Multiple factors can influence placental growth including nutrition, hormones, stress, genetics, maternal disease, and (of course with the topic of today's article) chemical exposure. 

The placenta develops from the cytotrophoblasts cells. At around 10 days post conception, these cells divide into invasion and syncytialization types.

Invasion types form the villus and embed themselves into the uterine lining, anchoring the embryo and starting the process of arterial remodeling. Issues with this process have been associated with placenta accrete, increta, or percreta that can result in pregnancy loss, or bleeding during pregnancy and birth. 

​Syncytialization types proliferate, lining the placenta villi and acting as a barrier between the maternal blood and the growing fetus. These cells produce progesterone, hCG, enzymes and other proteins. Poor syncytialization can cause poor progesterone production, and dysfunction in this process has been associated with preeclampsia and IUGR. 

Early placental development is heavily influenced on endocrine hormones, and thus the placenta is rich in endocrine receptors, making it a vulnerable organ to endocrine chemical disruption. The development of the trophoblast cells in early pregnancy becomes the foundation for the rest of pregnancy physiology. Changes in the genetic expression or development of the placenta, specifically, can affect fetal growth and birth outcomes.  Proper placenta development is dependent on genetic methylation, steroidogenesis, spiral arterial remodeling, cellular proliferation, and uterine invasion. All things that are influenced and affected by endocrine disrupting chemicals (EDCs).

Separating the different chemicals and measuring their effect is difficult. Mostly because the average pregnant person is exposed to over fifty different chemicals at once. EDCs are found in our everyday life, in plastics, cleaning productions, skin care products, cookware, food, and our drinking water...and often travel together. 

Instead of breaking down each chemical and what they do, I'm discussing the different changes seen in EDC exposure.

Invasion defines the ability of cells to use enzymatic secretions (catalyzed by zinc...by the way) to infiltrate the extracellular matrix of the uterine tissues and remodel the maternal arteries. Several EDCs have been shown to affect this function in both in vitro and in vivo studies. Of these phthalates, polybrominated diphenyl ethers (PBDEs), bisphenols (BPA), and polychlorinated biphenyls (PCBs) are the most associated. 

​Phthalates are in nearly 100% of people tested. Phthalates reduce cytotrophoblast invasion by activating PPARy in HTR-8/SVneo line cells, reducing this line of cell growth, which is associated with pregnancy loss. 

PBDEs are cytotoxic in the second trimester and known to cause unexplained stillbirth. Exposure in the first trimester disrupts cytotrophoblast migration and invasion through the HTR-8/SVneo cell line and changes the expression of metalloproteinases by these cells. 

BPA exposure negatively affects cytotrophoblast invasion through hypermethylation and downregulation of WNT2 gene, and an upregulation of DNMT. BPA exposure has also been shown to decrease the expression of metalloproteinases.

PCBs disrupt the invasion of HTR-8/SVneo cells by disrupting the balance between angiogenic and anti-angiogenic activities through inhibition of vascular endothelial growth factor. 

Syncytialization is the process of cellular fusion of cytotrophoblasts. These cells are hormonally active and create the labyrinth layer...the site of exchange between the maternal and fetal blood. Like the cells that divide to facilitate invasion, the syncytiotrophoblasts are sensitive to EDCs, possibly even more so than invasion cells, due to their hormone output. Of these chemicals, BPA, phthalates, PCBs organophosphates and organotin seem to have the most affect.

In vitro BPA exposure alters syncytiotrotrophoblast proliferation, reduces estrogen production, and alters P450 enzyme activity needed for proper steroidogenesis vis a reduction in corticotropin gene expression.

Histopathology observations of phthalate exposure of doses >20 kg/day showed a reduction in placental labyrinth formation, which is a noted defect found in IUGR. Phthalates concentrate more heavily in the placenta than another maternal organ.

PCBs cross the placental barrier and can directly affect the growing fetus. Placenta PCB concentrations have been associated with a decrease in syncytriotrophoblast volume. 

Organophosphates (think Roundup) alter pregnancy chemicals, specifically the production of hCG. Interestingly organophosphates accumulate more in male placentas than female placentas. Organophosphates reduce syncotriotrophoblast cell viability and cause apoptosis. 

Organotin has been shown to cross the placental barrier and lead to embryonic death. In vitro studies show that organotin affects gene expression associated with cytokine expression, hCG production, PPARy, and the retinoid X receptor.

Little research has been done on the effects of EDCs, fertility, and pregnancy, but the current evidence, EDC distribution, as well as the increase in reproductive issues and pregnancy complications begs us to increase research. 

Primary sources of these chemicals include everyday drinking water, body care products, and the foods we eat.

If you are concerned, talk to your provider about testing options, or reach out to our clinic. 

