|Vitamins for Fetal Development: Conception to Birth|
|Written by Chris Masterjohn|
|Sunday, 22 March 2009 22:29|
Table of Contents
Human life begins, biologically speaking, at conception. This is the moment at which the new organism possesses its own unique combination of some 20,000 genes and the moment at which it becomes capable of growth and cell division. The days and weeks following conception form a critical window within which the nutritional environment of the womb sets the tempo for fetal growth. But nothing more clearly illustrates the continuity between the new life within the womb and the adult he or she will become than the fact that the quality of nutrition during these nine months produces lifelong effects on the brain, kidneys, and the cardiovascular system; determines the risk of degenerative disease; and profoundly influences the quality of life that persists through adulthood and into old age.
Every human cell within a given human being has an identical set of genes, called a genome. These genes come in pairs: one copy from the mother and one from the father. Sperm and egg cells are the exception to the rule and carry only one from each pair. By shuffling the maternal and paternal genes into different combinations to produce each sperm or egg, a single man or woman could theoretically generate an incomprehensibly greater number of combinations than the number of atoms that make up the known universe, thus ensuring that no two human beings on the face of the earthâsave identical twinsâwill carry the exact same genome.1
During ovulation, an egg is released from the ovary and moves into a tube called the oviduct. At conception, the sperm and egg combine within the oviduct to form a zygote. The genes from each parent combine into pairs and the zygote possesses a new, unique genome that every cell into which it divides will inherit.
Over the course of the first seven days, the zygote divides into a hollow ball of cells as it moves through the oviduct toward the uterus. By the seventh day, it becomes embedded in the uterine wall. At this point it is called an embryo. The heart of the embryo heart by day 23; its brainwaves can be recorded at day 40; in the seventh week it begins sucking, touching its face, hiccupping, frowning and making various other spontaneous movements.
At eight weeks, all organ systems are present and functioning at which point the growing organism is called a fetus. Out of 4,500 body structures present in the adult, 4,000 are present at this eight-week point. The fetus has a firm grip, sucks its thumb, and somersaults by four months; in the beginning of the sixth month it nestles into position to sleep, stretches upon waking and can hear.2
At the turn of the third trimester, a dramatic increase in the likelihood that the infant will survive outside the womb if born prematurely takes placeâfrom 15 percent at 23 weeks to 79 percent at 25 weeks.3 In the last half of this trimester, rapid growth takes place, especially in the skeletal system. Infants born six weeks prematurely have only half the calcium and phosphorus laid down as infants carried to term.4
None of this growth and development can take place without nutrients. Fats and carbohydrates fuel the growth. Fats and cholesterol form cell membranes. Amino acids form structural proteins and enzymes. Vitamins and minerals act as cofactors for those enzymes or as regulators of the entire process of growth. These nutrients are uniquely supplied by the motherâs diet.
The provision of special pregnancy and preconception diets to mothers-to-be was a universal characteristic of the healthy traditional groups studied by Weston Price. In some cases, these groups provided special preconception foods to fathers-to-be as well.
All groups that had access to the sea used fish eggs; milk-drinking groups used high-quality dairy from the season when grass was green and rapidly growing. Some groups used other foods such as moose thyroids or spider crabs, and African groups whose water was low in iodine used the ashes of certain plant foods to supply this element.5 These foods were added against the backdrop of a diet rich in liver and other organ meats, bones and skin, fats, seafood and the local plant foods.
Fish eggs are especially rich in cholesterol, vitamin B12, choline, selenium, calcium, magnesium, and omega-3 fatty acids. They contain a modest amount of most fat-soluble vitamins but their vitamin K2 content is unknown (see Figure 1).6
The Maasai only allowed men and women to marry after spending several months consuming milk from the wet season when the grass was especially lush and the milk much denser in nutrients. Maasai milk is higher in fat and cholesterol and lower in sugar than commercial American milk. The highest quality Maasai milk used for preconception diets, however, is even richer: compared to commercial American milk, it has over twice the cholesterol, nearly three times the fat, and over five times the quantity of phospholipids (see Figure 2).7 The phospholipid content is particularly important. Since most of the choline in milk is contained in phospholipids,8 this means that high-quality Maasai milk is probably about five times richer in choline than the milk you would find in the grocery store.
Compared to grain-fed milk, grass-fed milk is much higher in fat-soluble vitamins, pigments, conjugated linoleic acid (CLA) and omega-3 fatty acids.9 Price showed that the content of vitamin A, activator X (which we now believe to be vitamin K2), and essential fatty acids markedly increased in butterfat during the rainy lush season.10 As the quality of grass increases, we can presume that the content of other grass-related nutrientsâsuch as pigments, vitamin E and CLAâwill also markedly increase in the milk.
Although modern science still has much research to accomplish in order to fully elucidate the value of traditional wisdom, it has already confirmed the fact that many of the nutritional factors that we now recognize as the most important to healthy embryonic and fetal development are the same ones emphasized in traditional pregnancy and preconception diets.
