics of Contra Costa County, California, in 1963. During the twelve and one-half years of the project, Tom supervised the prenatal management of over seven thousand mother from the lowest income group in the San Francisco Bay area. Over half the mothers belonged to ethnic minorities--Black, Mexican, American Indian and Oriental. Two-thirds of those having their first babies were teen-agers. All of these factors--poverty, race, age and number of pregnancies--contribute to what medical statisticians call a "high-risk" obstetrical population. These mothers, by all odds, should have had a great deal of trouble giving birth to healthy babies. They are considered to be especially likely candidates for developing toxemia and having low-birth-weight babies.

For example, during this period the university teaching hospital in Dallas reported that the toxemia rate in Blac teen-age mothers delivering there was 35 percent. At Jacobi Hospital in New York City the estimated figure was 20 percent of all mothers having first babies. A rising maternal death rate from convulsive toxemia was reported by Dr. Lester Hibbard at Los Angeles County Hospital in 1973.

Unlike these other situations, the incidence fo toxemia among mothers in the Contra Costa County project was 0.5 percent, with no cases reaching the convulsive stage.

What made the difference?

We credit four major changes made in daily clinical practices:

1. Redefining toxemia in a way that explained all cases;
   
2. Properly interpreting the classic signs of toxemia and refraining from merely treating them symptomatically;
   
3. Requiring that every mother attend nutrition counseling sessions with Tom;
   
4. Developing skills of communicating with mothers so they would understand and be motivated to follow the clinic nutrition program.

These departures from traditional methods were not easy to make. They evolved over a thirteen-year period of study and work in our southern states, the "eclampsia belt," so-called because of its persistently high rate of convulsive toxemia. Over these years it became necessary to rethink and reject much of what had become standard medical school teaching about the origin of the disease and its treatment.

Conclusions resulting from this laboratory and clinical research were published in 1966 in a handbook for the practicing physician, Metabolic Toxemia of Late Pregnancy: a Disease of Malnutrition. In it a separate disease entity of known origin, metabolic toxemia of late pregnancy (MTLP), was differentiated for the first time from the "toxemia syndrome"--the well-known signs and symptoms associated with the disease. The clue to this discovery was the realization that the signs and symptoms which accompany MTLP can also be caused by other conditions. Sorting out which conditions are responsible for which aspects of the "toxemia syndrome" in any individual case is a process called differential diagnosis. Undertaking differential diagnosis whenever a mother displayed the "toxemia syndrome" was not taught in medical school or OB/GYN residency programs in the past--nor is it now.

The prevailing teaching has been that the "toxemia syndrome" (also known as "pre-eclampsia/eclampsia") is a disease of hyper tension and kidney malfunction precipitated by an unknown underlying mechanism. This theory provided the physician no tools for use in the face of impending "toxemia," and since the cause was officially unknown, every pregnant woman has been managed as though she were likely to develop the illness. If the signs and symptoms arose, all the physician could do was institute one of the myriad therapies and hope for the best. Lacking knowledge of the underlying cause of the disease, there could be no efforts at true prevention.

The book advanced a simpler thesis which gave the obstetrician a clear course of action to take in preventing the disease. The major conclusion was that fundamental disturbances in metabolism, chiefly in liver cells, afflicted mothers with MTLP. These disturbances were caused by malnutrition and resulted in a malfunctioning liver. Thus, the "toxemia syndrome" of swelling, hypertension, protein in the urine and sudden weight gain must be viewed as the end result of metabolic derangement.

Characteristic liver lesions have been observed by pathologists for many years in mothers who have died of convulsive MTLP (eclampsia). In 1973 Sheehan and Lynch, two of England's leading pathologists, published a monumental review (11,719 references) of the world's literature on certain fatal diseases related to human pregnancy, including their own thorough autopsy reports on 677 obstetric patients. In 377 of these cases the mother had been suffering from "toxemia of pregnancy." Sheehan and Lynch described specific changes in the livers of these mothers which occur in no other recognized human disease. Sometimes these lesions are so severe that they cause rupture of the liver and intra-abdominal hemorrhage. Tom pointed out in his book that similar lesions have been produced experimentally in animals deprived of proteins and other essential nutrients during gestation. In areas of the world where malnutrition is widespread, liver ruptures resulting from MTLP are often reported.

While malnutrition has been an undeniable fact of life for women living in poverty throughout history, the swing in 1958 in American obstetrical practice to rigid weight control, salt restriction and diuretic therapy as methods of routine pregnancy management made malnutrition an ever-present threat to women in every economic group who followed such dietary prescriptions.