Copyright © 2022 Functional Maternity, all rights reserved.
The content in this article is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding your medical condition. ​

ALA is an organosulfur, fatty acid compound that is synthesized by the mitochondria in the cells. This synthesis is inconsistent, and studies confirm that dietary intake of ALA is essential for cellular health.

ALA works primarily as an antioxidant in metabolic functions and as a cofactor for metabolic enzymes. 

The formation of ALA in the cells requires octanoic acid, an 8-carbon fatty acid, protein, pantothenic acid (vitamin B5), and sulfur. The enzyme that catalyzes this reaction contains iron. 

In the diet, ALA is found in organ meat (liver, heart, kidneys) in significant amounts. In smaller amounts it is found in tomatoes, spinach, Brussels sprouts, peas, potatoes, broccoli, and brown rice. 

Once absorbed via the diet, ALA is reduced to dihydrolipoic acid (DHLA). Both ALA and DHLA work directly and indirectly in the body. 

In addition to its functions in metabolism, ALA has also been shown to have epigenetic regulation functions in the genes that express inflammatory factors, such as PGE2, COX-2, iNOS, TNF, IL6 and others. 

A 2015 survey that investigated the positive effects of ALA in the prevention of miscarriage followed two groups of pregnant women. The women were all within the first 13 weeks of pregnancy and had been diagnosed with threatened miscarriage or immediate loss, presented with a subchorionic hematoma between 20-50% of the gestational sac surface, vaginal bleeding, back pain, and/or contractions. One group was given 200mg vaginal progesterone 2x/daily. The second group was given the same progesterone medication plus ALA 300mg 2x/daily. The second group showed an accelerated recovery compared to the first group over the course of treatment. The group that received the ALA supplementation saw an 89% reduction in vaginal bleeding, 78% reduction in pain in 1 week. Within 15 days there was a 90% reduction in the hematoma in the ALA group. Within 3 weeks there was a 100% reduction in symptoms in the ALA treated group.

​Another study, from Italy, looked into vaginal administration of ALA for women with imminent miscarriage risk between 7-12 weeks gestation with and without subchorionic hematoma. The study compared the use of 10mg/day vaginal ALA to progesterone 400mg/day and a control group who received no support. After 20 days, the ALA group had an 80% reduction in subchorionic hematoma size, and a 100% remission in associated symptoms (pain and vaginal bleeding). 

This research is new, and there are still many questions that need to be sorted out, but it looks promising and could be an option for many women with chronic loss. 

The theory as to how ALA helps to reduce hematomas is via its immunomodulating and antioxidant effects. 

ALA reduces pro-inflammatory cytokines and increases anti-inflammatory cytokines, reduces COX-2 which in turn reduces PG2 and NO production. 

​The studies have used 300mg 2x/day in the dosage and have found this dose to be safe in pregnancy. 

All studies that have investigated the use of ALA in pregnancy, even early pregnancy, confirm its safety. No study has found adverse effects in either mom or baby. 

In fact, the use of ALA in the prevention of miscarriage and the treatment of subchorionic hematoma may have benefits that extend further into pregnancy. 

Having a subchorionic hematoma early in pregnancy increases the likelihood of developing preeclampsia later in gestation. 

​Spontaneous pregnancy loss is an all-too-common complication of early pregnancy. The clinical sign is vaginal bleeding. 18% of women who present with vaginal bleeding in pregnancy are diagnosed with a subchorionic hematoma. Of those women, 20% will miscarry, and 50% will have preterm labor or other pregnancy complications. 

ALA is a safe a viable treatment option to add to traditional progesterone treatment protocols that can increase recovery and provide preventative treatment for future pregnancy risk. 

Copyright © 2022 Functional Maternity, all rights reserved.
The content in this article is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding your medical condition. ​

There is a little something I want to touch on here, since we’re talking about B6 conversion, called the B6 paradox. We see this in supplements, typically high dose B complexes or isolated B6 supplements. One of the known side effects of B6 overdose is neurotoxicity with tingling in the extremities and neuropathy type presentations. Until 2017, the exact mechanism behind this was unknown. 

In this study they compared the neurological effects of different vitamin B6 forms, pyridoxine, pyridoxamine, pyridoxal, and P5P on different types of cells. What they found was that high doses of pyridoxine cause cell death, while none of the other vitamers affected the viability of the cells. Moreover, the P5P dependent enzymes were inhibited by the high dosed pyridoxine. This explains why symptoms of vitamin B6 toxicity mimic vitamin B6 deficiency since the supplemental pyridoxine causes a deficiency in P5P function. 

This is just one example of why vitamin form in supplementation is important. 