Vitamin E was originally named âFertility Factor Xâ in 1922 because rats could not reproduce without it. Two years later, researchers dubbed it âtocopherolâ from the Greek ÏÏÎșÎżÏ (tokos), meaning âchildbirth,â and ÏÎ”ÏÎ”ÎčÎœ (ferein), meaning âto bring forth.â Its precise role in rat fertility remains unclear and scientists have yet to conclusively demonstrate its essentiality to human reproduction.11
Mice lacking the gene for the protein that transports vitamin E across the placenta conceive offspring that die within 11 to 15 days. The nutritional transport system of the placenta is observably malformed by the ninth day. The human placenta makes the same protein, so the role of vitamin E in constructing the nutritional transport system of the human placenta is probably similar. Vitamin E, thenâdespite the lack of published proofâis almost certainly essential to human reproduction.11
Vegetable oils are high in vitamin E, but they are also high in polyunsaturated fatty acids (PUFA), which deplete the body of this nutrient.12 Palm oil is a much better source, having a vitamin Eto- PUFA ratio that is 8 times higher than that of soybean oil and 13 times higher than that of safflower oil.13 The vitamin E content of grass-fed animal fats is four times higher than that of grain-fed animal fats.14 Nuts, seeds, fresh fruits and vegetables and freshly ground grains also contain vitamin E.
In the years following the discovery of the role of vitamin E in rat fertility, researchers quickly began to realize that vitamin A was even more important to reproduction. In Nutrition and Physical Degeneration, Price described the early work on vitamin A deficiency during pregnancy and the preconception period. In diverse species of laboratory animals, this deficiency produced spontaneous abortion; prolonged labor and death of the mother and her offspring during labor; eye defects including the complete absence of eyes; defects of the snout, dental arches and lips; displacement of internal organs including the kidneys, ovaries and testes; and deafness due to degeneration of the nervous system.15
We now know that vitamin A is necessary for the differentiation and patterning of all of the cells, tissues, and organs within the developing body. It is especially important for the development of the communication systems between the sense organs and the brain.16,17 Even mild vitamin A deficiency compromises the number of functional units called nephrons in the kidneys, which could predispose a person to poor kidney function later in life.18 Vitamin A is also necessary during fetal development and through adult life to maintain the presence of cells lining the lungs that are covered in hair-like projections called cilia.19 These hairs sweep away debris and foreign material, protecting the lungs from pollutants and infectious diseases. During and after the formation of all these systems, vitamin A is necessary for their continued growth.
The RDA of vitamin A for pregnant women is 2,600 IUâjust 300 IU more than the RDA for women who are not pregnant. There are several problems with this figure, described in the sidebar below. We do not have exact figures for the vitamin A content of the preconception and pregnancy diets used by the groups that Price studied, but they were certainly higher than 2,600 IU per day. These groups prized organ meats, especially liver, and used them on a regular basis. Preconception and pregnancy diets added additional foods rich in fat-soluble vitamins.
The Weston A. Price Foundation recommends 20,000 IU per day from cod liver oil and additional vitamin A from milk, butter, eggs, and three to eight ounces of liver per week. Yet the medical profession warns pregnant women that this quantity of vitamin A increases the risk of birth defects. This belief can be traced to a single study published in 1995 that purportedly found an increase in the risk of birth defects among mothers consuming more than 10,000 IU per day. As discussed in the sidebar below, there are several important flaws in this study. Every other published study on this subject shows this amount of vitamin A to be safeâindeed, one major study of over 25,000 births showed that daily doses of vitamin A up to 40,000 IU cut the risk of birth defects in half.
Considering the ubiquitous role of vitamin A in the development of every organ system of the body and how tightly the body regulates the level of the activated form, we should expect a generous helping of vitamin A-rich organs and animal fats to help perfect fetal development, not to throw it off course. The preponderance of the evidence suggests that this is the case.
In the late third trimester, the fetal skeleton enters a period of rapid growth that requires calcium, phosphorus and vitamin D. An infant born six weeks prematurely has laid down only half the calcium into its bones as an infant carried to term.28 There is evidence that vitamin D plays a role in lung development,29 and it probably plays a much larger role in fetal development in general due to vitamin Dâs interaction with vitamin A. At birth, the infantâs blood level of vitamin D is closely correlated to that of the mother.30,31 Adequate levels of vitamin D protect the newborn from tetany, convulsions and heart failure.29
The rapid skeletal growth that occurs in late pregnancy taxes the vitamin D supply of the mother and her blood levels drop over the course of the third trimester. One study conducted in Britain showed that 36 percent of new mothers and 32 percent of newborn infants had no detectable vitamin D in their blood at all; another showed that 60 percent of infants born to white mothers in the spring and summer had levels under 8 nanograms per milliliter (ng/mL), a level that is overtly deficient.32
In 1963, the American Academy of Pediatrics acknowledged the increased need for vitamin D during the third trimester of pregnancy. The Academy lamented the lack of data elucidating the precise amount of this need and suggested that 400 IU per day would cover the requirements of mother and fetus.28
In 1997, however, the Institute of Medicine declared that the transfer of vitamin D from the mother to the fetus is so small that the motherâs vitamin D status is not affected. Citing a 1978 study showing that the average vitamin D level of pregnant women consuming small amounts of vitamin D at high latitudes was 9.1 ng/mL (25 percent under the level required to protect against overt deficiency) the Institute concluded that âthere is no additional need to increase the vitamin D age-related [adequate intake] during pregnancy above that required for non-pregnant women.â This conclusion is strange, not only because many of the mothers in this study must have had vitamin D levels below the average, but because the average level itself was already deficient. The Institute set the recommended intake at 200 IU, which it rather dubiously supposed âmay actually represent an overestimate of true biological need.â33
In 2003, the American Academy of Pediatricsâ Committee on Nutrition and its Section on Breastfeeding issued a joint statement in which they overturned the 40-year position of the Academy advocating 400 IU in favor of adopting the lower so-called âoverestimateâ of the Institute of Medicine.34
In the second part of this statement, the Academy directed mothers to keep their infants out of the sun, dress them in protective clothing, and liberally cover them in sunblock. In the last part of the statement, it emphasized that breast milk is deficient in vitamin Dâmaking no mention of the fact that the low intake of vitamin D during pregnancy and lactation that it advocates and the practice of keeping infants out of the sun are the precise factors responsible for low vitamin D levels in breast milk and infant vitamin D deficiency.