It became clear that preventing malnutrition is the key to preventing MTLP. The successful Contra Costa County project was based on this single idea.

As Tom explains, "My interest in MTLP began in 1950 when I was a medical student at Tulane University Medical School, rotating through the OB/GYN department. One of the instructors, Dr. James Henry Ferguson, had spent the years 1946 to 1948 studying maternal deaths and the nutrition of pregnant women in rural Mississippi. He included material from his field work in his lectures. Our obstetrics textbook mentioned a new "nutritional" theory of the origin of toxemia based on work done by Maurice Strauss and Bertha Burke at Harvard and Ferguson's research seemed to confirm it."

Toxemia was the number one cause of maternal death at that time throughout the South. In Mississippi seventy-six deaths from toxemia were reported in the first year of Ferguson's study. Rather than pore over medical records and state health department statistics, Ferguson chose a more direct way of finding out the conditions under which these unfortunate women had lived and died. He visited physicians and midwives who had had contact with a maternal death. He consulted public health nurses for information on the victim's background, home and diet. He visited some of their homes and personally interviewed over four hundred pregnant women coming to prenatal clinics in public hospitals. The picture that emerged was not a pretty one, nor one most well-fed and prosperous American physicians could accept as reality.

As Ferguson reported in the Journal of the American Medical Association in 1951:

The case reports in this study are heavily weighted with women who are poverty stricken. Seventy-nine percent of these women can be classified as being in the lowest socio-economic group.

He also published reports on the nutrition of the clinic patients he interviewed. Examples of some of the worst menus he encountered were:

Menu I

	Breakfast: 3 tablespoons grits 1 tablespoon butter 2 pieces of toast 1 cup coffee Lunch: 1 candy bar 1 apple 1 soft drink Dinner: No dinner

Menu II

	Breakfast: No breakfast Lunch: 1 root beer 2 plates field peas 4 biscuits (large) Dinner: 1/2 plate water gravy 1 1/2 plates fried okra 2 biscuits (large)

He found 94 percent of these mothers to be obviously malnourished: their diets were deficient in high quality proteins, iron, vitamin C, the B vitamins, calcium and many other nutrients recognized as essential. Eighty-nine percent did not receive a quart of milk a day and 57 percent had no eggs. More expensive sources of protein, such as lean meats, were way beyond their means.

The same miserable circumstances existed on the "toxemia ward" at Charity Hospital, Tulane's teaching institution serving the "medically indigent" from New Orleans and referrals from across Louisiana and Mississippi. The importance of taking in-depth histories detailing the life and dietary habits of the patient before entering the hospital was stressed in the internal medicine department.

Tom found, however, that on the OB/GYN service such histories were rarely taken. With over one thousand deliveries a month, 19 percent of which were complicated by the "toxemia syndrome," much of the patient care was on a strictly emergency basis. Only in the occasional case involving an internal medicine consultation was a detailed medical history attached to the patient's chart. The failure to take dietary histories on mothers admitted for "toxemia" denied the obstetricians an important clue to the underlying cause of the disease. It is impossible to get the right answers without asking the right questions. This missed opportunity left the doctors functioning in a vacuum. The only reality was the possibility that at any moment any one of the critically ill mothers on the ward might convulse.

One of the students' jobs was to go from bed to bed checking and recording the toxemic patients' blood pressures. As Ferguson had done in Mississippi, Tom asked the mothers what they had been eating before their admission to the hospital. They often volunteered that they had been vomiting for weeks off and on, then severely for a few days just prior to being hospitalized. Most were in the last trimester of pregnancy. The conversation:
"Did you have milk?"
"No, sir."
"Did you have eggs?"
"No, sir."
"Did you have meat?"
"Yes, sir."
"What kind of meat?"
"Fatback."
"Sow belly."
"Salt pork."
"Any lean meat?"
"No, sir."

Cornbread, grits, water gravy and field peas often constituted the rest of the diet.

In the crisis treatment center which was the "toxemia ward" in particular and the obstetrics service in general, the idea that malnutrition might be the cause of the problem was the farthest thing from the chief resident's mind.

It was his responsibility to supervise the anxious watch for convulsions, a sign that the disease had reached life-threatening proportions. The most important thing, when faced with rows of beds filled with patients who might convulse at any moment, was to ward off those convulsions! Repeated injections of mercury diuretics, magnesium sulfate and morphine had to be given in hopes of reducing gross swelling and achieving adequate sedation.