There have been several studies linking different nutritional deficiencies with an increased risk of developing gestational hypertension and preeclampsia. In this article I will address the individual nutrients linked in these studies, as well as nutritional principles that can help prevent, slow and support preeclampsia presentations. ​

Symptoms can include:

• Edema (specifically pitting in the ankles)
• Sudden weight gain
• Headaches
• Vision Changes
• In extreme cases, seizures, and death

It is a serious condition, but there are ways to lessen the incident. There is research that supports nutritional deficiencies to play a role in the onset of the disease

​​B5-pantothenic acid is essential in the formation of red blood cells, sex hormones, and the regulation of stress hormones.

It is also necessary for the absorption of riboflavin, so if you are deficient in pantothenic acid, you will become deficient in riboflavin. 

Like I mentioned above, folate is important for the methionine cycle that breaks down homocysteine and produces the methyl donor SAMe. 

The use of folic acid in supplementation has been the preferred method for decades. Newer studies are showing the inadequacy of the functional value of these supplements, and a better response from dietary folates. 

A 2015 study compared the severity of preeclampsia between non-folate consumers, folic acid consumers, and dietary folate consumers. What they found was the folic acid consumers has the same risk of severity of preeclampsia as non-folate consumers. In contrast, dietary folate intake was associated with a significant decrease in severe preeclampsia symptoms, but not mild symptoms.

Cobalamin along with folate and pyridoxine help to break down homocysteine. Dysfunctions in the methionine pathway and the increase in homocysteine is related to preeclampsia. There is quite a commotion around the MTHFR gene and mutations that limit the cells' ability to methylate folate.... but there are so many more genes in the process of breaking down homocysteine. Some of these genes produce enzymes that need cobalamin to function. 

In addition, many of the symptoms of HELLP syndrome mimic cobalamin deficiency and symptoms of cobalamin deficiency mimic HELLP syndrome. 

Vitamin D and K work together, and in combination with Calcium, Magnesium and Potassium.​ (More on those below)

Vitamin K2 is a fat-soluble vitamin that is produced through bacterial fermentation (either in the form of cultured food products, or by our digestive bacteria in our guts), or in cultured dairy products and bone marrow (bone broth). Its role in the body is only just starting to be understood.

Blood clotting issues in the placenta have been theorized to be a cause of preeclampsia progression. Preeclampsia is associated with low concentrations of protein Z. 

Protein Z is a plasma protein that regulates coagulation. We think of vitamin K as a nutrient that helps to prevent hemorrhaging, but what it really does is regulate blood clotting. Women with preeclampsia have lower concentrations of protein Z, which could be associated with a deficiency in vitamin K, and thus have issues with coagulation. Therefore blood clotting postpartum is more common in women with preeclampsia as well.

Calcium has long been associated with the progression of pre-eclampsia and HELLP syndromes. While most of the nutrients we are talking about work in prevention of preeclampsia from early gestation, in subsequent pregnancies, or are found deficient in preeclampsia women, calcium is the only nutrient (so far) that has been shown to reduce acute symptoms according to Cochrane. 

​Calcium regulates the hormones that function on the arteries (tightening and relaxing), and thus regulates blood pressure. In order to work properly, there must be enough Magnesium.

Oxidative stress is seen in preeclampsia women. During pregnancy serum levels of CoQ10 rise throughout pregnancy in conjunction with rises in cholesterol levels. Studies have theorized that this rise in maternal CoQ10 is protective against oxidative stress and helps to balance the inflammatory effects of late gestation metabolic changes and hormones. 

A 2003 study found a marked decrease in CoQ10 in women with preeclampsia. The theory is that increasing oxidative stress, “consumes” the CoQ10, and decreases mitochondrial function. Interestingly this difference is more prominent in women living at altitude than women living at sea level.

Choline is a dietary nutrient similar in structure to the vitamin B family. Your body can make some choline, but it is not enough to fulfill your needs. The body needs to be supplemented with dietary intake.

Choline plays a role in various body functions, including:

• Cell Membranes: Phosphorylated Choline makes the outer membrane of your cells
• Genetic Methylation: Along with Folate, B6, B12 and other methyl donors, choline is essential for genetic expression; important for fetal development
• Metabolism: Choline helps metabolize fats into energy, which is super important during the third trimester when most glucose is sent to your growing baby
• Mental Health: Choline makes up a neurotransmitter called Acetylcholine, which is important for memory, mood, and muscle control. 

There are two different forms of choline found in the diet: a water-soluble form and a fat-soluble form.

• Water soluble choline is absorbed through the small intestines and transported to the liver for storage, where it is phosphorylated into the fat-soluble form as needed to make up cell membranes. 
• The fat-soluble choline forms are more prominent in the diet and are the functional forms of the vitamin. These dietary nutrients are absorbed directly into the bloodstream and go to work throughout the body without needing to be processed in the liver.

Several factors determine choline demand and risk of deficiency.

