Nutritional Stress II

The following is a continuation of a chapter reprinted by permission from 21st Century Obstetrics Now! (David Stewart, PhD, and Lee Stewart, CCE, Editors), National Association of Parents & Professionals for Safe Alternatives in Childbirth, 1977. (p. 387)

The relationship between nutrition and development as enumerated in both prospective and retrospective studies, many of which were reviewed in the previous section and prior ones, should be viewed from a more direct perspective rather than a statistical one. In fact, such studies are hardly necessary in view of the known physiological phenomena pertaining to nutrition and development. Because of our emphasis on research, which is frequently done more for research's sake than its practical applications, and our failure to apply principles of internal medicine and nutrition science, numerous pregnant women have been subjected to risks of reproductive casualty in experiments which do not ensure an adequate intake of calories and nutrients.[24]

Proper nutrition during pregnancy is a sine qua non ["without which (there is) nothing"] for normal fetal development. This period of development is so rapid that an adult would be several times the size of the earth if he or she had grown at the fetal growth rate through adult life.[72] Most important, the brain develops more than any other organ during fetal development.[73] In fact, the head circumference of a newborn infant is approximately 65% of the full adult size.[47} At the age of five months, a child has approximately 80% of his or her adult capacity of brain cells.

Malnutrition directly and adversely hinders hyperplasia (cell division).[74-75] During the most rapid period of brain development, which occurs from the last trimester of pregnancy to the first month of life, malnutrition can cause irreversible neurological damage and permanent brain underdevelopment.[34,47,76] One study showed that malnutrition during pregnancy can result in a deficiency of as much as 60% of the expected number of brain cells.[75] In the same study, the brain weight, protein, RNA, and DNA of nine infants (who were between 1/2 and 11 months of age) who had been malnourished prenatally (indicated by triangles in the figures below) were compared with the same measures of brain development of two abortuses and eight infants whose mothers had not shown signs of clinical malnutrition (indicated by circles). The number of brain cells, as measured by DNA (at the age of six months, brain DNA is nearly the adult amount[74]), was significantly lower in the malnourished group. Note that the amount of RNA and protein per brain cell were comparable in the malnourished and better nourished groups. In Figures 4-7, the lines represent the range for normal children independent of data from the study.

Malnutrition during the latter half of pregnancy leads to a reduction in the number of glial cells,[77] which are more vulnerable to malnutrition than any other form of neurological development.[30] Glial cells, which form the myelin sheath (which insulates nerve fibers) around the axons, form the foundation for the most dominant type of neurological development, myelination, which progresses from approximately age one to age four.[77]

Even more significant neurological development than glial proliferation occurs concurrently with and is dependent on glial multiplication and myelination. Impairment in the formation and development of dendrites (which conduct impulses to cells) may affect learning potential more than a reduction in the number or size of brain cells. The interneural network is adversely affected by malnutrition.[30] The size of axons, which comprise a major component of the total nerve fiber, is also stunted by intrauterine and early postnatal malnutrition.

Malnutrition during the initial stages of brain development causes changes in the size, electrical activity, composition, and morphology of the central nervous system.[34] Because the cerebellum, which coordinates voluntary muscular movements, is largely developed between the 30th week of gestation and the first year of life, it is much more vulnerable to inadequate nutrition than the cerebrum,[78] which is developed over a longer period.[77]

After the age of two, poor nutrition basically retards the growth of individual brain cells.[34] Mental deficiency from malnutrition after this age, at which time brain cell proliferation has virtually ceased,[74] is much more likely to be reversible than brain underdevelopment caused by prenatal malnutrition.[34]

Maternal malnutrition also retards the growth of the placenta[26,74,79-80] and can lead to placental dysfunction and pathology.[81] Lechtig et al. discovered that malnutrition caused low birth weight primarily because of its effect on reducing the size of the placenta.[26] It is not surprising, then that placental weight and birth weight are highly correlated.[5] The Collaborative Perinatal Study also showed that low placental weight is related to perinatal death.