Trying to introduce the subject of meat, milk and eggs in this highly charged atmosphere must have seemed preposterous. At this late stage in the course of full-blown MTLP, any consideration of underlying cause appeared to be a speculative, academic matter. Even if anyone knew the cause, by the time the seriously toxemic mother reached the ward there was nothing to be done about the disease but treat it. Prevention was simply not part of the thinking of the time.

Thousands of hours spent pouring over scientific reports in Chemical Abstracts yielded little. Virtually every biochemical test known had been done on normal pregnant women and those with the "toxemia syndrome," but confusion was rampant. Conflicting results on the same tests done on the the same populations in different medical centers were the rule. Clearly the researchers were not all calling the same set of phenomena by the same name, or there were variables in their samples of which they were unaware.

During his internship at the city-county hospital in Houston, Tom noticed that the private attending physicians seemed not to worry about "toxemia." They often commented, "We have to come over here to Jeff Davis to see pre-eclampsia, eclampsia and abruptions of the placenta. We don't see these in private practice."

Tom notes: "Their remarks strengthened my growing belief that MTLP historically afflicted the poor because the poor were more likely to be malnourished. From 1955 to '58 in my private general practice in Fulton, Missouri, I saw no cases of MTLP in one hundred pregnancies. The absolute difference between the malnourished women of the 'toxemia wards' and this better-fed group of mothers confirmed what the Houston obstetricians had told me. MTLP was, at that time, a rare complication in middle-class women."

The subject came up occasionally during informal talks with other doctors in Fulton. They usually credited the absence of toxemia among their patients to the higher economic status and generally better health of the women in Fulton as compared to the women they had cared for in their training days. "Poverty" was the reason for all the troubles they had seen back in the inner city teaching hospitals. But the idea that poverty usually meant malnutrition and that malnutrition predisposed to disease never entered the conversation. The casual expectation of the doctors was that mothers who made up the bulk of private practice would go through pregnancy just fine and have a normal baby. The sharp contrast between this attitude and that which prevailed in the university centers helps explain a development in routine pregnancy management which in retrospect seems almost inconceivable.

A look at the medical journals of the 1950's and 1960's leaves little doubt as to which attitude gradually came to dominate the American OB/GYN consciousness and inadvertently lay the groundwork for middle-class pregnancy malnutrition on an unprecedented scale. The emphasis on pregnancy complications, crisis-management and drug therapies is so overwhelming that if one had no other source of information about pregnancy in mid-century America, one would be driven to conclude that it was a high-risk condition of the same order as impending heart attack. The journals reflect this point of view because they are written primarily by and for researchers in teaching institutions whose "material" for study is almost exclusively comprised of malnourished, poverty-stricken women who do indeed have many pregnancy problems.

Abetting the preoccupation with pregnancy pathology were drug company advertisements, each of which tried to outdo the others in convincing the physician of the efficacy of their products. Since claims made in these advertisements are based on research done in the university medical schools with grant money provided by the drug companies, it should not be surprising that journal articles and drug company promotions address the same concerns and reinforce each other's conclusions. Drug companies in this country, of course, are in business to make a profit. Advertising in medical journals is an important part of overall marketing strategy.

For thirty years [as of 1977] competition in the pregnancy "market" has been focused on developing new ways of dealing with that old problem, weight control. Excess weight gain has been implicated for decades in the onset of toxemia, so, to the traditionally trained obstetrician, any assistance he can get in preventing undue weight gain he tends to view as an aid to preventing toxemia. The drug company market analysts know of the university physicians' continual concern about toxemia, and their promotional campaigns ever since the late 1940's have featured advertisements in which the spectre of toxemia looms as an unspoken menace. By never allowing the obstetrician to forget the "toxemia ward" of his training, a "market" is created for weight control drugs which can only be obtained by prescription. Prescriptions mean profits.

The first category of drugs to be approved for use in pregnancy weight control were appetite suppressants (amphetamines or "speed"). At first promoted primarily for mothers who were overweight at the beginning of pregnancy, they were quickly taken up for use in enforcing rigid patterns of weight gain in normal mothers as well. Competition for dominance in the lucrative pregnancy weight control "market" was keen. The July 15, 1962 issue of the American Journal of Obstetrics and Gynecology probably represents the pinnacle of corporate contention: four major drug companies, each with full-page layouts.

