Preeclampsia: Nutritional Factors, Environmental Toxins: Prevention & Treatment

Preeclampsia in pregnancy is defined by systolic blood pressure levels greater than 140 or diastolic pressure greater than 90. In addition to elevations in blood pressure, other common clinical findings of preeclampsia may include: proteinuria (elevated urinary protein), elevated liver enzymes, edema (fluid retention), headaches and visual disturbances. Preeclampsia can cause several pregnancy complications, including seizures, pre-term birth and birth defects. The standard medical treatment for pre-eclampsia involves anti-hypertensive drugs, and in some cases anti-seizure medications. However, these treatments do not address underlying, etiological factors. A considerable body of scientific literature has identified that the primary risk factors for preeclampsia involve oxidative stress conditions, nutritional factors, including excess sugar and PUFA intake (polyunsaturated fatty acids), and importantly high levels of toxic elements lead (Pb), cadmium (Cd), arsenic (Ar) or mercury (Hg). Additionally, preeclampsia has been shown to feature low levels of antioxidant nutrients, Vitamins E, C, ß-carotene, selenium and CoQ10. Moreover, a variety of genetic risk factors for preeclampsia have been reviewed and selected for discussion. The nexus of this publication’s research findings suggests that preeclampsia is a highly heterogenous condition, and likely arise from a variety of different factors for each woman. From a clinical perspective, this requires careful examination of major etiological and contributing factors, preferably prior to pregnancy so that preeclampsia may be prevented. This review aims to evaluate the association between heavy metal toxicity, oxidative stress, genetics, and nutritional interactions in preeclampsia.

Preeclampsia: Oxidative Stress, Nutrition & Toxic Elements

Increased ROS (reactive oxygen species) and oxidative stress have long been identified as primary factors that can lead to pregnancy complications including: preeclampsia, gestational diabetes, adverse embryonic development, diminished placental integrity, including adverse effects on placental size and weight, spontaneous abortion, congenital malformations, as well as developmental delays after birth (Gubory, et al; 2010), (Duhig, et al; 2016), (Pietryga, et al; 2020).

Pregnancy, as a conditional state of maternal life and fetal development increases oxidative stress. This is due to the fact that the placenta increases the demand for oxygen respiration and growth processes that demand increased metabolic activities, which results in the generation of more reactive oxygen species (ROS). Pregnant women have a lower antioxidant capacity compared to non-pregnant women, as well as an increase in numerous oxidized molecules such as ox-LDL, and they develop a greater systemic inflammatory profile in the later term (Redman Sargent, 2003), (Belo, et al; 2004).

A heathy diet plays an essential role in preventing the sabotage of oxidative stress during pregnancy. A healthy diet includes nutrient dense whole food nutrition, which contains the fundamental and essential nutrients for life, nutrient cofactors and antioxidants which facilitate biochemical reactions, including those involved in reduction and oxidation. Anthropological evidence obtained from isolated, primitive cultures in the early part of the 20th century have succinctly identified the native people’s understanding of the criticality of a healthy diet, not only during pregnancy but in the years leading up to conception (Price, 1939). In the modern era, the prevention of pregnancy complications should be seen as a priority, even though modern conveniences and lifestyles are in many ways antithetical to preparatory practices of conception and birthing.

Large population cohort studies have identified significant dietary differences among women who develop preeclampsia versus women who do not. A U.S. based study in 2001 evaluated a total of 3,133 women, identifying that preeclampsia incidence is associated with higher intakes of dietary sucrose and PUFA’s (polyunsaturated fatty acids). Strikingly, women who developed early onset preeclampsia were found to consume more than 3 times the amount of sucrose from sugar-containing soft drinks (Clausen, Slot, et al; 2001). Other sizable studies that have investigated dietary associations with preeclampsia have found similar associations with processed food versus whole food diets. An Iranian study (n=511) found that intake of western-based diets is associated with a 6-fold increased risk of developing preeclampsia, compared to an 87.5% risk reduction when a healthy dietary pattern is used, and an 81.7% reduction when a traditional Iranian diet is used (Abassi, et al; 2019).