During pregnancy there is an increased demand for choline, with most of it going to the developing baby. A study from 2017 suggested that only 8.5% of pregnant women were meeting the choline demand in pregnancy, or over 90% of women were deficiency. As of this year, few prenatal vitamins contain choline.

There is also concern that the current AI for choline in pregnancy is too low, and that an increased demand during the third trimester warrants a change in the recommendations. 

The current AI for choline in pregnancy is 450 mg/day. In 2017 the American Medical Association (AMA) announced their support of increasing prenatal supplements to contain the 450mg/day of choline. Sadly, most prenatal supplements, including the top selling brands, do not contain ANY choline. 

Supplementation is only a safety net and should not account for the full intake of nutrition in pregnancy. Many vitamins and minerals are not absorbed as efficiently in supplemental form and are best consumed in the diet. 

Taking a prenatal supplement that contains adequate choline and increasing food sources is your best way at increasing functional choline in the body. 

But, where in the diet do you get Choline? The best sources are Eggs, and Liver!

One of my favorite foods for pregnancy is eggs. Eggs have nearly everything you need to grow a baby...that's what it does. In regard to choline, eggs give you a whopping 150 mg per egg. 

Eggs are also high in Vitamin A (needed for oxytocin receptor formation), Vitamin D (deficiencies associated with pregnancy complications), Vitamin E (an essential antioxidant found in the amniotic fluid), as well as protein and cholesterol (needed for estrogen and progesterone formation). 

In some traditional cultures, pregnant women were required to eat 9+ eggs per day to have healthy babies. I like to have my patients eat 2 per day with quality prenatal and other choline rich foods. 
Many women are nervous about consuming liver in pregnancy because they have been fed fearful information. Please read my other article on this subject. Consuming liver in the second and third trimesters is safe, and nutrient dense. 

3 oz. of Beef contains a whopping 350 mg of choline, not to mention everything you need to build blood - which is doubling in the second trimester. 

​Not everyone likes liver...I know, surprising, right? Sneaking it into food is sometimes easier on the pregnancy palate. Liver can be hidden in broth and ground meats easily. 

Vegans have a harder time accumulating enough dietary choline, as most sources are animal based...but it can be done! I'm not a practitioner that believes everyone should be paleo, all foods have a place in the diet. I am also not a practitioner that is going to try and change someone's philosophy on diet. My job is to make sure that you can maintain a healthy nutritional density with your beliefs. 

Some of the foods we focus on are: 

• ​Fermented Soy: yes fermented, always fermented! Tofu, Miso, Tempeh, and Natto all fall into this group. Sources on total choline numbers in this food varies, with some sources showing tempeh having 250 mg/2 cups.
• Wheat Germ: 1 cup (that's a lot of wheat germ) provides 200 mg
• Cruciferous Veggies (Brussel Sprouts, broccoli): These guys provide around 60 mg per 1 cup serving
• Broad Leaf Greens (Spinach, Collard Greens): Cook well and they provide between 50-90 mg per 1 cup serving depending on type.

Epigenetics is an emerging area of science that offers insight into the programming of genetics and the generational impact associated with these changes. Epigenetics is defined as modifications in DNA that occur without changing its sequencing, but results in altered gene expression and function. There are multiple epigenetic mechanisms, but the most researched in pregnancy is methylation.

DNA methylation occurs when a methyl group is added to a DNA material. These genetic changes during fetal development are influenced by maternal environment and diet. This is a complex process that is only recently being fully researched. 

The maternal diet and lifestyle, through DNA methylation, can have a positive or negative impact not only on the fetus, but the next generation. 

The lifestyle of the mother can have positive or negative effects on the development of her growing baby. 

Research on environmental exposure to plastics, such as BPA, and cigarette smoke shows negative genetic impacts on fetal DNA.

​Studies using agouti mice and the effects of environmental toxins on color development, and the use of methyl donors to reverse effects, show a direct epigenetic connection to color development. A study of genetically identical mice showed that exposure to bisphenol-A (BPA found in plastics) led to an increase in yellow coated offspring with an obese phenotype. When the BPA exposed dams (mother mice) were given dietary supplements of methyl donors the effect was reversed, and the offspring had darker coats with lean phenotypes. This study highlights the link between maternal methyl donor nutrients and epigenetic expression.

​Additional studies using the same mouse models have shown that alcohol and cigarette smoke during pregnancy also directly affect DNA methylation, gene expression, and infant phenotype. 

Maternal diet plays a crucial role in the epigenetic processes. Many key nutrients are important for fetal development as well as being methyl donors. These include folate, B6, B12, Choline, and Betaine from a variety of dietary sources. These nutrients are influential during pregnancy, but also throughout childhood development. 

