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The quality of daily food intake is the most important and most ignored factor determining pregnancy outcomes. Problems caused by chromosomal material such as in Downs syndrome, cannot be resolved with diet. However, in every case, the health of the fetus is determined by the woman’s diet, exercise and life style choices, not prenatal care. The only test that has been proven to improve outcomes is testing for blood type and treating Rh negative women who have Rh positive partners. Home visits and phone calls giving weekly feedback on diet and exercise regimes are effective while prenatal testing other than blood typing is not. However standard prenatal care is built upon blood, urine and ultrasound tests. Three examples of tests with little or no advantage to the fetus are routine OGTT test, routine ultrasound screening of the previous scar for vbacs and ultrasound screening for IUGR caused by placental insufficiency. The placenta is being continuously remodeled, villi constantly replaced as the placenta migrates upward, yet Doppler velocimetry is the new set of forceps used to terrorize and bedazzle pregnant people, instead of nutritional guidance. Obstetrical prenatal care that lacks intensive hours spent improving diet is designed for profit rather than to improve outcomes.  Women choose between optimizing birth outcomes with nutrition and exercise or providing the medical system with profit derived from prenatal testing.

Even in a country (like mine) with excellent socialized medicine, accepted prenatal ‘care’ is a series of blood screening tests, urine tests and cultures, routine screening ultrasounds and sometimes amniocentesis ( developed 1956) without diet, exercise or substance abuse history or discussion. Examples of tests and when they began to be used routinely, which are used to assess risks of “problems” that are lacking in solutions that significantly improve outcomes: ultrasound estimated birth weight (1980), ultrasound dating (1980), fetal Non StressTest (NST) (1986), Biophysical Profile (BPP) (1986), suspected low or high amniotic fluid (1987), Maternal Serum Alpha-Fetoprotein Screening (MSAFP) (1990), culture for suspected presence of Group B Strep in the vagina (1996), glucose tolerance test (1998), and suspected placental insufficiency diagnosed by uterine artery Doppler waveforms (2000).

The reason prenatal care is focused on testing is that providers are not reimbursed for time spent listening or counseling the pregnant woman. Although there is research (1) showing that preconception and intrauterine maternal nutrient deprivation causes an increase in fetal mean arterial blood pressure and an increase in fetal Adrenocorticotropic hormone (ACTH)(1), maternal preconception and pregnancy nutrition is basically ignored in favor of testing, worrying and more testing.

 

Because of current obstetric approach to pregnancy, it may bear repeating that pregnancy is a normal human function like breathing and digestion that happens by itself. The necessary ‘care’ needed is the same needed to promote breathing and digestion:

Preconception: Nausea and vomiting are a result of long term Vitamin B6 insufficiency before pregnancy. Tiredness after the first trimester results from anemia. Optimal nutrition and exercise result in no nausea or tiredness in the first trimester. Preconception folic acid deficiency causes neural tube defects. (2) There is unequivocal evidence that severe iodine deficiency in pregnancy impairs brain development in the child because of the body’s inability to make T4 without iodine. (9) The most serious consequence of iodine deficiency is profound mental retardation (cretinism). (9)

Pregnancy: Following a low glycemic, Mediterranean-type diet, rich in omega-3 fatty acids (including low-mercury risk fatty fish),adequate calcium from tehina and hummus, adequate sunshine to provide Vitamin D improves ovulatory infertility, decreases preterm birth, and decreases the risk of gestational diabetes.(2) Poor diet has been documented to cause preeclampsia and improved diet to prevent it. (3)

Quality of food intake is the determining factor of pregnancy outcome. There are many healthy diets and each woman should find what works for her. The Chinese made a science out of nutrition. By determining the yin and yang qualities of food over 3000 years, the Chinese culture evolved a balanced way of eating made available to western cultures mostly thru Macrobiotics. Sugar and chocolate are examples of extreme yin and meat is extreme yang and both are destabilizing to health. Daily intake of fresh and cooked green leafy vegetables such as parsley and beet leaves are obvious daily essentials. Eating adequate complete protein- about 45 gm per day is critical starting at 12 weeks. It has been established that fish 3 times per week significantly decreases premature birth and some evidence shows improved neurological development at 3 years of age. Obviously every person eats differently and has to figure out what is the ideal intake for them, but guidelines do exist. Chocolate and coke are not part of any of them.