In them we learn that Amber Extentabs, a combination of amphetamine (an "upper") and phenobarbitol (a "downer")--later in the ad described as a "balanced formula"--are "small...easy to take...suppress appetite for up to 12 hours...improve mood without 'jitters'...and help establish conservative eating habits." With Tenuate, the doctor can "control weight gain from test to term" by "suppressing appetite with no effect on heart rate, blood pressure, pulse, respiration and no alteration of basal metabolism rate (BMR)." The doctor might also consider Dexamyl Spansule, a brand of sustained release capsules containing Dexedrine and amobarbitol ("Warning, may be habit forming") especially effective "during pregnancy...to keep her weight right and her outlook bright." For those who had a few pounds to lose during pregnancy, the doctor could count on Desoxyn Gradumet, "the all-day appetite control from a single oral dose" which caused side effects such as insomnia, nervousness and palpitation in only 15 to 20 percent of patients!

These advertisements never pointed out that a mother could be obese because her diet was too high in carbohydrates, sugars and fats and low in protein, vitamins and minerals. Nor was there ever an intimidation that a more appropriate form of physician intervention would be to switch the mother to a higher quality diet, instead of counseling her to do anything she could to hold her weight down. Because doctors had been trained to think of the baby as a parasite and "toxemia" as a consequence of excess weight gain, the concept that dieting during pregnancy might be harmful to baby and mother completely escaped them. During no phase of their training had anyone made the link between malnutrition and poor pregnancy outcome, so it was easy for them to be seduced into prescribing amphetamines, unaware that reducing any mother's food intake below pregnancy requirements could harm the baby. This major clinical error could only have come about as the result of medical training which failed to take into account the malnutrition of the poorest mothers in the country. If doctors had fully recognized the role of malnutrition in human reproductive casualty, they could never have been induced to cooperate in the next phase of maternal starvation for profit--the campaign for sodium diuretics.

Capitalizing on their by-then well-established "market" for pregnancy weight control, the major drug companies added a new promotional twist in January 1958. With full approval of the Food and Drug Administration, the American Medical Association (AMA) and the American College of Obstetricians and Gynecologists (ACOG), a new category of drugs was introduced for use in pregnancy--thiazide diuretics. The journal ads for the thiazides displayed concern over one specific component of the "excess" weight gain targeted by the amphetamine ads, pregnancy swelling (edema). Since gross swelling is associated with severe toxemia, and responsible for the sudden increase in weight in toxemic mothers, the ads encouraged the physician to take charge of the situation as he had been trained to do on the "toxemia" ward. By prescribing a diuretic, the ads proclaimed, the doctor could "prevent pre-eclampsia or toxemia" and provide relief from the "discomfort of late pregnancy edema" without having to hospitalize the mother. Until this time, the most effective diuretic, mercury, had to be given by injection. Its use was of necessity limited to the critically ill who populated the "toxemia" wards.

With the advent of the thiazides, all that changed. Far more potent than any of their precursors, the thiazides acted directly on the kidney, effecting wholesale excretion of salt, water and potassium from the body. They were effective when taken by mouth, so even the mother on the most rigorous diuretic therapy could now maintain her customary activities.

Just as the amphetamine ads never adknowleged the different status of mothers who gained weight on sound diets from those who gained on poor diets, the ads for thiazides never distinguished between the multitude of conditions that could cause fluid retention in the pregnant woman. On the contrary, the ads give the impression that all edema is worth "treating"--and the sooner in pregnancy the better, so no serious problem could develop. Because doctors themselves had not been trained in differentiate between physiologic edema (which accompanies nearly every pregnancy to some degree) and pathological edema resulting from an underlying disease, all edema came to be viewed as suspect. Because edema is so common, the "market" for the new diuretics was much broader than that for amphetamines alone had been. Because edema can be associated with MTLP, doctors were interested in a drug which promised to help them eliminate this threat to their patients. Because few physicians reflected on the deleterious effects of interfering with the body's normal mechanisms governing salt metabolism, there was not a murmur of protest as drug companies took the position that all water retention is potentially harmful.

Sales of the thiazides zoomed as ten giants of the pharmaceutical industry engaged in a long-running battle for their share of the profit-laden "market." Huge advertising budgets were allotted to the diuretic campaign. Conferences, seminars and medical meetings, traditionally sponsored by drug manufacturers, were highlighted by attractive booths featuring the diuretics and, as usual, the industry reached the physician in his office with its direct mail promotion and 35,000 company representatives, the "detail men."