Folate affects fetal neural development in early pregnancy, and interacts with B12, methionine and homocysteine. It is also important for DNA methylation as a methyl donor. Homocysteine is a neurotoxin, which is typically converted to Methionine via Folate, or Betaine with the addition of B12. Betaine can be found in the diet or converted from Choline in the diet. 

Many of these above nutrients are found in foods such as green leafy vegetables, legumes, fruits, beets, pasture raised meats, organ meat, eggs, and fish. All foods that are deficient in the American diet. 

• 80% of American women of reproductive age do not consume the RDA for Vegetable intake.
• 60% of American women of reproductive age do not consume the RDA for Fruit intake.

Changes to this pathway can have long term effects on fetal health and are strongly influenced by environmental factors and diet. Mutations to the genes necessary for homocysteine metabolism (MTHFR, BHMT) can cause epigenetic changes to the growing fetus.

Several studies have linked maternal micronutrient deficiency and offspring DNA methylation.

​In addition, excess supplementation, especially with Folic Acid, has been associated with over methylation of DNA. 

Nutritional status of the mother at conception and during pregnancy affects not only their own health during pregnancy, but also the health and future health of their developing fetus. Increasing evidence points to the acute and long-term effects of poor diet choices during pregnancy.

​Consuming a healthy and nutrient dense diet is important before and during pregnancy to prevent long term complications and genetic changes. Choosing a prenatal vitamin that provides Folate and B12 in their methylated forms, and the recommended amount of Choline is increasingly important. 

Preconception is the ideal time to begin eating for pregnancy. If you have been diagnosed with a genetic mutation that limits your methylation abilities, consulting a trained professional for correct supplementation may be necessary. 

First off, we should address the WHY behind the number of women seeking natural options to encourage the onset of childbirth. 

The current medical model of birth is intimidating for the modern mother. The US birthing statistics are dismal. Currently the US is ranked 47th in maternal care in the world, just under Iran (Go USA). A 2016 report by the Center for Disease Control stated that 23.3% of births are medically induced. A survey done by Childbirth Connection found that 41% of women who delivered in US hospitals in 2011-2012 had their primary care provider attempt induction. Of those three out of four did have their labors induced.

Why are we concerned about medical induction? The standard care protocols for medical induction have changed over the years, with more focus being put on the ripening of the cervix and less on the initiation of contractions. But, with the decrease in Pitocin use comes the increase in synthetic prostaglandins. Prostaglandin therapy produces more vaginal births within 24hrs with fewer side effects compared to Pitocin inductions, but that doesn't mean zero side effects. 

​Although medical intervention can be lifesaving and the best option for some births, this is a frighteningly high number of inductions and complications, and would cause the most medically trusting woman to consider home options for labor induction.

When you read this, it is hard to see the faults. In theory Evening Primrose oil would seem a miracle for the induction of labor. It contains LA which comes down the cascade to produce both PGE1 and PGE2/PGF2 prostaglandins and is a balance of anti-inflammatory and inflammatory responses. And, also GLA which in theory would also induce the same response, increasing the prostaglandins as needed for either inflammatory or anti-inflammatory responses. Theories are always well placed, and in theory, if evening primrose is beneficial for other women’s health conditions, such as menopause and PMS, would it not also be beneficial for the pregnant mother. Although Evening Primrose Oil contains both dietary Linoleic Acid and Gamma Linolenic Acid, and the body can convert both into the correct inflammatory prostaglandins, there is concern over the wide use of Evening Primrose for the induction of labor, because dietary GLA works differently than converted GLA. 

One of Evening Primrose Oil’s claims to fame is its ability to raise PGE1 levels  
WITHOUT raising PEG2 levels. (And there is the snap) Several research studies have given this claim backing. Dietary GLA seems to skip the AA conversion steps, not sure why or how. When GLA is consumed orally, it is converted to DGLA while the AA levels remain the same, thus increasing the production of PGE1. While this is great for those with cardiovascular disease or PMS, this can be dangerous for those at the end of pregnancy.     ​

​Although the use of Evening Primrose Oil for the initiation of natural labor is often recommended as an herbal remedy to women looking to avoid the medical interventions that are ever growing in the United States, it may offer more risk than benefit.

Safe options are available, such as Acupuncture, Chiropractic, and the overall benefits of proper nutrition prior to delivery. If you want to decrease your overall risk for medical induction and complications, understanding how nutrition affects your natural labor and delivery processes is essential and should be part of modern maternity nutritional care.

Want to learn more about nutrition for childbirth success? Read my eBook, "A Patient's Guide to Childbirth Nutrition" or take my Practitioner's Course, "Advanced Nutrition in the Formation and Function of Childbirth Hormones."

