This note is not medical advice. It is really just common sense, but since obstetricians do not recognize it as such, I will label it “scientific speculation.” Every primitive culture knows the importance of maternal reserves (see Weston Price’s Nutrition and Physical Degeneration). Women who may become pregnant are put on a special diet before they conceive and are on extra-nutritious food throughout the pregnancy. Our doctors think prenatal vitamins are enough: this overestimates the importance of essential nutrients relative to accessory nutrients and conditionally essential nutrients.
The idea is this: a pregnancy is a 9 month sprint, start to finish. When the maternal bloodstream does not have adequate levels of a nutrient, the developing fetus borrows the nutrients from the mother’s bodily reserves, which are comprised mostly of muscle, fat, dense bone, and the extra blood that accompanies larger size. If the reserves are also inadequate, something still has to be done (there can be no pauses during a sprint like pregnancy), and inevitably, it is a botched job. There are more birth defects than doctors realize. Things they take for granted (like our overly narrow middle third of our faces, which give us unusually narrow nasal passages, which aggravate breathing problems) are not even seen in primitive cultures where women are better nourished.
A woman has and needs her own personal reserves. The reserve needed to carry a fetus to term is above and beyond her personal reserve.
Personal reserve can be estimated by plotting various appropriate morbidity indicators vs BMI – the first BMI level at which the morbidity indicators start to rise defines a physiological state with inadequate reserves. My guess for this number is that women with BMIs of at least 19 (maybe 20) have no more medical problems than women with BMIs of 21-25. But if their BMI is 18 or below, I expect to see a rise in the morbidity indicator functions.
The maternal reserves are in addition to the personal reserves and they can be estimated in the same way. One plots appropriate morbidity indicators during and after pregnancy (some birth defects are not seen right away) vs BMI and the first BMI where the indicator starts to rise is a BMI that is below the requisite maternal reserves. My guess for this is that women with BMIs of at least 20 should be safe, but it may be 21 or 22, and it will be higher the more inadequate her baseline nutrition. I am guessing that at least half the weight of the pregnancy (about 20-25 pounds) or about 10-12 extra pounds would provide the reserves that would be needed by an average woman consuming the average American diet and taking prenatal supplements. On a 5’6″ average frame, 10 more pounds is about another 1.6 BMI units.
Some reference values:
5’6″ 130 pounds – BMI 21
5’6″ 140 pounds – BMI of 22.6
Consider the sad case of the award-winning actress Audrey Hepburn (see her Biographical section on the IMDB database). She prided herself on always being under 103 pounds when she was not expecting. She was 5’7″ tall. This is a maximum BMI of just 16.1, way below the normal weight (135 pounds) and BMI (21.1) of a person of her height.
What were her obstetricians thinking of? What were her doctors thinking of?
Her BMI was well-below where I would expect a person to enjoy a long and healthy life. She died at just age 63, about 15 years less than the average American woman.
Her pregnancies: 5 out of 7 miscarriages (the actual percentage of miscarriage is probably higher because doctors do not count the frequent (?) failure-to-properly-implant-miscarriages). No surprise there. If my common sense estimates are correct, Audrey Hepburn did not have even remotely adequate personal reserves. Her maternal reserves were that much more negative. I am surprised that she carried two pregnancies to term. Nature finds a way. It is truly amazing, but doctors are amazingly deficient in common sense. She should have used surrogate mothers.
How common is this high miscarriage frequency, especially among actresses and models?
The fault is partly nature’s as well – the species probably does better in the long run if risky pregnancies are allowed to occur, in which either the mother’s health or the baby’s (or both) are actually at risk. Sad, if true. In a well-orchestrated system (i.e. if it were the product of design by both an intelligent and beneficent being), the hypothalamus would measure reserves and not release gonadotropin releasing hormone to start the next menstrual cycle unless there are adequate maternal reserves above and beyond her personal reserves. This problem also crops up in women who have serial pregnancies (one every 11-12 months) without time to adequately rebuild their reserves. Nature should block the menstrual cycle until the reserves are build back up, but it does not, and the results can be tragic. Hypothalamic amenorrhea, when it does occur, requires more extreme conditions than simply lack of adequate reserves: anorexia or over-training are common examples.
4/30/14 Good news: scientists are now catching on to what primitive cultures have always known. Consider this article:
Mother’s Diet Has Life-Long Effects on Child’s Gene Function
The months before and after conception, and though early pregnancy, are known to be critical. If mothers lack essential nutrients during this time, infants may endure developmental challenges and suffer deficiencies from which they never fully recover. Already, folic acid supplementation is used during the periconceptual period to prevent defects in embryos. Folic acid appears to have a role in a developing embryo’s epigenetics, which involve chemical changes to DNA. These changes leave DNA’s base sequences unaltered, but they still influence gene expression.
The connection between maternal nutrition and epigenetic change has been explored by researchers from the MRC International Nutrition Group, the London School of Hygiene and Tropical Medicine, and the Baylor College of Medicine in Houston. They have found the first evidence in humans that the “maternal biomarker status of substrates and cofactors required for methyl-donor pathways, measured around the time of conception, predicts the methylation patterns of metastable epialleles.”
Such patterns reflect the tagging gene of gene regions with chemical compounds called methyl groups. These changes, which can silence genes, occur in the presence of nutrients such as folate; vitamins B2, B6, and B12; choline; and methionine.
The researchers’ results appeared April 29 in Nature Communications, in an article entitled “Maternal nutrition at conception modulates DNA methylation of human metastable epialleles.” In this article, the authors note that the epigenetic influences of maternal diet were previously established in studies with mice. The current study, however, was able to extend these findings to humans because the researchers were able to take advantage of a unique “experiment of nature” in rural Gambia, where the population’s dependence on own-grown foods and a markedly seasonal climate impose a large difference in people’s dietary patterns between rainy and dry seasons.
Through a selection process involving over 2,000 women, the researchers enrolled pregnant women who conceived at the peak of the rainy season (84 women) and the peak of the dry season (83 women). By measuring the concentrations of nutrients in their blood, and later analyzing blood and hair follicle samples from their 2–8-month-old infants, they found that a mother’s diet before conception had a significant effect on the properties of her child’s DNA.
The researchers found that infants from rainy season conceptions had consistently higher rates of methyl groups present in all six genes they studied, and that these were linked to various nutrient levels in the mother’s blood. Strong associations were found with two compounds in particular (homocysteine and cysteine), and the mothers’ body mass index (BMI) had an additional influence. However, although these epigenetic effects were observed, their functional consequences remain unknown.
Andrew Prentice, Ph.D., professor of international nutrition at the London School of Hygiene and Tropical Medicine, and head of the Nutrition Theme at the MRC Unit, The Gambia, said: “Our ongoing research is yielding strong indications that the methylation machinery can be disrupted by nutrient deficiencies and that this can lead to disease. Our ultimate goal is to define an optimal diet for mothers-to-be that would prevent defects in the methylation process. Our research is pointing toward the need for a cocktail of nutrients, which could come from the diet or from supplements.”
Rob Waterland, Ph.D., of Baylor College of Medicine in Houston, who conducted the epigenetic analyses said: “We selected these gene regions because our earlier studies in mice had shown that establishment of DNA methylation at metastable epialleles is particularly sensitive to maternal nutrition in early pregnancy.”
The authors concluded: “Although the phenotypic consequences of these variations in methylation are not yet known, the possible implications of tissue-wide epigenetic variation at metastable epialleles induced by subtle differences in maternal micronutrient status and BMI at the time of conception are far reaching.”