In 1973, after certain studies showed that thiazides damaged mothers and babies, one major company voluntarily withdrew its promotions for its diuretic compound. The medical director of this firm disclosed that by the time the average drug hits the market, the company has spent five million dollars to develop it and that only after five years of intensive promotion will the product begin to make money. This often puts the company in the position of having to push the product even in the face of evidence that the drug might be harmful to the user. These economic imperatives account for the reluctance of the drug companies to remove the thiazides from the pregnancy "market." Not until the FDA acted in June 1976 to require a labeling change on these drugs did the other nine firms in the diuretic business abandon their pregnancy promotions, despite the fact that reported side effects from the thiazides, as listed on the package for the doctor's information, ran the gamut of insults to mother and baby. Loss of appetite, stomach irritation, diarrhea, constipation, cramping, jaundice, pancreatitis, hyperglycemia, hypertension, dizziness, headache, thrombocytopenia, sugar in the urine, depression of bone marrow function and allergic reactions were noted.

In addition to those side effects of the drugs themselves, several of which--like loss of appetite--have direct bearing on the mother's nutritional status, the detail man carried with him an adjunct to diuretic therapy which made it even more hazardous: the low-salt, low-calorie diet sheet. The low-salt provision supposedly reduced the likelihood that a mother would retain excess sodium in her tissues, thereby heading off edema from the very start of pregnancy. The low-calorie provision kept alive the notion that weight control was necessary in the fight against "toxemia."

The diet sheets, several of which were authored by professors in prestigious departments of OB/GYN, were a great blow to the concept of sound nutrition in pregnancy. Because they, like the new diuretics, were intended to be used by every pregnant woman as a preventive measure against the onset of "toxemia," even the healthiest mother in the country would be exposed to the hazards of malnutrition if she followed the regimen. In the original research on the thiazides, mothers had been permitted to use as much salt as they wished while they were on experimental diuretic therapies. So, even though the thiazides depleted the body's supply of sodium, mothers could keep up with their requirements by taking in more. When the diuretics were used rigorously in conjunction with the low-salt diets, however, metabolic consequences were likely to be catastrophic. Not only would the mother have a much higher risk of developing MTLP, but her baby's rate of intra-uterine growth would be slowed due to a reduced supply of blood to the placenta.

Estimates of how widespread the use of diuretics and low-salt diets became are mind-boggling. A survey conducted in 1963 in Tulsa, for instance, showed 93 percent of doctors responsible for prenatal care reporting that they used thiazide diuretics exactly as they had been promoted: in the treatment of edema, for weight control, and to treat and prevent "toxemia." Diuretic therapy became an accepted part of routine prenatal care in the United States and has been going strong ever since 1958. There is evidence that up to two million pregnant women a year have taken diuretics and even more mothers have been managed with salt restriction and weight control as essential, unquestioned practices.

Tom became deeply disturbed by the promotions for the thiazides when they first appeared in 1958. "I was convinced from my own experience and study," he relates, "that adoption of this approach to pregnancy management would produce MTLP, not prevent it. The malnutrition and dehydration resulting from the diet and drugs would make any woman subject to the same diseases and complications of pregnancy suffered by women in poverty for generations. In the case of the middle-class mother, though, this nutritional deprivation would be engendered by the advice of her physician. I decided to undertake further research to try to find a way to prevent MTLP. I was especially interested in the relationship between malnutrition and liver dysfunction since many researchers had called attention to certain liver lesions unique to patients with MTLP."

In his last year at Miami's Jackson Memorial Hospital, Tom became chief OB/GYN resident with the authority to test one of the results of his research: a new method of managing the mother acutely ill with MTLP.

There are two central problems presented by these patients. Solving each provided a strategy for true prevention of the conditions which precipitate MTLP. These mothers have markedly contracted blood volumes (hypovolemia) and they have impaired liver function due to malnutrition. Neither of these problems was taken into consideration by the standard protocol for treating "toxemia." With the advent of the more potent thiazide diuretics, the patient with hypovolemia was at even greater risk than before.

One of the earliest signs of developing MTLP is a fall in the serum albumin levels in the mother's blood. Albumin is a protein which keeps water in the circulation. It is manufactured by the liver. More albumin is required during pregnancy to maintain the normally expanded maternal blood volume. When the mother's diet is inadequate, the liver cannot synthesize enough albumin levels to keep up with the extra demands of pregnancy and albumin levels in the blood fall, allowing water which should be in the circulation to leak out into the mother's tissues. More significantly, her blood volume falls and the ability of the placenta to function starts to decrease.

Result: she appears swollen and puffy from the abnormal accumulation of water. The extra water retention also causes a sudden increase in weight.