TABLE 24
ASSOCIATION OF PLACENTAL WEIGHT WITH
LOW BIRTH WEIGHT AND PERINATAL MORTALITY

Weight of Placenta (g)	# Live Births With Known Birth Weight	% Low Birth Wt.	Total Births	% Perinatal Mortality
0-199	122	88.5	318	86.5
200-249	311	83.6	374	33.5
250-299	1,129	51.9	1,192	9.4
300-349	3,555	26.2	3,616	2.9
350-399	6,150	12.1	6,205	1.6
400-449	7,283	5.1	7,331	1.4
450-499	5,879	2.8	5,921	1.0
500-549	3,744	1.3	3,764	1.0
550-599	2,056	0.9	2,072	1.0
>600	1,737	0.5	1,771	2.7
TOTAL	31,966	10.13	32,564	3.03

Inadequate nutrition frequently leads to hepatic dysfunction,[36,82-83] which frequently precedes placental pathology. Hepatic storage of many nutrients, including albumin, is significantly related to birth weight.[33]

Various dramatic physiological and biochemical adjustments, particularly hormonal changes, accompany pregnancy. One major such adjustment is an increased retention of sodium, the principle electrolyte of the extracellular fluid.[85-86] Potential sodium depletion, which is frequently iatrogenic, is counteracted by a five to tenfold increase in aldosterone, an adrenal hormone which facilitates tubular reabsorption of sodium, representing the largest pregnancy renal adjustment.[42,86] The increase in aldosterone secretion is the last stage of the salt conservation mechanism (known as the renin-angiotensin-aldosterone homeostasis), which helps maintain a near constant concentration of sodium in the extracellular fluid. When this homeostasis is over-stressed (i.e., when the pregnant woman's sodium requirements are not met), juxtaglomerular degranulation [a process in the glomerulus of the kidney, which is caused by elevated BP, which in pregnancy is caused by high levels of renin, which in pregnancy is caused by low blood volume] can occur with its attendant morbidity and mortality.[87]

See the following studies for more information about "juxtaglomerular degranulation"

"The low sodium pregnant group had less juxtaglomerular granulation than the corresponding nonpregnant group or the other pregnant groups. Despite this degranulation, the low sodium pregnant animals had the widest zona glomerulosa and conserved the greatest percentage of dietary sodium. It is suggested that in this group juxtaglomerular degranulation was due to a rate of renin secretion exceeding the rate of production, thereby reducing the number of secretory granules present in the cells."

"The attempt to quantitate the amount of histamine liberated by degranulation of J-G cells has been less successful than with degranulated connective tissue mast cells, owing to the low J-G cell/parenchyma ratio in the kidney...The presence of mast-cell-like elements at the vascular pole of the kidney glomerulus is stressed in view of their possible role in the functional activity of the nephron, owing to the fact that degranulation of these cells is capable of releasing anticoagulant and vasoactive substances like heparin, histamine, and serotonin proximal to 1 of the most important circulatory districts of the body." [emphasis by Joy]

"Juxtaglomerular granular cells were examined in rats killed at 1, 2, 4, 6, and 8 weeks after adrenal enucleation. No evidence was found to indicate a change which would be expected to initiate a blood pressure rise and the degranulation observed was interpreted as the result rather than the cause of the blood pressure change." [emphasis by Joy]

Accumulation of granules in the juxtaglomerular cells occurred in rats which were maintained for 5 to 6 weeks on a diet low in sodium, chloride...Two per cent sodium chloride taken in the drinking water consumed for 4 weeks by similar animals caused degranulation of the juxtaglomerular cells...A hypothesis is suggested that the juxtaglomerular cells are involved in the hormonal regulation of sodium metabolism and/or blood pressure.

In an extensive study of 2,019 pregnant women, Robinson demonstrated unequivocally that sodium is an essential nutrient during pregnancy.[88] The women were divided into a high salt group (these women were told to increase their salt consumption) and a low salt group (these women were instructed to decrease their salt intake). Other than dietary sodium advice, the women in the two groups, who were of comparable age, parity, and socioeconomic status, were not placed on diverse dietary or medical regimens. The rates of miscarriage, perinatal death, toxemia, edema, and placental infarcts were much higher among the women who were told to restrict their salt concumption than among the women who were told to use additional salt.