In addition to dietary associations, a considerable body of literature has found associations between toxic, heavy metals and preeclampsia. This is particularly true of the toxic elements, lead (Pb), mercury (Hg), cadmium (Cd) and arsenic (Ar). Supplementation with antioxidants, namely Selenium (Se), NAC (n-acetyl cysteine), Vitamin E, Vitamin C, Lycopene, Zinc, as well as Calcium have shown positive results with respect to preventing preeclampsia, as well as mitigating the toxic effects of heavy metals in some cases (Alves, et al; 2023), (Rahnemaei, et al; 2020), (Motawei, et al; 2018).

Preeclampsia: Nutrients & Antioxidants

Dietary antioxidants are essential for normal cellular metabolic processes. This includes the protection from free radicals and the biotransformation and detoxification of toxic elements.

Women with preeclampsia have lower levels of plasma antioxidants, compared to pregnant women who do not have preeclampsia. The most significant associations include: Vitamin E, Selenium, Melatonin, ß-Carotene, Vitamin C, and CoQ10 (Xu, Guo, et al; 2015), (Cohen, et al; 2015), (Mikhail, et al; 1994), (Shaban, et al; 2004), (Vaillancourt, et al; 2012).

Vitamin E, PUFA’s & Preeclampsia

According to a 2009 systematic review, preeclampsia is associated with elevations in increased oxidative stress markers, including lipid peroxides and malondialdehydes (MDA’s), (Gupta, et al; 2009). The oxidation of polyunsaturated fatty acids (PUFA’s) leads to increases in lipid peroxides. Importantly, Vitamin E plays an essential role in preventing and scavenging lipid peroxides that are derived from PUFA’s, such as MDA. Higher PUFA intake is associated with both preeclampsia, and with Vitamin E deficiency. (Valk, Hornstra; 2013), (Hassan, et al; 1966). Moreover, some cases of preeclampsia will present with elevations in liver enzymes, and concomitant NAFLD (non-alcoholic fatty liver) (Memari, et al; 2018). In these cases, Vitamin E is critical here. Meta analysis research has found that supplemental Vitamin E is capable of improving all histological and clinical parameters of NAFLD, including reductions in ALT & AST liver enzymes, reductions in glucose, leptin and LDL cholesterol (Vadarlis, et al; 2020).

Selenium, Toxic Elements & Preeclampsia

Selenium plays a vital role in the antioxidant defenses, acting in 25 selenoproteins, including glutathione peroxidases, selenocysteine and thioredoxins. As such selenium plays an important role in the biotransformation and detoxification of reactive oxygen species, as well as toxic elements such as mercury and cadmium. Pregnancy features an increase demand for antioxidants, including selenium, because there is an increased demand for metabolic oxygen respiration (Osmond, et al; 2000). This demand may increase with higher levels of toxic elements.

Meta-analysis research has identified that selenium levels are inversely associated with preeclampsia (Xu, Guo, et al; 2015).

A 2016 meta analysis evaluating 16 total studies and a total of 1,515 participants found that Selenium supplementation significantly reduces the incidence of preeclampsia. The average dosages of selenium used in the RCT studies are between 60-100mcg daily. (Xu, Guo, et al; 2015).

Importantly, antioxidant enzymes such as glutathione peroxidase exist in the mother, the placenta, the fetus, and in the umbilical cord. The maternal intake of antioxidants such as selenium will affect the activities of all of these.

Lower placental levels of selenium are associated with higher placental levels of cadmium and preeclampsia (Laine, et al; 2015), whereas higher placental selenium levels are associated with normal birth weight for gestational age (Klapec, et al; 2008). Increased maternal red blood cell (RCB) selenium is associated with an infant’s improved psychomoter function at 1.5 years of age, including language comprehension and expression (Skroder, et al; 2015).