The Weston A. Price Foundation recommends 2,000 IU per day of vitamin D from cod liver oil, and small additional amounts from fatty fish, shellfish, butter, and lard. Although no studies have directly assessed the use of this dose during pregnancy, a study of over 10,000 infants in Finland conducted between 1966 and 1997 showed that direct supplementation of 2,000 IU per day to infants in the first year of life virtually eradicated the risk of type 1 diabetes over the next 30 years.35
Compared to vitamins A and D, very little is known about the role of vitamin K in embryonic and fetal development. The enzyme that uses it to activate vitamin K-dependent proteins first shows up in the skeletal and nervous tissue of the embryo.36 Two vitamin K-dependent proteins, bone Gla protein and matrix Gla protein, are present in the first trimester.37 These proteins help lay down calcium salts in bone tissue and keep calcium out of the soft tissues where it does not belong.
In 1997, an infant was born to a mother who took Warfarin during pregnancy. This drug interferes with the normal clotting mechanism of the blood by creating an effective vitamin K deficiency. During the early development of the middle third of her face, the cartilage of her septum calcified; at birth, her nose was a stub. Since only twenty percent of the septum protrudes from the face, a mere ten percent reduction in its length can cut the length of the nose in half. She also had cavities and plaques in her spinal cord; she required oxygen due to respiratory distress at birth; and she was quadriplegic by twenty months.37
This tragic case of severe deficiency illustrates the essential role of K vitamins in the development of proper facial proportions and the much more important and fundamental development of the nervous system.
Vitamin K2 has a higher rate of transport across the placenta than vitamin K1.38 When mothers receive injections of vitamin K2, the placenta rapidly accumulates it and then releases it slowly to the fetus over time.39 Vitamin K1 is found in leafy greens while vitamin K2 is found in fermented foods and grass-fed animal fatsâespecially natto, goose liver, cheese, and to a lesser extent butter and egg yolks.40
The fetus, infant and adult can all convert the omega-3 fatty acid found in plant oils, alpha- linolenic acid (ALA), into docosohexaenoic acid (DHA)âbut the rate of this conversion is no more than one percent at all ages and stages of development. DHA may be necessary for the formation of neurons and for the synthesis of the important brain lipid phosphatidylserine; it is also the precursor to an important compound that protects neurons when they are assaulted by oxidative stress. The fetus hoards DHA from the mother and incorporates it into its brain at ten times the rate at which it can synthesize it.41 DHA can be obtained primarily from cod liver oil and fatty fish and in small amounts from grass-fed animal fats.
The best source of DHA and vitamins A and D is high-vitamin cod liver oil. Cod liver oil also provides another omega-3 fatty acid, eicosapentaenoic acid (EPA). A number of studies have demonstrated the benefits of using cod liver oil during pregnancy and lactation. Rats that are fed cod liver oil during pregnancy give birth to offspring that have higher cognitive performance than controls at six months. If rats are fed a protein-deficient diet during pregnancy, their offspring have disturbed glucose metabolism; if they are also fed cod liver oil, however, the glucose metabolism of their offspring is normal.42
The benefits of cod liver oil during pregnancy have been verified in humans as well. Use of cod liver oil during pregnancy is independently associated with birth weight.43 A double-blind, placebo- controlled study showed the use of cod liver oil during pregnancy and lactation to increase the childâs IQ at the age of four years. In this study, the control group received the same amount of fat-soluble vitamins as the cod liver oil group, so the effects are most likely due to the DHA.44 In Norway, use of cod liver oil during pregnancy was associated with a 70 percent reduced risk of type 1 diabetes.45
The Weston A. Price Foundation recommends 20,000 IU of vitamin A and 2,000 IU of vitamin D from cod liver oil during pregnancy. This can be obtained from 1ÂŸ teaspoons of the high-vitamin variety. This amount also supplies about two grams of omega-3 fatty acidsâthe same amount shown in one study to prevent premature delivery.46
Biotin is a B vitamin but has also been called âvitamin H.â Researchers have studied its role in pregnancy for decades but only recently have discovered that marginal biotin deficiency during this critical period is the norm.