During pregnancy the liver is working overtime to meet the stress of increased metabolic functions of all kinds. If the mother is malnourished in the last half of pregnancy, impairment of albumin synthesis can occur in a matter of weeks!

If the mother's diet is not improved, the blood volume continues to fall. Her body compensates in at least three ways:

1. the kidneys start to reabsorb water in an effort to restore fluid to the circulation. But without sufficient albumin, the reabsorbed water also leaks into the tissues, thus aggravating the edema;

2. blood pressure rises in an attempt to maintain adequate blood flow to all organs;

3. if blood volume becomes critically low, the kidneys shut down completely causing urinary output to dwindle to zero.

At this point in the traditional management of the severely toxemic patient, the answer has been to administer ever more potent diuretics to the mother in hopes of boosting her urinary output and reducing abnormal swelling.

In these circumstances, the diuretics are lethal. They act in the body only to remove more water from the already perilously shrunken blood volume. They are unable to affect the abnormal swelling because they do not contain any substance capable of attracting tissue fluid back into the circulation. Instead they rob the patient of the very fluid she needs in her bloodstream to keep heart, lungs and brain functioning.

With repeated doses of the diuretics, the mother eventually lapses into hypovolemic shock: exactly the same condition as if she had been in an auto accident and were bleeding uncontrollably. In both cases the mother lacks enough blood to sustain normal body functions. Tom witnessed several maternal deaths in the hospital following such a course of diuretic therapy.

Later reports in the literature indicated that this phenomenon was widespread. Advocates of the new diuretics overlooked the problem of hypovolemia. They maintained it was the "toxemia" which killed the mother, not the drugs.

In one case in 1969, a Vallejo, California, mother with three previous normal pregnancies died of MTLP along with her unborn twins in a famous medial center. The family sued the physician for malpractice.

During the trial, the plaintiff's attorney entered in evidence drug company literature warning against using the most potent diuretics, Lasix and Edecrin, at any time during pregnancy. This woman had been given both drugs in the hospital to combat her swelling.

The doctor's defense: we all use these drugs, anyway. Five of his colleagues testified that the doctor had done all he could do and, despite his efforts, the mysterious "toxemia" had finally killed her. The treatment he gave was just what they all would have given. The jury found the doctor innocent.

Tom's new approach to the patient with MTLP involved giving the mother the substance her damaged liver could not synthesize--human serum albumin. If the theory were right, the woman's urinary output should markedly increase and her abnormal swelling should begin to disappear after administration of the albumin. This course of treatment would not heal her liver, but at least she would be spared hypovolemic shock and kidney shutdown.

It worked. Since then other researchers have confirmed his clinical trials. Dr. Peggy Howard of Chattanooga and Dr. Stella Cloren of Basel, Switzerland, working independently, have administered serum albumin to more than 175 mothers with MTLP. Their reports of excellent results lend weight to the original study.

The albumin experiment was gratifying because it linked liver impairment to the classic signs of MTLP. However, the primary goal was not to rescue women suffering from advanced MTLP, but to prove that sound nutrition alone could improve the conditions of mothers who were developing MTLP and prevent it completely in all other mothers if adopted as routine prenatal management.

Tom instituted an experimental dietary intervention program at Jackson Memorial which had several unconventional features:

First, mothers with MTLP were placed on a high-protein (120 grams per day) diet. Dr. Maurice B. Strauss, the Harvard internist, had shown thirty years before that high-protein diets improved the conditions of mothers with what he termed "nutritional toxemia."

Second, the mothers were placed on regular, rather than salt-restricted diets. A salt shaker appeared on the tray at each meal and the mother was instructed to salt her food to taste.

Third, the women were encouraged to stay out of bed as muc as possible, even to do chores on the ward if they were willing, rather than being ordered to the customary bedrest.

Fourth, diuretics and drugs to lower blood pressures were not used.

Fifth, following the work of Poth on the most effective way to suppress bacterial flora in the bowel, patients received oral antibiotics to reduce the detoxication load on their damaged livers.

Sixth, Tom personally discussed the program with each mother to obtain her permission and cooperation, then made a conscientious effort to see that each followed her diet well.

Not every patient admitted to the hospital with the diagnosis of "toxemia" was accepted for the high-protein feeding program. Often after consultation and laboratory work, it would turn out that the mother did not have MTLP at all. Though she presented the same set of signs and symptoms--the "toxemia syndrome"--characteristic of MTLP, it was found she could have a problem totally unrelated to liver malfunction. For instance, physiologic edema, bladder and kidney infections, nephritis, chronic hypertension and obesity were often misdiagnosed as toxemia.