Elevated blood mercury levels are associated with both moderate to severe preeclampsia, and higher mercury levels are associated with lower birth weight (Wang, et al; 2022). Across all forms of life, a lower selenium to methyl mercury ratio is associated with the increased, deleterious effects of mercury toxicity (Kalisinska, et al; 2017).

Melatonin & Preeclampsia

Melatonin has emerged in recent decades as being a powerful, pleitropic hormone, with remarkable antioxidant properties. Melatonin improves oxidative phosphorylation, and supports several parameters of mitochondrial function. As a nocturnally-secreted hormone, it has long been recognized as a core regulator of circadian biology, in part acting to modulate the emission of biophotons (Naveed, et al; 2017). In addition to this, melatonin is a potent antioxidant, as well as a notable anti-hypertensive agent. Blue light exposure from artificial lighting sources, including computer and cell phone screens are known inhibitors of melatonin secretion. Importantly, melatonin plays essential roles in fetal development.

In normal pregnancy, melatonin is synthesized and secreted into the bloodstream, where it is taken up by the placenta, and the uterus. Additional melatonin can be made locally within the uterus, and remarkably both the trophoblast and placenta can synthesize melatonin (Vaillancourt, et al; 2008). Maternal levels of melatonin gradually rise until birth. The placenta contains melatonin receptors, MT1 and MT2, respectively, which leads to the activation of this important indolamine hormone. Importantly, new born babies do not produce their own melatonin until weeks 9-12, and are entirely dependent upon melatonin in the mother’s milk.

Melatonin possesses potent antioxidant properties, and it is capable of increasing the expression of other endogenous antioxidants in various tissues, including glutathione, superoxide dismutase and catalase. Importantly, melatonin works in conjunction with oxytocin to produce uterine contractions during labor, and it has been proposed that nocturnally secreted melatonin is the reason why most births occur at nighttime (Reiter, et al; 2013).

• Low melatonin levels are associated with poor fetal growth in the first trimester (Gitto, et al; 2005)
• Exposure of light at nighttime in pregnancy suppresses melatonin, and this leads to increased risk of low fetal weight, miscarriage, pre-term delivery, preeclampsia, as well as adverse developmental events for the developing baby (Gomes, et al; 2021)
• Experimental studies have found that maternally suppressed melatonin levels due to constant light exposure alters the circadian clock genes of the fetus, reduces intrauterine growth, and disrupts the cortisol rhythm (Mendez, et al; 2012).
• In preeclampsia, circulating levels of melatonin are lower at nighttime, compared to women with normal pregnancy (Bouchlariotou, et al; 2013)
• In preeclampsia, expression of melatonin’s MT1 and MT2 receptors in the placenta are reduced (Vaillancourt, et al; 2012)
• In a small phase 1 clinical trial, 20 women with early onset, severe preeclampsia were given 10mg of melatonin, three times daily. Compared to historical pregnancy duration from preeclampsia onset to delivery, there was an average 6 day increased gestation length with melatonin treatment. The blood pressure was not overall different, but the treated mothers required a lower dose of blood pressure-lowering drugs at certain intervals, including at delivery. Notably, this study also involved the use of a placental explant in vitro evaluation of melatonin. In these regards, melatonin improved molecular parameters of endothelial function, including reduction of isoprostanes, and improved antioxidant expression of Nrf2 (Hobson, et al; 2018)
• In women with preeclampsia, administration of 6mg of melatonin was shown to significantly increase glutathione peroxidase in the chorion, within hours following administration (Okatani, et al; 2002)
• In vitro preeclampsia research found a potent synergistic effect between melatonin, Vitamin C and Vitamin E in the ability to inhibit lipid peroxidation in placental mitochondria (Milczarek, et al; 2010)
• Melatonin enhances antioxidant function in the placenta and in the endothelium (Hannan, et al; 2018)
• In a trial study of babies born with asphyxia, 80mg of melatonin spread out over several hours resulted in reduced levels of lipid peroxides, and 100% survival (Fulia, et al; 2001)
• Melatonin acts as a chelating agent for a variety of toxic metals (Reiter, et al; 2016)
• An experimental animal study found that melatonin administration protects against cadmium-induced fetal growth restriction, protects the placental barrier and modulates intestinal dysbiosis (Zhang, et al; 2022)
• An experimental animal study found melatonin counters the toxic effects of Pb on developing rat brain, including restoration of glutathione and SOD, while improving Pb-induced histological damage to Pirkinje cells (Bazrgar, et al; 2015)