Several years ago investigators tracked the biotin status of thirteen pregnant women through the course of their pregnancies, measuring a marker of deficiency in their urine. The deficiency marker increased during both early and late pregnancy in all thirteen women; in nine, it increased above the upper limit. These women, however, had none of the traditional symptoms of deficiency such as skin problems or depression. 47
In pregnant rats, a five percent egg white diet produced a marginal biotin deficiency. The activity of biotin-dependent enzymes declined 10 percent in the mother. Yet in the fetus, the activity of these enzymes decreased a full 50 percent. Although the mother had no obvious symptoms herself, her offspring suffered an increased risk of limb and palate defects. These effects were all reversed when biotin was added to the diet in addition to egg whites.47
Whether marginal biotin deficiency causes birth defects in humans is an open question, but the results of the rat studies merit attention to increasing oneâs intake during pregnancy. Most foods contain some of this vitamin, but it is primarily found in liver and egg yolks (see Figure 4).48
Egg whites contain a glycoprotein called avidin that strongly binds to biotin and prevents its absorption. Cooking neutralizes avidin, but not completely. Frying destroys 67 percent, boiling the egg white directly for two minutes destroys 60 percent, and poaching only destroys 29 percent.49 Raw egg whites, then, should be strictly avoided, and cooked egg whites should be consumed in moderationâand never without the yolk. The addition of pure egg yolks to smoothies and ice cream will help boost biotin status.
Folate is probably the vitamin whose essential role in pregnancy is most widely known. It is necessary for the production of new DNA, and new DNA is needed for new cells. The growing life within the womb engages in constant cell division, and the mother must expand her blood supply with the production of new red blood cells as wellâthese activities demand a generous supply of folate.50
Adequate folate intake prevents neural tube defects (defects of the brain and spinal cord) and increases birth weight. It may also prevent spontaneous abortion, mental retardation and deformations of the mouth, face, and heart.50
The pregnancy RDA for folate is 600 micrograms (mcg) per day. This figure is based on the amount needed to prevent the folate concentration of the motherâs red blood cells from dropping during pregnancy and on urinary markers indicating the amount of folate being used.51 It assumes that only half of the vitamin is absorbed from food, although this figure is just an average; the rate of folate absorption is dependent on zinc status.
Synthetic âfolic acidâ is a chemical that is not normally found in foods or the human body. It can be converted into usable forms of folate, but this conversion is limited to about 200 mcg per single dose in healthy volunteers;52 it may be even more limited during long-term exposure or in certain people. Synthetic âfolic acidâ does not cross the placenta; folate crosses the placenta as the naturally occurring 5-methyl-tetrahydrofolate.50 Since the synthetic supplements do prevent neural tube defects, pregnant women should use them if they are not going to eat folate-rich diets; whenever possible, however, it is best to meet the folate requirement from foods. Folate-rich foods include liver, legumes, and greens (see Figure 5 and Figure 7).
Choline is related to folate because the body can turn it into a compound called betaine that can be substituted for folate in certain chemical reactions. Perhaps for this reason, a low intake is associated with a four-fold increased risk of neural tube defects.53
Choline has a much more direct role, however, in the development of the brain. It is especially important for the formation of cholinergic neurons (neurons that use the neurotransmitter acetylcholine), which takes place from day 56 of pregnancy through three months postpartum; and for the formation of the connections between these neurons, called synapses, which occurs at a high rate through the fourth year of life.53
Rats fed three times the normal choline requirement during pregnancy give birth to offspring with remarkably resilient nervous systems. These offspring have a lifelong 30 percent increase in visuospatial and auditory memory; they grow old without developing any age-related senility; they are protected against the assaults of neurotoxins; they have an enhanced ability to focus on several things at once; and they have a much lower rate of interference memory. Interference memory is when a past memory interferes with an immediate memoryâfor example, when a past memory of where you parked your car interferes with your ability to find it when you exit the store.53
The RDA for non-pregnant women is 425 milligrams (mg) per day. The RDA for pregnant women is 450 mg per day, only 25 mg more. The increase is based on the typical transfer of choline to and accumulation in the fetus.54 Rat studies, however, suggest that an amount two to three times this may provide the offspring with lasting benefits. Choline can be obtained from liver, egg yolks, and high-quality grass-fed dairy; it can be obtained to a lesser extent from meats, crucifers, nuts, and legumes (see Figure 6 and Figure 7).
The amino acid glycine is conditionally essential during pregnancy. Usually, we are able to make enough of it ourselves to meet our basic survival needs; during pregnancy, however, it must be obtained from food. It is the limiting factor for protein synthesis in the fetus, and thus almost certainly a limiting factor for fetal growth.55
The fetus can obtain glycine from two sources: the placenta transports glycine from the motherâs blood, and it uses folate to manufacture it from another amino acid called serine. The mother can obtain glycine primarily from collagen- rich foods such as skin and bones or bone broths (see Figure 8).56
Glycine is depleted in the detoxification of excess methionine, another amino acid. Eggs and meat are the main sources of methionineâit not only constitutes a greater percentage of their total protein but these foods are also higher in total protein than plant foods (see Figure 9).56 It is important, therefore, for the expectant mother to liberally match her eggs and muscle meats with glycine-rich skin and bones and folate-rich liver, legumes and greens.
The scientific community is showing increasing interest in what is called the âdevelopmental origins theory.â This theory postulates that the nutritional environment in the womb affects not only the risk of defects immediately apparent at birth, but also the lifelong risk of degenerative disease.