It became clear why other researchers had experienced such difficulty in understanding toxemia. Their definition had been imprecise, and even the simplest biochemical tests done on women with MTLP and women with nephritis, for example, turn up very divergent results.

Ten patients over two years met the program admission requirements. Nine improved, doing significantly better by all measures than women on traditional toxemia management.

The one mother who did not respond to the dietary program was carrying twins. She had made eight prenatal visits to the county clinic. At each visit she had complained about constant nausea and vomiting, but no steps were taken to help her correct it. As a consequence she had a very poor diet with low-protein intake. After nine days in the hospital, during which she was unable to eat an adequate diet, she spontaneously went into labor and gave birth to twins weighing three and a half and four pounds.

Tom observed: "This mother was so severely malnourished that her protein reserves had been depleted. After delivery and subsequent mobilization of her edema fluid, she weighed only 72 pounds (height 5 feet, 2 inches) and looked as if she had just come out of a concentration camp. Her liver had been so compromised by malnutrition that nothing short of delivery could initiate the healing process."

This result was encouraging because it showed that poor nutrition, not some mysterious substance manufactured by the placenta, was responsible for the onset of MTLP. Also significant was the fact that no mothers got worse after being placed on the program--a clear refutation of all those who claim that eating salt leads to toxemia, that eating to appetite results in excess weight gain which leads to toxemia, that diuretics must be given to prevent toxemia, that forced bed rest could improve the conditions of women with MTLP.

In 1963 Tom began the broad-based toxemia prevention project in the Contra Costa County prenatal clinics to which we have referred. He thought,"If MTLP can be eliminated among the group of mothers considered to be at greatest risk of developing the disease, then perhaps these nutritional methods would be tried and confirmed by others. These clinical tests of the approach, I hoped, would form the basis of a new set of standards for routine prenatal care which would be institutionalized all over the country."

The major innovation of the Contra Costa County project was the weekly nutrition seminar conducted with new clinic patients. The authority of the physician in charge was a crucial psychological factor in altering the behavior of the mothers in his care--especially in the culturally influenced area of food habits.

The informal discussion format encouraged mothers to ask questions and volunteer information about their past pregnancy experiences. In this way, mothers learned from one another as well as from the doctor what some of the hazards of malnutrition were. In addition to explaining the physiologic changes the mother could expect as pregnancy advanced, the importance of good nutrition in promoting these changes and facilitating an easier birth and postpartum period was stressed.

The unique feature, though, was reviewing how many common complications of pregnancy are concretely linked with poor nutrition. When mothers learned the consequences of malnutrition for themselves and their babies, they became serious about eating correctly. No supplemental foods were distributed at the clinic. Nutritional counseling given by the physician was the sole mode of dietary intervention.

At each follow-up visit with individual mothers, the initial educational talk was reinforced. During these conversations the mother could report on how well she was following the prescribed diet, discuss the problems she was having with it or ask any questions she might have. Every mother was reminded to continue to eat good foods to appetite and to salt her food to taste. No mention was made of weight gain, except in cases where underweight mothers were failing to gain.

In this situation, where the authority of the doctor was used to encourage sound nutritional habits and not to impose strict limits on weight gain, convulsive MTLP never once occurred in twelve and a half years, and mild MTLP was reduced to 0.5 percent.

As the Contra Costa County project progressed, Tom gradually became confident that the nutritional thesis of MTLP was correct. As is customary, he published journal articles about the project and began to lecture at medical meetings and hospitals around the country, urging obstetricians to try these methods and abandon those being promoted by pharmaceutical interests. He also started petitioning the FDA to hold a hearing on the use of diuretics and low-salt diets in pregnancy. This campaign was to take ten years to come to fruition.

As he traveled, he found that clinics everywhere were being run as they had been when he was a medical student in 1950 and an OB/GYN resident in 1960. Although some clinics had introduced dietary counseling provided by nutritionists, the authority of the doctor in charge almost always ran counter to their best efforts. One nutritionist from Mobile, Alabama, summed up her experience:

It has been our major teaching point to emphasize foods high in protein--specifically, lean meats, milk and eggs. We have an interview with every patient on each maternity clinic visit to instruct her in normal nutrition.

The nutritionists here have been confronted with conflicting ideologies concerning prenatal nutrition. The low-calorie, low-sodium, diuretic treatment is used by the majority of obstetricians. This has caused a head-on collision with the purpose of the nutritionists.