	# of Women	Perinatal Mortality Rate	% Toxemia	% Edema	% Placental Infarcts
Restricted Salt Intake	1,000	50.0	9.7	28.7	1.3
Increased Salt Intake	1,019	26.5	3.7	16.0	3.2

It may seem ironic that those who restricted their salt intake had the higher rate of edema, which is usually thought of as being caused by excess sodium intake. The inverted conception of the role of sodium in pregnancy represents one of the most misunderstood aspects of internal medicine.[36] The prevailing theory that sodium restention is a pathological condition caused by excess sodium intake has led to a vast amount of maternal and infant morbidity and mortality. Low-salt diets further deplete the woman of the essential nutrient, causing her renin-angiotensin-aldosterone mechanism to be stimulated even further to retain more sodium, the vicious cycle of which can lead to pathological edema.[84,86]

The speculative theory that sodium should be restricted provided some justification for the drug industry to promote diuretics, which cause sodium depletion. Despite the publication of double-blind studies which conclusively demonstrated that diuretics are of no value in human pregnancy,[89-91] approximately half of all obstetricians still prescribe them [as of 1977].[2] Besides leading to impaired placental function [92] and fetal growth, diuretics can lead to fetal malformations,[92] neonatal thrombocytopenia,[93] hypoglycemia,[36] or electrolyte imbalance [36,92] and maternal complications, such as toxemia [36,41-42] or pancreatitis.[94]

The use of diuretics and low-salt diets can, especially in malnourished women, lead to maternal death.[38,95] One obstetrician attributed the increase in maternal deaths from 5 to 19 during three-year periods at one hospital center largely to the indiscriminate use of low-salt diets and diuretics.[95] In reviewing the medical records of 67 maternal deaths from toxemia, he stated:

The incidence of toxemia can be sharply reduced simply by encouraging pregnant women to salt their foods to taste and refraining from prescribing diuretics. In one clinic where such management was followed, there was only one case of toxemia in 5,300 pregnancies,[41] which is far below the U.S. incidence of 7%.[96] At a nearby clinic, where the hazardous regimens are utilized, the toxemia rate was 98 times higher.

Infant deaths are also associated with the administration of diuretics. In a study of more than 17,000 pregnant women, the infant mortality rate among full-term infants was 16% higher in those who had been prescribed diuretics.[97]

The FDA recently [as of 1977] cited all of the nine drug firms which manufacture diuretics for pregnant women for promoting the drugs on no scientific basis.[98] In stating new regulations for the use of diuretics (which in essence state that the drug is contraindicated and possibly hazardous during pregnancy), the FDA noted:

The restriction of salt during pregnancy (and the justification for the prescription of diuretics) is based upon the historically accepted, but never proven, speculation that toxemia is caused by impairment of salt excretion.[86] In reality, among toxemic women, salt retention is not a cause of toxemia but, rather, an impending sign of sodium depletion, which causes the toxemia.[99]

A major reason that the myth that sodium restriction is a prophylaxis of toxemia continues to predominate obstetrical thinking is that physiological edema is seldom differentiated from pathological edema. Physiological edema usually signifies a normal pregnancy, whereas pathological edema reflects pretein/calorie, sodium, and/or related dietary deficiencies or a medical disorder unrelated to pregnancy. Differential diagnosis as well as a thorough dietary history can invariably determine the origin of the edema.[36]

Approximately 60% of all healthy pregnant women will develop edema, including generalized edema.[36,100] A study of nonproteinuric women showed that edema was associated with a 58% reduction in perinatal mortality.[93]

	# of Women	# of Still- Births	# of Neonatal Deaths	Perinatal Mortality Rate
No Edema of Hands or Face	2,268	33	40	32.2
Edema of Hands or Face	1,890	15	10	13.2

As has been shown above, edema, instead of being physiologic, can develop as a result of sodium deficiency. Pathological edema can also result from protein and/or calorie deficiency. This type of edema is mediated by a decrease in the plasma proteins as a result of lowered serum albumin concentration.[101-102]

By measuring the serum osmotic pressure of 65 pregnant women, all of whom were at seven months' gestation, Strauss demonstrated that the pressure was directly related to protein intake.[102] Serum osmotic pressure, serum albumin, and dietary protein were highest among the 35 nontoxemic women in the study, second highest among the 20 women who had nonconvulsive toxemia, and lowest among the 10 women who had eclampsia.

At the eighth month of gestation, 15 of the 20 nonconvulsive toxemic women were placed on a diet which consisted of 260 grams of protein and were given vitamin injections; the other 5 were placed on an isocaloric diet which provided 20 grams of protein. The osmotic pressure among the women on the high-protein diet increased by an average of 7%; that of the latter group declined 9%. Strauss noted that the average daily protein intake of the 20 women was less than 50 grams.

After three weeks on the high-protein diet,the symptoms of toxemia (including a reduction in the blood pressure of all 15 women) subsided. There was not one case of fetal mortality. The women lost an average of 6 1/2 pounds. In contrast, only two of the five toxemic women who had been placed on a low-protein diet showed a reduction in blood pressure. In addition, they gained an average of 1/2 pound.