​The development of an embryo is a complex and fascinating event that requires several different, and equally important nutrients. During the initial development of an embryo there are genetic and cellular changes happening at a very rapid rate, with a small human being present by week eight with limbs, ears, and facial features (how cool is that!). Magnesium deficiency is associated with an increased occurrence of birth defects, due to its critical role in embryonic gastrulation...huh? Gastrulation is one of the very first steps in embryonic development. It is the step in which the initial single layer of cells is converted into a multilayered structure of cells and occurs around the third week of gestation. This is the beginning of cellular differentiation, and this process sets the foundation for the development of each organ system. Therefore, preconception nutrition is MORE important than prenatal nutrition in the prevention of birth defects...all of this is happening before a mother even knows she is pregnant most of the time.

A little-known fact about Mg+ is that it is necessary for oxytocin to bind to its receptor on the uterus. In fact, for oxytocin to function in the uterus, there must be adequate amounts of both Mg+ and cholesterol available. If not, oxytocin cannot bind to the receptor and cannot do its job effectively.

​Diagnosing Mg+ deficiency is a bit of a puzzle, that often needs a skilled strategist to uncover. Serum Mg+ testing is inaccurate. The majority of Mg+ in the body is intracellular, meaning it is found inside cells doing its job, not floating around in the blood, lazily. This electrolyte has a job to do, and it does it. So, relying on blood testing to diagnose deficiency isn't a good idea. So, how do we assess for Mg+ deficiency? To be honest, experience and analysis of lifestyle and dietary choices. There are certain aspects of life and diet that make a person more likely to have a Mg+ deficiency. 

Magnesium is primarily found in whole grains, green vegetables, nuts, and seeds. By looking at someone's diet and analyzing their daily intake of these foods, we can determine if they are getting enough (which most are not). A pregnant mother needs a MINIMUM of 350mg of dietary magnesium per day.... MINIMUM, let me say it one more time.... MINIMUM! Now, even if someone is consuming these food groups, I want to know how they are consuming them. Food preparation methods are important. All of these food sources that contain high amounts of Mg+, also contain chemicals that keep them locked up within those plants, these are called anti-nutrients. They can affect mineral absorption from these food sources. In order to remove these anti-nutrients, specific cooking and food preparation methods need to be employed. Making sure a mother is doing this increases her absorption and decreases her likelihood of deficiency. 

Certain medications have been shown to decrease the body's Mg+ levels: Antacids, Corticosteroids, Antibiotics, Birth Control, Certain Cardiovascular medications, and Diuretics. If you have been taking any of these for an extended period, such as those with asthma, or birth control prior to conception usage, the risk of deficiency is greater.

Looking into case history can also give us a clue. There is a close relationship between Iron deficiency and Magnesium deficiency because they are often found in the same food sources. If you have iron deficiency anemia, your risk of magnesium deficiency is greater.

Another key to identifying low levels of Mg+ are patient symptoms. Certain conditions that are considered common pregnancy complaints can be a sign of a Mg+ deficiency: leg and food cramps, restless leg syndrome, increased occurrence of headaches, and edema.

​Prevention is key! Preconception diet and a good prenatal vitamin can go a long way in prevention of Mg+ deficiency in pregnancy. 

If you find yourself in a situation in which an additional Mg+ supplement may be needed...PLEASE...PLEASE...PLEASE DO NOT purchase and use a Magnesium Oxide or Citrate supplement. These are the most unabsorbable forms of Mg+ (they are also the cheapest). Consult a trained professional to determine the correct form for your presentation. I know there are many different Mg+ compounds on the market, and each is designed to work for specific presentations. So, differentiation is important.

​That doesn't mean, though, that it cannot be treated without prescription antifungals. In fact, the success rate in treatment with diet (with or without medication) is greater than medication alone.

​Yeast infections during pregnancy are much more common than you would think. Some estimate up to 75% of pregnant women have some level of yeast infection, with 30-40% needing treatment. 40% of those treated with antifungals will have a relapse and need a second dose of medication in treatment.

The severity and location of symptoms can vary significantly depending on the woman's microbiome, and immune health. But in general symptoms can include:

• Cottage Cheese like discharge (you'll never look at cottage cheese the same again...)
• Yeasty or bread like smell (...or bread)
• Vulva inflammation
• Vulva and Vaginal itchiness
• Pain with urination
• Pain with Intercourse (because sex while pregnant is already awkward enough, why not add candida)
• Symptoms worsen after intercourse

Yeast infections during pregnancy are common and can be caused by several different underlying conditions. Yeast plays a key role in eating the dead cells of blood, skin, and mucosal layers. When there is an imbalance in the diet, bacteria, or hormones, candida can overgrow and become a problem. 