Weston Price supported an early version of this theory in the 1930s and 1940s. In Nutrition and Physical Degeneration, for example, he proposed that an increased risk of tuberculosis was largely determined by a deformation of the chest cavity that began taking shape in the womb and paralleled the deformation of the dental arch that causes crowded teeth. He also demonstrated an association between delinquent behavior and deformities of the dental arch and found the same association with non-delinquent but mentally retarded children as well. In one case, he induced puberty and rapid mental development in a teenager by surgically broadening his maxilla to stimulate his pituitary. The maxilla is the upper jaw bone; it is one of the bones of the middle third of the face, which Price so often found underdeveloped in people who grew up on modern foods.57
The modern developmental origins theory (described in greater detail in the sidebar on page 34) observes that birth weight is determined in part by embryonic and fetal nutrition; and low birth weight is in turn associated with an increased risk of heart disease, stroke, high blood pressure, diabetes and kidney disease. To explain these observations, the theory proposes that poor nutrition during pregnancy causes changes in the growth and development of the internal organs, which in turn affects the lifelong risk of degenerative disease. Since poor nutrition during this period can result in lower birth weight, an indirect association between birth weight and the risk of degenerative disease arises.58
The ideal birth weight according to these studies appears to be between 8.5 and 9.5 pounds. These figures exclude infants whose birth weights are low because of premature delivery; it is the rate of fetal growth, not the birth weight itself, that counts.59 The theory does not suggest that the risk of disease is affected only by the rate of growth within the wombâsimply that the nutritional environment during this period makes an incomplete yet permanent contribution to that risk.
Genetics has little if anything to do with birth weight. A 1995 study examined 62 cases of egg donor pregnancies. The birth weight of the baby was not correlated with the donorâs weight, the donorâs birth weight, or the birth weights of the donorâs other children; it was, however, correlated with the recipientâs weight.61 This study shows that birth weight is determined by the environment that the womb provides rather than the genome present at conception.
An intake of meat protein below 25 grams per day during late pregnancy and an intake of carbohydrate above 265 grams per day during early pregnancy are associated with a decrease in birth weight. A low intake of animal protein relative to carbohydrate is also associated with an increase of blood pressure at forty years of age.62 In order to obtain adequate glycine for growth, meat and egg protein should be balanced with the liberal use of liver, skin, bone broths, legumes and green vegetables.
The use of cod liver oil is independently associated with birth weight.43 Seven out of twelve trials have shown folic acid supplementation to increase birth weight.50 Iron deficiency compromises fetal growth,46 and a major deficiency in any vitamin or mineral is likely to do the same.
In general, the role of vitamins and minerals in providing for robust fetal growth is understudied and probably much more important than the scarcity of the available literature would suggest.
Although the quantity of growth is a useful marker for the risk of disease, the determining factor is the quality of growth. Choline may confer remarkable benefits to the developing nervous system without having much of an impact on head circumference, and vitamin A may provide for robust kidney function without having much of an impact on the size of the waist or torso.
We must take the same care in preparing the human womb for the seed of life to be planted therein that we take to prepare the womb of the earth for the seeds of the plant life from which we and our animals will take nourishment. A generous intake of all nutrientsâespecially the fat-soluble vitamins, essential fatty acids, biotin, folate, choline and glycineâwill supply the soil of the womb with everything the life developing within it needs for robust and vigorous growth and a long, healthy life to come.
Nutrient Content per 100 grams (% pregnancy RDA)
FIGURE 2. COMPARISON OF COMMERCIAL U.S. MILK AVAILABLE IN 1970 TO MAASAI MILK IN DRY AND WET SEASONS IN NAROK DISTRICT OF KENYA
The folate requirement for pregnancy can be met by one of any of the following (volume after cooking):
The RDA for choline during pregnancy can be met by one of any of the following:
* This figure assumes that Maasai milk during the wet season is five times higher in choline than commercial American milk, as discussed above.
Any combination of three meals and one snack and most combinations of three meals will exceed the pregnancy RDA for both nutrients. Folate from raw milk is accompanied by a protein that doubles its absorption. Absorption of folate from food in general is dependent on zinc status. High-quality grass-fed milk may be three to five times richer in choline.
Gluten-Free Casein-Free (GFCF)
Glycine is found primarily in skin and bones.
Animal products have a higher percentage of their total protein as methionine than plant products. Although not shown in the chart, they also contain much more protein per unit of weight or volume. The main sources of methionine in the diet, then, are eggs and muscle meats.
The RDA of vitamin A for pregnant women is only 2,600 IUâjust 300 IU more than the RDA for women who are not pregnant. To obtain this figure, the scientists at the Institute of Medicine (IOM) made the following calculation: first, they ascertained from previous reports the amount of vitamin A stored in the livers of fetuses that were spontaneously or voluntarily aborted between 37 and 40 weeks; second, they doubled this figure, assuming that half of the fetal vitamin A stores exist in the liver; and third, they divided this amount over the number of days in the last trimester, during which they presumed this vitamin A would accumulate.20
There are several problems with this calculation. Since the fetuses were aborted, we have no idea what their future health would have been likeâtheir visual acuity, their hearing, their intelligence, their facial and dental features, their reproductive health, or their length of life. And the function of vitamin A, of course, is not to be stored but to be used. The fetus does not simply hold on to vitamin A to use it after birth, but rapidly uses and metabolizes it to regulate the entirety of its growth and development. Granted, the IOM acknowledges that it has only used this data because better data do not existâyet it is important to emphasize just how little the data tell us.