In addition to proper diet, optimal outcomes are a result of one hour of daily exercise 7 days per week in addition to activities of normal living, no substance abuse and not living near a leaking nuclear power plant or some other environmental disaster. The correct exercise to do is the one that you will do every day.

Although quality of diet is far more important than weight gain, recommended weight gains are 10–12 kg for women of BMI <18.0, 7–10 kg for women of BMI 18.0 to 24.0, and 5–7 kg for women of BMI >24.0. (4) In the presence of these enforced weight gain restrictions, the unexplained stillbirth rate in Japan was about 0.9/1000 for the years 1998–2005. This figure is 300% less than the unexplained stillbirth rate in the UK during the same period (3.9/1000) (5). Therefore Japanese experiences support the intake of a healthy, low sugar diet as a means to producing smaller, healthier babies at decreased risk of stillbirth, prematurity and shoulder dystocia. Obesity increases the risk of diabetes, stillbirth, perinatal mortality, shoulder dystocia and cesarean section. By 1999, only 35% of Americans were normal weight, with 65% of Americans were overweight or obese (35% BMI 25–29, 30% BMI >30) (6).

A woman can eliminate all pregnancy disease except fetal genetic defects by proper diet, exercise, life style and environment before and during pregnancy.

Some women benefit from counseling to determine diet and exercise appropriate for them and/or to discuss individual areas of concern. It is very clear from a single home visit, if you open the fridge and the cabinet, to know exactly what a woman is and isn’t eating. A time saving strategy would be having the women write down and analyze everything they eat, and have one home visit to see what is in her fridge if she has one, and determine her social needs.

But most often what women get are tests that produce profit, not improved outcomes.

The most obvious unnecessary routine is the Oral Glucose Tolerance Test (OGTT) known as the sugar test. This test reminds me of a test I saw on daytime TV. The guest was promoting his brilliant new test that would enable you to know if you are overweight. You had to take a pinch of fat from one very specific part of your body and measure the pinch exactly in inches, and if it was more than a certain amount, then it was scientifically determined that you were overweight. Such a test is completely unnecessary. If you want to know if you are fat, take off your clothes and look in the mirror. Same goes for the OGTT. If you are obese, you are eating too much. You either over eat or don’t exercise enough or both. You don’t need an OGTT to know whether you are eating healthy. Look in the mirror! Look in the fridge! Look in the cabinet! Look at your itemized grocery bill! If you are eating chocolate, cake or candy every day, you should not need an OGTT to tell you to stop. Anyway, you can fool the OGTT. It only reflects eating too much sugar for the past 3 days. Regardless of whether you have gestational diabetes, if you fast for 3 days before you take the OGTT, it will come out normal. You will have gained nothing, but the clinic always profits and gets paid for the taking the test!

Another example is the current ‘care’ for vaginal births after cesarean (VBACs). Vbacs are supposed to undergo ultrasound to see if their scar is strong enough to undergo labor. This test cannot predict uterine rupture.(7) The scar can be seen as thin or thick by ultrasound but it will not predict anything accurately because ultrasound is an inaccurate view of things.  It is sound waves bouncing off the body.

The size of the fetus DOES predict uterine rupture.  If the fetus is 2500 g at birth, the risk of uterine rupture is 1 in 1000, whereas if the fetus is 4200 g at birth, the risk of uterine rupture is 1 in 50. (8) This is not pointed out to women because either the doctors don’t believe in the woman’s ability to control their food intake during pregnancy in order to have a healthy but smaller fetus, or don’t care to spend the time necessary to do nutritional counseling to result in good outcomes. It is too time consuming. Some doctors promote the myth that birth weight has no relation to diet, but is genetic. Birth weight is directly dependent on maternal nutrition as shown by the many studies on children born after to pregnancies affected by the Dutch Famine in 1945.