• ​Normal Flora & Candida: There should be a natural balance between the yeasts and bacteria of the body. When the balance is off, with a higher ratio of candida to bacteria, we get overgrowth. 
• Pregnancy Hormones and Candida: Estrogen helps Candida grow! In lab studies, candida that is exposed to Estradiol (the estrogen of pregnancy) increased in size and structure…it grows and multiples and becomes stronger. Estrogen exposed candida are also more resistant to medications.
• Minerals and Candida: Candida binds minerals like Iron, Zinc, and Magnesium and uses them as fuel. This becomes tricky in pregnancy, as your body needs more minerals for hormones and growth processes. Too much though and you can be fueling candida growth. Because of this connection, chronic candida infections can increase the risk of anemia in pregnancy.

​It's sad to me that most western medicine providers on not trained in dietary and nutritional therapy. They are, however, well trained in medication therapy (which is sometimes the best course of action). 

1. ​Antifungals: There are multiple types of antifungals available for treatment. In general, all antifungals are hard on the body. The primary type of anti-fungal used in pregnancy are the azole antifungals (a mix of imidazole and triazole antifungals) in topical form. Topically these are safe. Oral azole antifungal treatment is considered a secondary line of defense in severe cases as it is associated with an increased risk of miscarriage and birth defects.
2. ​Antiseptics: Topical boric acid is sometimes used in place of antifungals in treatment during pregnancy. Boric Acid interferes with the natural life cycle of candida, thus killing them. Although it is considered safe in pregnancy, and absorption through the vaginal mucosa is limited, some research has linked boric acid use to severe fetal deformities.
3. ​Corticosteroids: Corticosteroids do not treatment the cause of candida, or kill the candida, they are used to alleviate the irritating symptoms caused by candida. These are usually topical creams used on the exterior labia to alleviate itching and redness associated with infection. 3% of the steroid cream is absorbed through the skin. Some studies link topical steroid use in pregnancy to an increase in cleft palate and other deformities.

Common medication treatment runs the risk of interactions and birth defects. If symptoms are mild and caught early, treatment with natural supplements should be a first line defense. Even if treatment with antifungals is necessary for the prevention of childbirth and pregnancy complications such as preterm labor, these supplements can be used to increase medical treatment success and prevent relapse.

1. Probiotics:​ Probiotics, in a hefty dose, are crucial to treatment. Lactobacillus rhamnosus is the most important for controlling yeast overgrowth, second is Lactobacillus Acidophilus, as are soil bacteria (not found in lactic acid fermentation) …dosages can and need to be high starting at 100billion per day and going up to 300billion per day. Some of the brands that I personally like are Prescript-Assist (soil bacteria), and Klaire Labs Ther-Biotic Complete Powder. The Klaire Labs powder can be used mixed with Coconut Oil as a vaginal topical. 
2. Sitz Baths: Taking baths with Baking Soda can be helpful at reducing exterior inflammation and removing infection from the vagina.
3. Garlic: Fresh garlic is best, as the anti-bacterial properties of Allicin (the active ingredient) are lost quickly after crushing the clove. 

The goal of dietary therapy in most candida diets is to starve out the yeast by depriving it of the foods likes, such as sugars and dairy. I have another approach as well. In my Candida diet we increase the foods that have been shown to have antifungal properties. Some of these foods are often left off of most other candida diet lists because they are high glycemic. In phases of pregnancy, we need additional glucose to fuel fetal development so depriving the body of all carbs (even the good ones) may not be the best idea. The general guidelines of my candida diet are not just about macronutrients, but about the micronutrients and lifestyles needs during pregnancy.

• Remove Simple Carbohydrates: This includes breads and pastas, natural sugars like pasteurized honey (raw, unfiltered is different because it contains anti-microbial compounds), Maple Syrup, and many types of fruits (some are okay, as they contain compounds that are anti-microbial as well and kill candida). 
• Avoid Starchy Vegetables: The sugars and carbs in the veggies can feed candida. (There are exceptions to this rule, like Sweet Potatoes)
• Avoid Dairy: Milk is full of lactose and estrogen (naturally occurring), which Candida loves. Aged cheeses are made with molds, and for the time being even yogurt should be avoided. Grass-Fed Butter is the only exception, as the nutrition it provides is important in pregnancy and the treatment of candida
• Avoid Xenoestrogens: Xenoestrogens fuel candida growth among other horrible things. Environmental estrogen is found in our body care products, detergents, pesticides, etc.…
• Increase Dietary Fats: Our dietary fats are nutritional powerhouses for our cells. Many are also Candida killers, and anti-inflammatory. 
• Stay Hydrated: Hydration is, of course, important in pregnancy. With Candida, you will feel dryer and flakier. Staying hydrated the correct way is more important. 
• Increase Culinary Herbs: Many, like Garlic, Turmeric and Cinnamon, are anti-microbial and kill candida. Fresh is best and use them to flavor and spice up meals.