The claim that intakes of vitamin A over 10,000 IU per day can increase the risk of birth defects can be traced back to a 1995 paper published by a group of researchers led by Dr. Kenneth Rothman of Boston University.21 The researchers followed almost 23,000 women over the course of their pregnancies and found that women who consumed more than 10,000 IU of vitamin A during the first trimester gave birth to offspring with a 2.4-fold greater risk of total birth defects and a 4.8-fold greater risk of cranial-neural-crest defects (a rather broad group of defects whose classification is controversial). Among the 188 women who consumed this amount of vitamin A from âfoodâ alone, there was an 80 percent increase in the risk of total birth defects and two times the risk of cranial-neural-crest defects. Because there were so few women consuming vitamin A from âfoodâ alone, however, the researchers could not conclusively distinguish the association from the effect of chance.
This study has a number of important flaws. Most of the vitamin A came from multivitamins. The authors did not distinguish between various food sourcesâand most âfoodâ vitamin A comes from fortified breakfast cereals. Three groups of experts wrote to the journal questioning the authorsâ classification of cranial-neural-crest defects.22,23,24 Perhaps most important, the authors may have underestimated the rate of certain types of birth defects. The rate of total birth defects among the 20,000 women consuming less than 10,000 IU was only 1.5 percent; by contrast, the generally accepted background rate is 3-4 percent. The rate of defects among the 3,000 women consuming more than 10,000 IU of vitamin A was 3 percentâon the lower end of normal.24
The most important objection to this study is the fact that it conflicts with all the other evidence:
The preponderance of the evidence clearly favors the view that 20,000-25,000 IU of vitamin A during pregnancy is safe and may even reduce the risk of birth defects.63
The British researcher David J. Barker first proposed the developmental origins theory in the 1980s to explain a puzzling paradox: as British prosperity increased, so did heart disease; yet geographically, the most heart disease was found in the poorest places in Britain. Barker found geographical associations of heart disease with infant mortality, but not with smoking or dietary fat. Yet even infant mortality had declined over the course of the century, just as prosperity had gone up. When he accounted for a time lag between cause and effect of more than 50 years, however, the paradox was resolvedâsomething was determining the risk of disease at or near birth, not late in life when the disease develops.58
Barker and his team of researchers then studied the birth weight of individuals born between 1911 and 1930 in Hertfordshire, UK. This allowed them to study the association at the level of individuals rather than local districts. Infants carried to term with birth weights between 8.5 and 9.5 pounds had a 45 percent lower risk of heart disease than infants carried to term weighing less than 5.5 pounds; they had a similarly lower risk of stroke, a nearly 70 percent lower risk of insulin resistance, and a slightly lower blood pressure in the seventh decade of life. The risk declined steadily and evenly between 5.5 and 9.5 pounds and began increasing thereafter. Later, other researchers found similar trends in the United States and southern India.59
Data from the three-month Dutch famine that occurred during World War II suggests that specific types of diseases are associated with specific windows of development during pregnancy. Women who were exposed to this famine during their first trimester gave birth to offspring with an increased risk of cardiovascular disease; women exposed during their second trimester gave birth to offspring with an increased risk of kidney disease; women exposed during their third trimester gave birth to offspring with an increased risk of insulin disorders.60
Developmental origins theorists have offered several explanations for these associations: poor nutrition could alter the development of the pancreas, which secretes insulin, and the liver, which secretes cholesterol and blood clotting proteins; muscle tissue could program itself for insulin resistance in order to spare glucose and amino acids for the brain when the supply of these materials is limited; overgrowth of the left ventricle of the heartâwhich itself is independently associated with cardiovascular diseaseâcould be a response to the need to supply a greater volume of blood to the brain at the expense of the other tissues.59
Just as Weston Price had associated the skeletal defects that occur because of poor prenatal nutrition with the risk of disease in childhood and adolescence, researchers are now associating the defects of the internal organs that occur due to poor nourishment with the risk of disease in adulthood and old age.
1. Ayala FJ. The Mechanisms of Evolution. Scientific American. 1978;239(3):56-69.
2. âMilestones of Early Life,â http://www.abortionfacts.com/literature/ literature_9438MS.asp. Accessed November 16, 2007.
3. Allen MC, Donohue PK, Dusman AE. The Limit of Viability â Neonatal Outcome of Infants Born at 22 to 25 Weeksâ Gestation. N Engl J Med. 1993;329:1597-1601.
4. American Academy of Pediatrics, Committee on Nutrition. âThe prophylactic requirement and the toxicity of vitamin D,â Pediatrics, March 1963; 512-525.
5. Price WA. Nutrition and Physical Degeneration: 6th Edition. La Mesa, CA: Price-Pottenger Nutrition Foundation (2004) pp. 399-403.
6. NutritionData (ND): Nutrition Facts & Calorie Counter. âNutrition Facts and Analysis for Fish, caviar, black and red, granular,â http://www.nutritiondata.com/facts-C00001-01c2138.html. Accessed November 16, 2007.