Ross, who discovered that the incidence of eclampsia was extremely high in areas where beriberi, pellagra, and other diseases of nutritional deficiencies were found, stated: "We have been struck with the number of patients in eclampsia who are in a very poor state of nutrition...The type of patient we see in eclamptic convulsions is the patient who subsists on a 2900 calorie diet consisting of bat meat, field peas, rice, hominy, grits, cane syrup, brown gravy, lard, and cornmeal...which is deficient in Vitamins B₂, A, C, and D, iron, calcium, phosphorus, and complete proteins."[103]

Hypovolemia (and usually hypoalbuminemia) precedes the onset of metabolic toxemia of late pregnancy.[36, 104] Hypovolemia, which is frequently iatrogenic (when low-salt, low-calorie diets are recommended), is caused by a deficiency of protein, calories, sodium, and/or protein-metabolizing vitamins.[104] Also, hepatic dysfunction usually precedes the clinical symptoms of metabolic toxemia of late pregnancy. Hypoalbuminemia and hypovolemia impair the liver's ability to synthesize sufficient albumin and thereby maintain its detoxification ezymatic functions.[82-85] The fact that severe preeclampsia and eclampsia frequently result in specific hepatic ischemia or periportal lesions or infarction further indicates that maternal malnutrition leads to hepatic dysfunction.[105]

	# of Women	Serum Albumin (g/100 ml)	Standard Deviation (Sic)
Toxemic	8	3.87	.03
Nontoxemic on Regular Diets	42	4.04	.04
Nontoxemic on High Protein Diets	12	4.90	.09
Nonpregnant	--	4.90	.06

In the 1930's, Dodge and Frost eradicated eclampsia by instituting a high-protein diet. Toxemic women who were placed on a daily diet consisting of six to eight eggs, one to two quarts of milk, meat, and legumes improved dramatically. The authors discovered that the average serum albumin level among toxemic women was 21% lower than that of those who had been on a high-protein diet and who didn't have toxemia. The probability that the relationship between albumin, toxemia, and protein intake (as exhibited in Table 27) is not significant is infinitesimal.

Tompkins and Wiehl also lowered the incidence of toxemia through dietary supplements.[56] They stated "the so-called 'toxemias of pregnancy' are in reality nutritional deficiency states."

TABLE 28
INCIDENCE OF TOXEMIA
AMONG SINGLE, VIABLE BIRTHS
BY TYPE OF SUPPLEMENTATION (IF ANY)

Group	# of Patients	% With Toxemia (Number of Cases in Parentheses)
Control	170	4.12 (7)
Vitamin Supplementation	244	3.28 (8)
Protein Supplementation	186	2.69 (5)
Protein & Vitamin Supplementation	160	0.63 (1)
TOTAL	760	2.76 (21)

In a previous prospective study of 750 pregnant women who received nutrition education and vitamin supplementation, Tompkins eradicated preeclampsia and eclampsia.[16] Among 750 controls (representing women who attended the same clinic as the well-nourished women but who did not participate in the nutrition program), there were 5 cases of eclampsia and 59 of preeclampsia, for a total incidence of 8.6%.

Quality of Prenatal Diet	# of Infants	% Women Who Developed Toxemia
Excellent or Good	31	0
Fair	149	8
Poor or Very Poor	36	44

Burke also demonstrated the relationship between prenatal diet and toxemia.[17,19] Toxemia did not occur in any woman whose daily protein intake was at least 68 grams.

Perhaps the first physician to establish a rigorous nutrition education program for the sole purpose of reducing the incidence of toxemia, Hamlin eradicated eclampsia in 5,000 deliveries and significantly reduced the rate of preeclampsia.[108] He observed:

Brewer, who also implemented a scientific nutrition education program, significantly reduced the incidence of metabolic toxemia of late pregnancy (p<.01).[109] Retrospectively, Brewer discovered that the three women who had developed preeclampsia (none contracted eclampsia) had been inadequately nourished.

	# of Women	Metabolic Toxemia Of Late Pregnancy
Participated in Nutrition Education Program	546	0.55%
Did Not Participate in Program	369	2.98%

For more than 20 years, Grieve, by insisting that pregnant women consume one pound of beef every day, has also nearly eradicated toxemia.[110] The differences in toxemia, abruptio placentae, and perinatal death between the 7,331 women whom he considered to be well nourished and the 4,145 whom he considered to be poorly nourished are all extraordinarily significant (p 10^-15).