The latest addition to prenatal testing is Doppler velocimetry used for the diagnosis of suspected intrauterine growth restriction or retardation (IUGR) which also goes by the name Fetal growth restriction (FGR). IUGR/FGR is variably defined as infants with birth weights below the 10th, 5th, or 3rd percentiles for gestational age. With more than 4 million live births in the United States each year, the number of growth-restricted infants ranges from 120,000 to 400,000 per year, depending on the percentile used. The most recent American College of Obstetrics and Gynecology Committee Opinion mentions 20+ possible causes. (10)


Since ultrasound is at best is 80% accurate, and since FGR depends on ultrasound, diagnosis of FGR is always uncertain. Ultrasound in the hands of the most experienced expert estimates fetal weight to the nearest +10% plus - 10% or about 80% accurate. An estimate of 2000g means the fetus is between 1800 and 2200 g. An estimate of 3000g means the fetus is between 2700 and 3300. Ultrasound cannot distinguish between a mother who eats a healthy balanced diet and has a very healthy small fetus and substance abuser who has a very unhealthy, drug addicted, malnutritioned small fetus. Whereas during a home visit, it is very easy to distinguish between the two.

IUGR by definition exists in 10% of fetuses. Due to the known inaccuracy of ultrasound, IUGR diagnosis is ALWAYS SUSPECTED, but never actually known to exist. Yet of all the women who undergo prenatal testing, regardless of lifestyle, no matter what the reality, 10% or more will be told that their fetus is growth retarded or restricted.

The given justification for diagnosing IUGR is because IUGR babies are at higher risk of miscarriage and stillbirth. The piece of the puzzle that is rarely mentioned is that diagnosing IUGR has no usefulness because it has never been shown to decrease miscarriage or stillbirth. The real justification is profit. It would be effective, but not profitable to doctors, not to do any ultrasounds but to spend hours per week from 12 weeks discussing nutrition, smoking, drugs, exercise, stress, and life situation. No solution for suspected IUGR is offered other than delivery, which in no way guarantees a better outcome. Nurse midwives have been shown to lower prematurity rates from 10% to 6.6% because of their emphasis on nutrition and life style and emotional support.(11) Instead of insurance paying for this kind of care, it pays for prenatal testing. (11)

Doppler velocimetry is the latest test added to the basket. The language is purposely mystifying but is unraveled here for the curious reader.

How the placenta works

Nutrients enter the placenta via villi, made up of a double layer of cells, the same process by which food is absorbed in the intestines. Active transport is used to transport these nutrients thru the villi. Active transport means the process which busses the nutrients uses energy. The placenta uses up some of the O2 and glucose transporting food to the fetus. Normally the placenta consumes 40% of the O2 and 70% of glucose during the transport of food to the fetus. (12) After the placenta takes its O2 and sugar needs, the blood carrying the O2 and sugar that is left, continues on to the fetus. Next the blood is forked between the fetal liver and the fetal heart, where normally, about 75% of umbilical blood delivered to the fetus goes to the fetal liver, and 25% to the heart. Next the blood from the liver and heart continues to the brain and body before being recycled back for reoxygenation.

What happens in the case of malnutrition?

With malnutrition, the placenta is not provided with less nutrients and/or O2 to adequately supply the fetus. For example, smokers have lower O2 levels at times and therefore have smaller babies. Average fetal growth is depends on the O2 and glucose delivered to the uterus exceeding what the placental needs to function. When less is supplied, the placenta compensates for low nutrient supplies by continuously remodeling during pregnancy. (13) The placenta is constantly moving upwards, discarding old villi and building new ones, gravitating north during the pregnancy.

There is no uniform clinical picture of placental insufficiency (13) because each case depends on which nutrients are deficient and to what degree. When there is insufficient O2 and sugar, the ductus venosus shunts a larger percent of oxygenated blood toward the fetal heart, rather than the liver. Sometimes the adrenal glands and spleen may show evidence of enhanced blood flow which results in increased oxygenated blood to the heart and brain and faster pumping out- blood moving at slightly faster pace out the umbilical arteries for re-oxygenation. Blood flow changes minute to minute.  Nutrient deprivation, endocrine imbalance and lower blood oxygen levels have been seen to temporarily alter organ function and maturation. But the effects are temporary and when long term studies look at these children later in life, there are no long term consequences to these compensations of the placental and fetal blood vessels. Neither continuous, absent or reversed end-diastolic umbilical artery flow have been shown to have long term effects on health later in life.(14)  Now if you want to understand that sentence read on.

Doppler velocimetry measures the velocity of the blood flow between heart beats. The two vessels yielding the best information in the fetus with intrauterine growth restriction are thought to be (because nothing is definite with ultrasound, even after over 30 years of testing Doppler velocimetry) the umbilical artery (UA) and middle cerebral artery (MCA). (15)

Already there is a problem with this description because there are 2 umbilical arteries. Which do they mean? Why are there no detectable problems with the supply, but only the velocity of the blood exiting the fetus?

“The MCA can be studied easily with an angle of zero degrees between the ultrasound beam and the direction of blood flow. “(15) This is the second problem: Doppler velocimetry is not at all accurate or reproducible unless there is an exact angle between the ultrasound beam and the direction of blood flow. (15) There is no way it can be EASY to get an angle of exactly zero degrees in a 2mm wide artery in a live, moving fetus.

“In placental insufficiency, there is an elevated placental vascular resistance, which is reflected as a decreased diastolic component of the umbilical artery Doppler waveforms. An abnormal umbilical artery waveform has a resistance index (P.I.), or systolic-diastolic ratio value above the normal range. As the placental insufficiency worsens over time, the diastolic velocity decreases because of greater resistance to blood flow, with reduced forward velocity when the ventricles are not actively contracting. In this progression the end diastolic forward velocity can eventually disappear altogether. At the extreme, there is reversal of the direction of flow in the umbilical artery during cardiac diastole.”  This description harkens back to the secret use of forceps in 1750. When forceps were invented, doctors would not let anyone see the forceps. (16) It is purposely confusing.  

Doppler velocimetry is a simple concept like forceps, and like forceps Doppler velocimetry is either useless or dangerous. If a baby can be delivered by forceps, clearly there was no need for them. There was room for the baby to come out. Get the women pushing in squatting and you never need forceps. Feed a woman a perfectly balanced adequate diet before and during pregnancy and have her walk three miles per day, and you don’t need Doppler velocimetry. Even in suspected IUGR fetus, the usefulness is questionable. Doppler velocimetry measures the velocity of the blood leaving the fetus between heart beats. There is no logical explanation for why the pressure of the blood flow between heart beats inaccurately measured by ultrasound can predict stillbirth. And, it should come as no surprise that it doesn’t.

The ability of the placenta to compensate to most situations and lack of evidence of long term effects is not emphasized. (17) “Deteriorating venous Doppler results indicate major (i.e. minor) changes in the fetal circulation as a consequence of hypoxia (i.e. supposed hypoxia), and reflect preferential blood flow to the brain and myocardium (i.e. heart) (i.e. albeit temporary), accompanied by reduced perfusion to the splanchnic organs (i.e. the intestines) and the extremities. (17) This translates to: a temporary deficiency of healthy nutrients causes increased blood flow to the brain and heart. This happens every day during fight or flight episodes. None of the Doppler velocimetry research looks at the nutritional intake, stressors of the mothers involved.

The use of the term placental insufficiency was coined around 1975 from sheep experiments in which scientists disconnected half the blood vessels supplying the uterus and found that the sheep fetuses grew poorly. This is comparable to placental abruption, not nutritive lack. In complete placental abruption, the placenta separates off the uterine wall, which immediately results in no blood flow to the placenta, which leads to immediate fetal demise. In the case of a marginal, incomplete placental abruption of less than 50%, usually weeks of hospitalization proceeds delivery and outcomes are not necessarily affected by the partial abruption. (18)

Placental insufficiency is diagnosed where IUGR, preeclampsia, miscarriage or stillbirth occurs and no disease or genetic mutations are found. There are no uniform test results that accurately predict IUGR, preeclampsia, miscarriage or stillbirth. There is no one clinical picture because the possible nutritional lacks are infinite.  Are we saving babies by delivering fetuses with suspected IUGR? No. Even among fetuses less than 1000 g, the evidence is weak, small retrospective studies that show any benefit of Doppler studies. (22)    Women do have a choice. They can be exacting in their diet and exercise and life style choices and optimize neonatal pregnancy outcomes. Or they can undergo a barrage of profitable tests for the provider that will not improve their pregnancy outcomes.

 

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2.Barger MK. Maternal nutrition and perinatal outcomes. J Midwifery Womens Health. 2010;55(6):502-11.

3. Newman V, Fullerton JT. Role of nutrition in the prevention of preeclampsia. Review of the literature. J Nurse Midwifery. 1990;35(5):282-91.

4. Japan Society of Obstetrics and Gynecology. 1997. Committee of Nutritional Guideline Nippon. Sanka Fujinka Gakkai Zasshi 51:N-507-510.

5. Sameshima H, Ikenoue T, Miyazaki Perinatal Data Group. 2008. Risk factors for perinatal deaths in Southern Japan: population-based analysis from 1998 to 2005. Early Hum Dev 84(5):319-23.

6. Wellman NS, Friedberg B. 2002. Causes and consequences of adult obesity: health, social and economic impacts in the United States. Asia Pac J Clin Nutr 11(Suppl 8):S705-9.

7. Varner M.Cesarean scar imaging and prediction of subsequent obstetric complications. Clin Obstet Gynecol. 2012;55(4):988-96.

8. Cohain JS. Can Low Glycemic Diet Increase VBAC Success? MIDIRS Midwifery Digest 2009:19(1)71-75.

9.Skeaff SA. Iodine deficiency in pregnancy: the effect on neurodevelopment in the child. Nutrients. 2011;3(2):265-73.

10. Greer LG, Ziadie MS, Casey BM, Rogers BB, McIntire DD, Leveno KJ. An immunologic basis for placental insufficiency in fetal growth restriction. Am J Perinatol. 2012;29(7):533-8.

11. Levy BS, Wilkinson FS, Marine WM. Reducing neonatal mortality rate with nurse-midwives. J Midwifery Womens Health. 2005;50(2):e10-8.

12. Fetal responses to placental insufficiency: an update. BJOG: an International Journal of Obstetrics and Gynaecology. 2004:111:1031–1041.

13. Hromadnikova I. Extracellular nucleic acids in maternal circulation as potential biomarkers for placental insufficiency. DNA Cell Biol. 2012;31(7):1221-32.

14. Makikallio K, Shah J, Slorach C, Kingdom J, Redington A, Jaeggi E. 2012. The impact of placental insufficiency on cardiovascular function in early infancy: a prospective longitudinal study. Ultrasound Obstet Gynecol, 40: 26.

15. Detti L, Mari G, Cheng CC, Bahado-Singh RO. Fetal Doppler velocimetry.Obstet Gynecol Clin North Am. 2004;31(1):201-14. Review.

16. Gelbart NR. The King's Midwife, a History of Madame Du Coudray, 1998. Berkeley, California: University of California Press.

17. Porat S, Yagel S, Anteby EY. Placental insufficiency is associated with reduced head circumference and femur length.Ultrasound in Obstetrics & Gynecology 2003. 22(S1)Poster216

18. McCormack, R., et al. 2008. Antepartum bleeding of unknown origin in the second half of pregnancy and pregnancy outcomes. BJOG 115: 1451–57.

19. Haws RA, Yakoob MY, Soomro T et al (2009). Reducing stillbirths: screening and monitoring during pregnancy and labour. BMC Pregnancy Childbirth 9(Suppl1):S5.

20. Smith, GC, and RC Fretts. 2007. Stillbirth. Lancet 370 (9600): 1715–25.

21. Apel-Sarid L, Levy A, Holcberg G, Sheiner E. Term and preterm (<34 and <37 weeks gestation) placental pathologies associated with fetal growth restriction. Arch Gynecol Obstet. 2010;282(5):487-92.

22. Chalubinski KM, Repa A, Stammler-Safar M, Ott J. Impact of Doppler sonography on intrauterine management and neonatal outcome in preterm fetuses with intrauterine growth restriction. Ultrasound Obstet Gynecol. 2012:39(3):293-8.

 

 

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
Sayer Ji
Founder of GreenMedInfo.com

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