7. Ho K-J, Biss K, Mikkelson B, Lewis LA, Taylor CB. The Masai of East Africa: Some Unique Biological Characteristics. Arch Path. 1971;91:387-410.
8. Zeisel SH, Mar M-H, Howe JC, Holden JM. Concentration of Choline-Containing Compounds and Betaine in Common Foods. J Nutr. 2003;133:1302-1307.
9. EatWild, âGrassfarming and Human Health,â http://www.eatwild.com/references.html. Accessed November 17, 2007.
10. Price, op cit., p. 435.
11. Pfluger P, Kluth D, Landes N, Bumke-Vogt C, Brigelius- Flohe R. Vitamin E: underestimated as an antioxidant. Redox Rep. 2004;9(5):249-54.
12. Harvey RA and Champe PC, eds., Biochemistry: 3rd Edition, Baltimore: Lippincott Williams and Wilkins (2005) p. 389.
13. Enig MG. Know Your Fats: The Complete Primer for Understanding the Nutrition of Fats, Oils, and Cholesterol. Silver Spring, MD: Bethesda Press (2000) pp. 188; 122-3.
14. EatWild, âNutritional Benefits of Grassfarming,â http://www. eatwild.com/healthbenefits.htm. Accessed November 17, 2007.
15. Price, op cit. pp. 334-349.
16. Luo T, Sakai Y, Wagner E, DrĂ€ger UC. Retinoids, eye development, and maturation of visual function. J Neurobiol. 2006;66(7):677- 86.
17. Rawson NE, LaMantia AS. Once and again: retinoic acid signaling in the developing and regenerating olfactory pathway. J Neurobiol. 2006;66(7):653-76.
18. Gilbert T, Vitamin A and kidney development. Nephrol. Dial Transplant. 2002;17:78-80.
19. Biesalski HK, Bohr D. Importance of vitamin-A for lung function and development. Mol Aspects Med. 2003;24:431-440.
20. Panel on Micronutrients, Subcommittees on Upper Reference Levels of Nutrients and of Interpretation and Use of Dietary Reference Intakes, and the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press (2000) pp. 82-61.
21. Rothman KJ, Moore LL, Singer MR, Nguyen U-SDT, Mannino S, Milunsky A. Teratogenicity of High Vitamin A Intake. J Engl J Med. 1995;333:1369-73.
22. Werler MM, Lammer EJ, Mitchell AA. Teratogenicity of High Vitamin A Intake. N Engl J Med. 1996;334:1195-1196.
23. Brent RL, Hendrickx AG, Holmes LB, Miller RK. Teratogenicity of High Vitamin A Intake. N Engl J Med. 1996;334:1196.
24. Watkins M, Moore C, Mulinare J. Teratogenicity of High Vitamin A Intake. N Engl J Med. 1996;334:1197.
25. MartĂnez-FrĂas ML, Salvador J. Epidemiological Aspects of Prenatal Exposure to High Doses of Vitamin A in Spain. Eur J Epidemiol. 1990;6(2):118-123.
26. Shaw GM, Wasserman CR, Block G. High maternal vitamin A intake and risk of anomalies of structures with cranial neural crest cell contribution. Lancet. 1996;347:899-900.
27. Mills JL, Simpson JL, Cunningham GC, Conley MR, Rhoads GG. Am J Obstet Gynecol. 1997;177(1):31-6.
28. American Academy of Pediatrics, Committee on Nutrition. âThe prophylactic requirement and the toxicity of vitamin D,â Pediatrics, March 1963; 512-525.
29. Devereux G. Early life events in asthma â diet. Pediatr Pulmonol. 2007;42(8):663-73.
30. Hoogenboezem, T. Degenhart, H. J. De Muinck Keizer-Schrama, et al., âVitamin D Metabolism in Breast-Fed Infants and their Mothers,â Pediatric Research, 1989; 25: 623-628.
31. Ala-Houhala, M. Koskinen, T. Terho, A. Koivula, T. Visakorpi, J. âMaternal compared with infant vitamin D supplementation,â Archives of Disease in Childhood, 1986; 61: 1159-1163.
32. Bishop, N. âPerinatal Vitamin D Actions.â In Feldman, D. Pike, J.W. Glorieux, F.H. eds., Vitamin D: Second Edition, Burlington: Elsevier Academic Press, 2005; 803-810.
33. Institute of Medicine, Food and Nutrition Board, Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. âVitamin D.â In: Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride, Washington, DC: National Academy Press, 1997; 250-287.
34. Howe AM, Lipson AH, de Silva M, Ouvrier R, Webster WS. Severe Cervical Dysplasia and Nasal Cartilage Calcification Following Prenatal Warfarin Exposure. Am J Med Genet. 1997;71:391-396.
35. Hypponen, E. Laara, E. Reunanen, A. Jarvelin, M. R. Virtanen, S. M. "Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study," The Lancet, 2001; 358: 1500-03.
36. Berkner KL. The Vitamin K-Dependent Carboxylase. Annu Rev Nutr. 2005; 25: 127-49.
37. Howe AM, Lipson AH, de Silva M, Ouvrier R, Webster WS. Severe cervical dysplasia and nasal cartilage calcification following prenatal warfarin exposure. Am J Med Genet. 1997;71(4):391-6.