Want to know more? Check out my eBook, "A Patient's Guide to Candida in Pregnancy." For a more in depth look into dietary treatment for Candida.

I love liver. Yes, I do, and so do my children. My family is a subsistence meat eating family, meaning we hunt for our meat. Every fall we fill our freezer with some of the highest quality meat to be found, this includes the organs. My children will fight each other over the last sliver of heart fajitas (a fall delicacy at our home). You've also never seen two little girls more excited over the giblets in a bird. There is nothing more enjoyable than watching them "patiently" wait for the fried liver and heart of little game birds and chickens. 

Not everyone loves liver as much as I do, for several reasons. But no one hates liver more than the modern medical system. There have been several myths over the decades, regarding liver, (that have been debunked) that given this previously common table staple a bad name. Like the "it filters toxins and therefore is toxic." Which we know is not the case. The liver is not a storage organ for toxins, it is a storage organ for vitamins...which is why it is one of my superfoods. 

​In 1995 an article written in the New York Times stirred the prenatal nutrition pot. This article Study Links Excess Vitamin A to Birth Defects created a swirl of thought and discussion over the dietary intake of foods high in Vitamin A, like liver. The article stated...

Let's come back to this. First, before I continue, it is pertinent to explain what Vitamin A is, exactly.

Vitamin A comes in 2 dietary forms: Provitamin A carotenoids (beta-carotene, alpha-carotene, beta-cryptoxanthin) and preformed vitamin A retinoids (retinol, retinal, and retinoic acid).

There are also synthetic versions of vitamin A. These are created in the laboratory, and are often used in supplementation, and in research. They tend to be more water-soluble, and easier to regulate in trials, so are often the forms used in medical research. This form is also more toxic. 

Carotenoids in the diet are converted to retinol (the more usable form of vitamin A). The Liver stores vitamin A in an alcohol-based form called retinyl esters. (Which is why it is such a nutritional powerhouse for dietary retinol - esters are converted to retinol in the small intestines). There is a negative feedback mechanism in place that "measures" the levels of retinol in the liver. When there are adequate levels of vitamin A in the body, there is an inhibition of both absorption of carotenoids from the diet and a decrease in conversion to retinol in the liver.  The ratio varies from 4:1 to 55:1. Conversion is also limited in the presence of other nutritional deficiencies, such as zinc. 

Carotenoids are potent antioxidants. There are over 750 of them found in plants with only beta-carotene, alpha-carotene and beta-cryptoxanthin being able to convert to vitamin A retinol. Beta-carotene is the one most referenced. On their own, Carotenoids are potent antioxidants that help neutralize toxins in the body. To provide an actual function, they must be converted to retinol. Their main dietary function is to serve as a source of retinol, as retinol is the true vitamin A.
​
When you hear "Vitamin A" what you should really be hearing is "Retinol." This is the usable form of vitamin A in the body. It is ESSENTIAL for human health and development. It is converted into retinal and retinoic acid dependent on the body's needs.  Retinol functions on a cellular level, controlling cellular development and growth. Retinol plays an important part in the development of embryos. Retinal is used in eye health and development. Retinoic Acid is necessary for hormone function and genetic expression, as well as tooth and bone growth...all crucial functions for pregnancy, childbirth, and fetal development.

So, this specific study that is mentioned in the New York Times was a survey study done at Boston University School of Medicine. Meaning the Dr. conducting the study interviewed 22,748 pregnant women. He did in-depth interviews into the supplements they were taking and the foods they were eating. 98.6% of the women interviewed were well under the toxic amount of vitamin A. Those that were consuming higher amounts, received the majority of this Vitamin A in synthetic form from prenatal vitamins and fortified foods. When you read the actual article published in the New England Journal of Medicine, little of the vitamin A supplied was via natural foods. The majority was via supplementation.

This isn't the only study that has been done. In fact, there have been several, dating back to 1967 in fact.  The findings were slightly varied, based on methods, but there are some key features in these articles that need to be addressed.

The link between dietary Vitamin A and birth defects is, literally, non-existent. In fact, you would need to consume more than 20,000 IU per day of retinol (not beta-carotene) over the course of weeks/months to induce an overdose dietarily. (If you are eating that much liver, you like liver way more than I am giving the population credit for.) Not a single study links beta-carotene consumption to birth defects.

Because liver is a rich source of retinol (via esters), it has been the dietary black sheep for the prenatal diet since the first study linked elevated levels of vitamin A (via synthetic). The amount of vitamin A reserves found in liver is not static and can range from 3,000 IU per 3 oz to 12,000 IU per 3 oz, with some sources (depending on region and diet) can be upward of 25,000 IU per ounce serving. This includes your cod liver oil fish oil supplements. 

​​So, to reiterate: