As I stated earlier in this course, reducing the risk of jaundice lies in addressing the 3 most preventable causes of physiological newborn jaundice (poor cellular hydration ((aka, mitochondrial dysfunction)), circadian dysfunction, and preterm birth).
Overall, the goal is to have a healthy, full-term pregnancy and physiological birth. That's why I think this protocol could just as easily be called the Thriving Bioelectric & Circadian Pregnancy Protocol!
Connect to nature via grounding and alternating solar light and nighttime darkness.
Remember:
“Your relationship with your physical, geographical location on Earth is where bioelectric cellular hydration and mitochondrial health meet the circadian processes of cell growth and recycling to promote the utmost integration into your local ecosystem, and your family’s health thereby.”
This protocol includes a small amount of nutrition research, as certain deficiencies are associated with worse outcomes, but these are not very different from any other nutritional advice you would receive in pregnancy—though this may give you a deeper understanding of why it is important for pregnant women to have excellent nutritional intake.
The things in the protocols that may be less known to you are the ways that families can make meaningful connection with the local environment to reduce oxidative stress, improve mitochondrial function, and strengthen circadian rhythms.
In a way, it may even be obvious in retrospect in that jaundice can be seen in some ways as a (sun)light-deficiency. After all, light itself is the most common jaundice treatment.
And the research shows Vitamin D, which is also highly correlated to sunlight exposure, is often lower in babies that have jaundice.
The one piece of nutritional research that may less obvious represents the final paradigm shift I want to share with you:
No more synthetic folic acid—get back to natural folates. Folic acid, though more shelf-stable than folate, depends on an enzyme in the body that is rare in the body, but even more rare in pregnant women. Plus, many pregnant women take supplements as well as eat fortified foods. This can lead up to build-ups of unmetabolized folic acid. Excess unmetabolized folic acid is associated with cognitive impairment, depression, and cancer in adults1, and can also cause a masked B12 deficiency. B12 deficiency is highly correlated with newborn jaundice. In fact, the rates of B12 deficiency directly correlate with newborn jaundice rates (both are currently ~50-60% worldwide)2. Based on this information, this protocol teaches what is known about optimizing folate without the use of folic acid. Folate metabolism is circadian (ie, folate is destroyed in the day and built up in the night, both parts of which are important), so the circadian-balancing lifestyle choices also support folate. Additionally, folate can’t be considered independently of the other B vitamins or its other cofactors, because a folate-rich diet won’t work if the other factors are missing.
Finally, physiological birth supports physiological jaundice (if jaundice is part of that baby’s journey). In the reading for this module, notice how birth interventions change a baby’s risk of jaundice.
The effect of medical and operative birth interventions on child health outcomes in the first 28 days and up to 5 years of age: A linked data population-based cohort study
Infants who experienced an instrumental birth after induction or augmentation had the highest risk of jaundice, adjusted odds ratio (aOR) 2.75 (95% confidence interval [CI] 2.61-2.91) compared with spontaneous vaginal birth
Because of its role in DNA synthesis, vitamin B12 (VitB12) is essential for cell multiplication during pregnancy. VitB12 (stored in liver) is crucial for maturation and proliferation of red blood cells (RBCs). Deficiency of VitB12 causes failure of RBC maturation leading to cell lysis. RBC lysis causes excess heme production that ends with hyperbilirubinemia. Since in newborn the functional capacity of liver is only about 1% of the adult liver, we supposed that excess bilirubin due to RBC lysis and low functional capacity of liver would result in inefficient clearance of bilirubin so that indirect hyperbilirubinemia develops. In this study, we aimed to evaluate the role of VitB12 in neonatal hyperbilirubinemia (NNH) with prolonged jaundice and to compare patients with control group who did not develop hyperbilirubinemia.
Here in our study, VitB12 level was analyzed for a risk factor of NNH. We found that low VitB12 level is a risk factor for developement of NNH. VitB12 deficiency is a correctable cause for hemolysis. The mechanism of hemolysis in this condition is ineffective erythropoiesis, where in immature erythrocytes are lysed within the bone marrow itself, resulting in the release of excess quantities of biliverdin, which is ultimately converted to indirect bilirubin.
VitB12 (cobalamin) is essential for folate metabolism and DNA synthesis, acting as a cofactor for key enzymatic reactions. Deoxyadenosylcobalamin, one of the coenzyme forms of cobalamin, is a cofactor for methionine synthase, the enzyme which converts homocysteine to methionine. In maternal VitB12 deficiency, the products homocysteine and methylmalonic acid accumulate and can be transmitted to the fetus. Raised levels of these products have been detected on newborn screening of infants with low VitB12 stores. Thus, screening for methylmalonic acid cannot be relied upon to detect in- fants with low VitB12 stores.
VitB12 deficiency in newborn, in most cases, results from a maternal deficiency.
Low folate levels in pregnant women have been linked to birth abnormalities, such as neural tube defects, and Poor levels of folate are also linked to increased cancer risk. Therefore, supplementation with folate is common. Fortifying foods with synthetic folic acid is actually mandatory in countries such as the US, Canada and Chile. The real problem is that supplements and fortified foods contain folic acid and not the natural folate.
Folate is the natural form of vitamin B9. The active form of vitamin B9 is known as levomefolic acid or 5-methyltetrahydrofolate which is also called 5- MTHF. In the digestive system, the majority of dietary folate is converted into 5-MTHF before entering the bloodstream. However, folic acid is a synthetic form of vitamin B9, which is known as pteroylmonoglutamic acid. It is used in supplements and added to processed food products, such as flour and breakfast cereals. For many years, folic acid was thought to be much better absorbed than natural folate. But a diet containing a variety of folate-rich foods has been shown to be almost as effective. Unlike most folate, the majority of folic acid is not converted to the 5-MTHF in the digestive system. Instead, it needs to be converted in the liver, but this process is slow and inefficient. After taking a folic acid supplement, it takes time for the body to convert all of it to 5-MTHF. Even a small dosage, like 200 to 400 mcg/day, may not be completely metabolized till the next dosage is taken. This crucial problem is even worse when fortified foods are eaten along with folic acid supplements as most pregnant women do, and the extra will remain in blood. Therefore, un-metabolized folic acid is usually detected in the bloodstreams of pregnant women, even in the fasted state. This should be of concern, since high levels of un-metabolized folic acid have been associated with several health problems and the most important is the cobalamin deficiency. However, one study suggests that taking folic acid along with vitamin B6, makes the conversion more efficient, but as the organ meat, which is high in vitamin B6, consumption has been decreased, this should be of a concern as well.
From all aspects of this perspective research, folic acid supplementation during pregnancy not only leads to folate deficiency due to malabsorption of synthetic folic acid, but also causes high levels of unmetabolized pteroylmonoglutamic acid which is one of the main cause and masking of cobalamin deficiency in pregnant women. Vitamin B12 deficiency is a great concern since it leads to the increasing of bilirubin in neonates which cause neonatal jaundice after delivery. Many factors in prenatal nutrition can chelate folate like sulfur deficiency and high levels of glyphosate in the diet, therefore, the replacement of synthetic folic acid with natural folate may help absorption and reducing the amount of unmetabolized folic acid serum in the blood of pregnant women.
At present, it is generally accepted that the methods for assessing the risk of neonatal hyperbilirubinemia at home and abroad are based on the age of the newborn; total serum bilirubin and/or transcutaneous bilirubin are measured, risk factors are assessed (such as hypoxia, acidosis, head hematoma, sepsis, hypoglycemia), and neonatal jaundice hour bilirubin nomograms are evaluated (Bhutani curve). There are many complex causes of neonatal hyperbilirubinemia. Common causes include infection, G6PD deficiency, breastfeeding-related jaundice, alloimmunization (ABO hemolysis or rhesus monkey incompatibility, etc.) or other severe hemolysis; there are also numerous unknown factors that lead to hyperbilirubinemia, and these factors need to be further explored.
In addition to participating in the formation of vitamin D, the liver also plays a key role in converting indirect bilirubin into direct bilirubin. Although the metabolic pathways of the two are different, they may affect each other during the biosynthesis stage of the liver. At present, the relationship between vitamin D levels and neonatal hyperbilirubinemia has attracted wide- spread attention. There have been many epidemiological studies on the relationship between vitamin D levels and neonatal hyperbilirubinemia, and some reports have shown that new- borns with hyperbilirubinemia are negatively correlated with their serum vitamin D levels. However, there are also studies suggesting that there is no significant correlation between serum vitamin D levels and neonatal hyperbilirubinemia. It is controversial. Therefore, we conducted a meta-analysis of the correlation between neonatal hyperbilirubinemia and serum vitamin D levels to determine whether there is a correlation between the two. The findings will provide evidence regarding the etiology of, risk factors for, and prevention of neonatal hyperbilirubinemia.
At present, the mechanism of the relationship between vitamin D and neonatal hyperbilirubinemia is unclear. The reported biological views are mainly as follows.
1. Indirect blood bilirubin is mostly decomposed by red blood cells. Erythropoietin is the main hormone that promotes red blood cell production. Studies have shown that vitamin D can reduce the level of erythropoietin, so vitamin D deficiency may increase the occurrence of neonatal jaundice.
2. Studies have shown that neonatal red blood cells are susceptible to oxidative damage, and vitamin D has certain antioxidant effects, so some people believe that vitamin D helps prevent the increase in bilirubin levels caused by red blood cell oxidative damage.
CONCLUSION
Vitamin D levels were observed to be lower in neonates with hyperbilirubinemia as compared to term neonates without hyperbilirubinemia in this study. This can possibly suggest that neonates with lower vitamin D levels are at higher risk for developing hyperbilirubinemia.
Shulpekova, Y., Nechaev, V., Kardasheva, S., Sedova, A., Kurbatova, A., Bueverova, E., Kopylov, A., Malsagova, K., Dlamini, J. C., & Ivashkin, V. (2021). The Concept of Folic Acid in Health and Disease. Molecules (Basel, Switzerland), 26(12), 3731. https://doi.org/10.3390/molecules26123731
Eroglu, N., Kandur, Y., Kalay, S., Kalay, Z., & Guney, O. (2015). Neonatal hyperbilirubinemia in a Turkish cohort: association of vitamin B12. Journal of clinical medicine research, 7(7), 556–559. https://doi.org/10.14740/jocmr2158w