38. Iioka H, Akada S, Hisanaga H, Shimamoto T, Yamada Y, Moriyama IS, Ichijo M. A study on the placental transport mechanism of vitamin K2 (MK-4). Asia Oceania. J Obstet Gynaecol. 1992;18(1):49-55.
39. Iioka H, Moriyama IS, Mormoto K, Akada S, Hisanaga H, Ishihara Y, Ichijo M. Pharmacokinetics of vitamin K in mothers and children in the perinatal period: transplacental transport of vitamin K2 (MK-4). Asia Oceania J Obstet Gynaecol. 1991;17(1):97-100.
40. Masterjohn C. On the Trail of the Elusive X Factor: A Sixty-Two-Year-Old Mystery Finally Solved. Wise Traditions. 2007; Spring:14-32.
41. Innis SM. Dietary (n-3) Fatty Acids and Brain Development. J Nutr. 2007;137:855-859.
42. Joshi S, Rao S, Girigosavi S, Daware M, Kale A, Hegde M. Differential effects of fish oil and folic acid supplementation during pregnancy in rats on cognitive performance and serum glucose in their offspring. Nutrition. 2004;20(5):465-72.
43. Olafsdottir AS, Magnusardottir AR, Thorgeirsdottir H, Hauksson A, Skuladottir GV, Steingrimsdottir L. Relationship between dietary intake of cod liver oil in early pregnancy and birthweight. BJOG. 2005;112(4):424-9.
44. Helland IB, Smith L, Saarem K, Saugstad OD, Drevon CA. Maternal supplementation with verylong- chain n-3 fatty acids during pregnancy and lactation augments childrenâs IQ at 4 years of age. Pediatrics. 2003;111(1):e39-44.
45. Stene LC, Ulriksen J, Magnus P, Joner G. Use of cod liver oil during pregnancy associated with lower risk of Type I diabetes in the offspring. Diabetologia. 2000;43(9):1093-8.
46. Sparks JW, Cetin L. Determinants of Fetal Growth. In: Thureen PJ, Hay WW, eds. Neonatal Nutrition and Metabolism: Second Edition. Cambridge, MA: Cambridge University Press (2006) p. 26.
47. Mock DM. Marginal biotin deficiency is teratogenic in mice and perhaps humans: a review of biotin deficiency during human pregnancy and effects of biotin deficiency on gene expression and enzyme activities in mouse dam and fetus. J Nutr Biochem. 2005;16(7):435-7.
48. Linus Pauling Institute Micronutrient Information Center. âBiotin.â http://lpi.oregonstate.edu/infocenter/ vitamins/biotin. Accessed November 20, 2007.
49. Durance TD. Residual Avidin Activity in Cooked Egg White Assayed with Improved Sensitivity. J Food Sci. 1991;56(3):707-709.
50. Tamura T, Picciano MF. Folate and human reproduction. Am J Clin Nutr. 2006;83(5):993-1016.
51. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline and Subcommittee on Upper Reference Levels of Nutrients, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, DC: National Academy Press (1998) pp. 196-305.
52. Kelly P, McPartlin J, Goggins M, Weir DG, Scott JM. Am J Clin Nutr. 1997;65(6):1790-5.
53. Zeisel, SH. The fetal origins of memory: the role of dietary choline in optimal brain development. J Pediatr. 2006;149:S131-S136.
54. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline and Subcommittee on Upper Reference Levels of Nutrients, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, DC: National Academy Press (1998) pp. 399-422.
55. Rees WD, Wilson FA, Maloney CA. Sulfur amino acid metabolism in pregnancy: the impact of methionine in the maternal diet. J Nutr. 2006;136(6 Suppl):1701S-1705S.
56. http://www.nutritiondata.com. [Corresponding entries for each food.] Accessed November 8, 2007. Glycine content of bone broth calculated by assuming bone protein is 95% collagen and collagen is 33% glycine.
57. Price, op cit. pp. 350-1; 355; 357; 367-71.
58. Barker DJP. The origins of the developmental origins theory. J Intern Med. 2007;261:412-417.
59. Barker DJP. Fetal nutrition and cardiovascular disease in later life. British Medical Bulletin. 1997;53(1):96-108.
60. Symonds ME, Stephenson T, Gardner DS, Budge H. Long-term effects of nutritional programming of the embryo and fetus: mechanisms and critical windows. Reprod Feril Dev. 2007;19:53-63.
61. Brooks AA, Johnson MR< Steer PJ, Pawson ME, Abdalla HI. Birth weight: nature or nurture? Early Human Dev. 1995;42(1):29-35.
62. Godfrey K, Robinson S, Brker DJP, Osmond C, Cox V. Maternal nutrition in early and late pregnancy in relation to placental and fetal growth. BMJ 1996;312:410.
63. Mastroiacovo P, Mazzone T, Addis A, Elephant E, Carlier P, Vial T. High vitamin A intake in early pregnancy and major malformations: a multicenter prospective controlled study. Teratology. 1999;59(1):7-11.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Winter 2007.
Vitamin A cutting birth defects in half
written by Celestia , Jul 18 2012
|Last Updated on Tuesday, 31 January 2012 14:06|