The Contra Costa project results confirmed those of Dr. Reginald Hamlin of Sydney, Australia, who, while chief of OB/GYN at the Crown Street Women's Hospital, also taught nutrition to clinic mothers from 1948 to 1951. For the preceding ten years there had been one case of convulsive MTLP in every 350 deliveries in his hospital. By the third year of his nutrition education efforts, there was not one case in 5,000 consecutive deliveries. As Hamlin expressed it, MTLP is caused by "a relative deficit of first class proteins and vitamins." He attributed his success to a program which "was aimed strategically at the occult basis of the disease instead of at its summit of classical late signs and symptoms." The result:

The humicribs (incubators) were often empty now. By 1949 nurses and medical students were beginning to ask why they were no longer seeing enough eclamptics (patients with convulsive MTLP)...By 1950 it was felt that one could say to the skeptics: Eclampsia will no longer afflict the patients of this hospital if the present methods of prevention are followed meticulously.

Hamlin's remarkable work, like that of Strauss, Burke, Ferguson and others who linked MTLP with malnutrition, remains almost completely unknown in American obstetrics today [as of 1977 and unfortunately apparently continuing to 2008].

The conclusion that MTLP is completely preventable by sound nutrition has been brushed aside in the rush to ever more far-fetched therapies. In the 1960's it was diuretics which were going to prevent toxemia. Now, technological detection of fetal illness and warehousing of large numbers of "high-risk" mothers and babies in regional perinatal centers are the rage. Rarely in the academic centers does one hear or read of the protective effects of scientific nutrition during gestation. At a recent meeting [1977] of the International Federation of Obstetricians and Gynecologists, for instance, eighty papers were presented. Thirty of them dealt with fetal monitoring and its special applications in the "high-risk" case.

Examination of the current OB/GYN journals turns up the same preoccupation with diagnosis and treatment of disease. Those investigators who write on toxemia spend years of their lives painstakingly measuring biochemical irregularities in mothers with the disease. Though they write copiously documented reports of their efforts, these researchers rarely say a word about prevention.

Even the obstetrics textbooks, which thirty years ago [as of 1977] gave some credence to the nutritional thesis of MTLP, today contain no reference to the possibility that the disease can be prevented. New chapters on fetal medicine direct the medical students' attention even farther away from the concepts of sound nutrition by elaborating on all the latest techniques for assessing the developmental retardation of babies suffering from intrauterine malnutrition. All the doctors in training who learn their obstetrics from these textbooks will continue to be taught the wrong approach to these problems.

There is a common idea that it is just older doctors, with rigid training from the past, who block acceptance of the nutritional line of research into pregnancy complications. As they retire, the thinking goes, younger people with the correct ideas will come forward and change practices. However, this bright outlook can never materialize while medical schools, professors and textbooks continue to train doctors in traditional methods.

Since the bulk of practitioners continue to give traditional care when it comes to nutrition, a non-profit organization committed to the establishment of scientific standards of nutrition management in American obstetrics was founded in 1972, the Society for the Protection of the Unborn through Nutrition (SPUN). Only when official OB/GYN practice standards have been set for sound maternal nutrition will the idea become incorporated into medical school teaching. Until that time, every mother and every unborn baby will continue to be at risk from the known hazards of nutritional deprivation during pregnancy.

The Contra Costa County clinic project demonstrated that no mother who is able to eat, digest, absorb and metabolize a diet adequate for pregnancy will develop MTLP.

Whenever a mother in the project developed the "toxemia syndrome," one of two things was happening.

Either she was not following the diet.

Or she had something else.

See "Mistaken Diagnosis" here

What Every Pregnant Woman Should Know available here

Salt in Pregnancy

	High Salt Diet	Low-Salt Diet
Toxemia	37/1000	97/1000
Perinatal deaths	27/1000	50/1000
C-section	9/1000	14/1000
Abruptio placenta	17/1000	32/1000

Nutritional Deficiency in Pregnancy

Complications	Control Group (750)	Nutrition Group (750)
Preeclampsia	59	0
Eclampsia	5	0
Prematures (5 lb. or less)	37	0*
Infant Mortality	54.6/1,000	4/1,000

Prevention of Convulsive MTLP (Eclampsia)

	Number of Pregnancies	Cases of Convulsive MTLP (Eclampsia)
Tompkins 1941	750	0
Hamlin 1952	5,000	0
Bradley 1974	13,000	0
Davis 1976	500	0
Brewer 1976	7,000	0
Total	26,250	0

Perinatal Support Services: pregnancydiet@mindspring.com