	# of Women	% Toxemia (Hyper- tension, Edema, and Proteinuria)	% Abruptio Placentae	Perinatal Death Rate
Hemoglobin Level At Least 10 g/100ml and Weight Gain of Less than 39.5 lb.	7,331	.01	.03	19.2
Hemoglobin Level Under 10 g/100ml or no Greater than 12 g/100ml and Weight Gain Greater than 39.5 lb.	4,645	.82	1.38	50.6

The fact that protein deficiency causes toxemia was verified in a recent study [as of 1977] in which the administration of protein immediately alleviated the toxemic process.[111] Among the 37 severe toxemics who were given albumin, there was not one instance of RDS and all of their babies received high pediatric ratings.

	# of Women	Induction of Labor	Perinatal Mortality	Abruption of the Placenta
Study Group	135	5%	0.9%	0%
Control Group	297	25%	3.7%	3%

Numerous complications, such as toxemia, low birth weight, abruptio placentae, and anemia, have been linked with inadequate prenatal nutrition. As will be shown herein, contrary to prevailing teachings, complications of labor and delivery are much more likely to occur among underweight births than those of higher weight. Major delivery complications, including an increase in the rate of cesarean sections, have been linked to low-weight babies born to inadequately nourished women.[17,19]

Ebbs et al., in a prospective study of 380 pregnant women, showed the direct relationship between prenatal nutrition and lack of complications during pregnancy, labor, and delivery.[28-29] The incidence of toxemia was more than twice as high among the 120 poorly nourished women than among the 90 women whose diets had been supplemented during the latter half of pregnancy (prior to that their diets were just as deficient as those of the former group) or the 170 women who had been on good diets throughout pregnancy.[28] In addition, the duration of labor and postpartum recovery was highest among the 120 poorly nourished women.[29] Among these women, 24.2% of them had dystocia in contrast to 2.3% of the women on supplemented diets and 5.9% of those on good diets.[29] In addition, the average duration of labor was five hours shorter in the good diet group than in the poor diet group.[28] It is noteworthy that the obstetrician who diagnosed these and other complications was not aware of the group to which any of the 380 women had been placed.

Quality Prenatal Diet	# of Women	% Not Having Compli- cations	% Having Major Compli- cations	Statistical Signif. Level Compared With Poor Diet Group
Good	170	48.5	12.2	p<10^-6
Supplemented	90	45.9	9.2	p<10^-5
Poor	120	30.3	36.2

A similar improvement in maternal health and lowered risk of complications during delivery were achieved by Higgins, who implemented a sound nutrition program. Among the 1,736 women who participated in her program, [the] rate of toxemia was 69% lower than that of other clinic patients and 39% less than that of private patients who received prenatal care at the same hospital.[112] Among the nutrition program's participants, who generally delivered larger babies than women who were not involved in the program, there was a much higher incidence of spontaneous deliveries and a lower rate of cesarean sections.[32]

TABLE 34
OBSTETRICAL RATING OF THE
LAST 3 TO 4 MONTHS OF PREGNANCY
TO THE 6th WEEK POSTPARTUM

Quality of Prenatal Diet	Excellent	Good to Fair	Poor	Bad
Good	30.6%	54.1%	14.2%	1.1%
Supplemented	34.5%	59.6%	5.9%	0.0%
Poor	13.1%	52.9%	22.6%	11.3%

Pasamanick and Knobloch, who advanced the sophisticated concept of a "continuum of reproductive casualty"[112-114] to designate "the sequelae of harmful events during pregnancy and parturition resulting in damage to the fetal or newborn infant, and primarily localized to the central nervous system,"[113] were the first to extensively link maternal health with infant and childhood health and development. Their mammoth research disproved the prevailing theories that developmental disabilities are primarily caused by chromosomal abnormalities, genetically transmitted metabolic disturbances, and unknown causes.[115]

Their scientific research delineated an association between prenatal and perinatal complications and a gradient of reproductive casualty,[114] including, in descending order of significance, spontaneous abortion, perinatal death, cerebral palsy, mental retardation, and behavioral disorders.[116]

Knobloch and Pasamanick found toxemia, which they linked to malnutrition, to be highly associated with the birth of children who had minor degrees of cerebral palsy.[115] They also noted that among mothers of infants who had a D.Q. under 80 (90% of the infants in the study had a D.Q. between 90 and 120), the incidence of toxemia was twice that of all the mothers whose children they examined.[63]

In a prospective study they analyzed the relationship between behavior and emotional stability and birth weight.[92] In a series of examinations given at age three, the higher birth weight children received better results in the examinations which tested organization of behavior, discrimination, judgement, emotional stability, attention span, perserverance, irritability, restlessness, and quality or integration. The authors concluded:

Table 35 summarizes the results of several well-controlled retrospective studies.[113] The data document the dramatic association between low birth weight, maternal complications, and neonatal abnormalities and various neurophysical disorders.

TABLE 35
ASSOCIATION OF NEUROPSYCHIATRIC DISORDERS WITH PRENATAL AND PARANATAL COMPLICATIONS

Neuro- Psychiatric Disorder	# of Children In Study Group	LOW- Study Group	-BIRTH- Control Group	-WEIGHT Signif. Level	COMPLICATIONS- Study Group	-OF- Control Group	-PREGNANCY Signif. Level	NEONATAL- CYANOSIS- Study Group	-CONVULSIONS, -or- -ASPHYXIA Control Group
Autism	50	21.0%	12.0%	ns	51.0%	17.0%	p<.0005	64.0%	28.0%
Behavioral Disorders	840	8.8%	2.8%	p<10^-8	40.9%	31.7%	p<.0005	4.7%	2.7%
Cerebral Palsy	561	22.0%	5.0%	p<10^-13	38.0%	21.0%	p<10^-10	- -	- -
Epilepsy	396	13.6%	6.4%	ns	34.8%	26.4%	p<.05	16.1%	5.0%
Hearing Disorders	124	16.1%	7.3%	p<.05	24.0%	11.5%	p<.01	17.1%	13.3%
Mental Deficiency	639	17.1%	8.7%	p<.0005	43.8%	36.2%	p<.05	14.2%	7.0%
Reading Disorders	205	11.5%	4.6%	p<.05	37.6%	21.5%	p<.0005	7.8%	3.9%
Strabismus	398	13.6%	7.8%	p<.01	22.9%	16.1%	p<.02	22.4%	13.8%

Pasamanick et al. observed that infants who were of low birth weight and/or born to mothers who had complications during pregnancy frequently are afflicted with minimal brain damage,[113] which they felt usually originates during the prenatal period. Pasamanick also showed that hyperactivity is highly associated with low birth weight and complications.[113,118]

In perhaps the most thorough, well-controlled study of the relationship between birth weight and neurological function and intellectual potential, Knobloch et al. tested 500 singleborn, low birth weight children and compared their results with 492 higher birth weight singleton controls.[119] Developmental, neurological, and physical examinations were performed on all 992 infants at ages ranging from 34 to 69 weeks. The examiners were not aware of the group to which any child belonged.[119-120]

As is shown in Table 36, the rates of both neurological abnormalities and intellectual defects increased as birth weight decreased.[119] Among the 57 lowest birth weight infants, 61.4% had minor neurological damage to severe intellectual deficiency; 44% of them had severe neurological or visual impairment in contrast to 2.6% among the control group infants. Moreover, none of the infants whose birth weight was under 2001 grams (4 pounds 6 1/2 ounces) had superior intellectual potential, whereas 6.3% of the normal birth weight infants were found to have such potential. The results would have been even more significant had the authors not standardized the test results of the low birth weight infants to adjust for their degree of prematurity.[119-120]

Birth Weight	# of Infants	NEURO- Normal to Indeterminate Neurol. Funct.	-LOGICAL Minimal Brain Damage	STATUS Possible CP to Overt Neurol. Defect	INTEL- Superior to High Average	-LECTUAL Average to Dull	POTENTIAL Borderline Defective to Defect.
1500 g or less	57	50.9%	22.8%	26.3%	5.3%	77.1%	17.6%
1501--2500 g	443	76.7%	16.0%	7.2%	16.3%	81.9%	1.8%
Composite of Low Birth Wt. Group Adjusted for Birth Wt.	(500)	75.5%	16.3%	8.2%	15.7%	81.6%	2.6%
Control Group (2501 g or more)	492	88.4%	10.0%	1.6%	21.8%	76.6%	1.6%

The results of tests given at age three were highly correlated (p<.05) to the initial ones.[120] The correlation between the two test results was 0.75 among the children who, as determined by the initial tests, exhibited a neurological abnormality and/or intellectual impairment.

It is noteworthy that, in virtually all of their studies, Pasamanick et al. found no major differences in the rates of dystocia and delivery procedures,[113] thereby refuting the myth that delivery-related factors are major etiologic events in influencing infant health and the presence or extent of neurological damage. Lilienfeld and Parkhurst, in a thorough retrospective analysis of 561 consecutive singleton cerebral palsied children, determined that low birth weight and complications of pregnancy were not independent factors influencing the development of cerebral palsy, as had been previously believed, but instead are caused by the same factor(s) that cause(s) the cerebral palsy.[121]

In upstate New York, birth weight and complications among the 561 cerebral palsy cases were compared to like factors among infants who were born in upstate New York in 1948 and who survived the neonatal period. The low birth weight incidence among the cerebral palsied children was 22.2% in comparison to 4.8% among the neonatal survivors (p<10^-15). Nearly 38% of the former group were born to mothers who had had complications, whereas the incidence of complications among the 1948 neonatal survivors was 19% (p<10^-9). Among women who had not had complications, the low birth weight rate was six times higher among the cerebral palsy cases.

As is evident in Table 37, as birth weight increased, the incidence of cerebral palsy decreased. Note that the table, which is based on data from the group of neonatal survivors, shows that the incidence of cerebral palsy among children who weighed under 1500 grams at birth and whose mothers did not have complications during pregnancy was 22 times higher than expected from an unbiased population of neonatal survivors.

TABLE 37
RATIO OF OBSERVED TO EXPECTED CASES
OF CEREBRAL PALSY BY BIRTH WEIGHT
ACCORDING TO PRESENCE OR ABSENCE
OF COMPLICATIONS

Birth Weight	Cases in Which the Mother Had No Complications	All Cases
Under 1500 grams (3 lb, 5 oz or less	22.00	15.00
1500-1999 grams (3 lb, 5 oz to 4 lb, 6.5 oz)	12.69	11.22
2000-2249 grams (4 lb, 6.5 oz to 4 lb, 15.5 oz)	3.90	3.39
2250-2499 grams (4 lb, 15.5 oz to 5 lb, 8 oz)	2.04	2.24
At least 2500 grams (5 lb, 8 oz or more)	.61	.82

Table 38 reveals the rates of complications among the cerebral palsy cases for which complete records were available and other populations. Premature separation of the placenta and toxemia, both of which have been shown herein to be caused by malnutrition, were the complications most overproportionately frequent among the mothers of the cerebral palsy population and the 1942-1945 group of mother who gave birth to stillbirths or whose neonates died.

TABLE 38
INCREASED RISK OF DEVELOPING COMPLICATIONS
AMONG MOTHERS OF CEREBRAL PALSIED CHILDREN
OR STILLBIRTHS OR NEONATAL DEATHS

	Complications During Pregnancy	Abruptio Placentae	Toxemia of Pregnancy
1940-1947 Cerebral Palsy Group (517 cases)	37.8% (10^-9)	1.0% (.01)	3.3% (.02)
Average per Year of 1942-1945 Group of Neonatal Survivors (377,764 cases)	20.9%	0.3%	1.8%
Average of 1942-1945 Group of Stillbirths and Neonatal Deaths (12,820 cases)	62.4% (10^-15	10.8% (10^-21)	10.3% (10^-12)
Average of 1942-1945 Total Births (395,588 cases)	22.8%	0.8%	2.2%

In Figure 8 the ratios of the actual number of instances of various complications to the expected number (as based upon a population of neonatal survivors for the cerebral palsy group and a total birth population for a group of stillbirths and neonatal deaths for the same period) are provided.

Consistent with the findings of Pasamanick et al., operative procedures used during delivery were not significantly associated with cerebral palsy births. Consequently, as evidenced by its dramatic association with low birth weight and complications of pregnancy (both of which are largely preventable by sound prenatal nutrition), cerebral palsy is primarily caused during the prenatal period.

Physiologically, cerebral palsy has been linked with periventricular venous infarction (death of tissue resulting from cessation of blood supply), which is a basically preventable lesion found around the cavities of the brain.[122] This lesion, which is common among premature infants, also is associated with and perhaps leads to epilepsy, mental retardation, and behavioral disorders.[123] Anoxia (oxygen deficiency), which usually results from maternal malnutrition, precedes periventricular venous infarction.