Folate, Preeclampsia & MTHFR Genetics

Folate, also known as Vitamin B-9 is an essential nutrient that plays a crucial role in DNA synthesis. Adequate folate during pregnancy has long been recognized as essential for preventing birth defects, including neural tube defects. While folic acid is still to this day recommended as the choice form of folate, existing research has identified that folic acid, a synthetic form of folate may not be the proper form for many people. Individuals who carry the genetic polymorphism of the MTHFR C677T variant (which exists in 10-25% of different worldly populations) have an impaired ability to synthesize the active form of folate, known as 5-methyltetrahydrofolate. The inability to synthesize the active methylated form of folate could create symptoms of folate deficiency, even if folic acid is given.

Associations between preeclampsia risk and the MTHFR 677T genetic polymorphism have been established and confirmed to be statistically significant by meta analysis (Wu, et al; 2015). The mechanism of preeclampsia for carriers of the MTHFR polymorphism involves the elevation in homocysteine, which is a risk factor for endothelial inflammation, and subsequent hypertension. In these cases, active 5-methylfolate supplementation should be considered during pregnancy, along with monitoring of plasma homocysteine.

Preeclampsia & Heavy Metal Toxicity: Lead (Pb), Mercury (Hg), Cadmium (Cd)

Pb (lead) is a common environmental heavy metal that has been flagged as a developmental toxin for decades. A 2018 meta analysis pooled 12 studies that evaluated the relationship between pre-eclampsia and Pb toxicity, involving a total of 6,069 pregnant mothers. The authors identified that a 1 ug/dl increase in blood lead (Pb) levels is associated with a 1.6% increase in the likelihood of preeclampsia. According to the study this association “appears to be the strongest risk factor for preeclampsia yet reported.” (Poropat, Laidlaw, et al) .

Pb (Lead) & Preeclampsia: Mechanisms of Action

Pb toxicity has been long associated with hypertension, cardiovascular disease risk factors and endothelial inflammation. Pb can cause hypertension and induce preeclampsia through several mechanisms of action:

• Pb (lead) increases a vasoconstrictive peptide known as Endothelin (Metryka, et al; 2018)
• Pb (lead) lowers levels of the primary endothelial vasodilation molecule, nitric oxide (Carmignani, et al; 2000)
• Pb (lead) increases the pro-inflammatory cytokine IL-8 (Metryka, et al; 2018). IL-8 serves as a potent chemoattractant, and inflammatory promoter for endothelial cells. Compared to normal pregnancy, elevated IL-8 is found in women with preeclampsia (Arikan, et al; 2012).
• CRP levels are elevated in preeclampsia (Arikan, et al; 2012). Higher levels of CRP are a risk factor for hypertension (Jayedi, et al; 2019). Higher Pb levels are associated with elevations in CRP (Khan, et al; 2008) Elevated CRP levels serve as a marker of endothelial cell inflammation (Metryka, et al; 2018)
• Elevated Pb (lead) levels are associated with increases in the inflammatory cytokine IL-6 (Lu, Xu, et al; 2018). IL-6 is elevated in preeclampsia (Lau, et al; 2013).

How Pb (Lead) is Toxic to a Developing Baby

• As a toxic element, Pb (lead) is capable of crossing the placental barrier and altering the mitochondrial DNA of developing fetuses (Guerra, et al; 2019)
• Pb (lead) is a neurodevelopmental toxin. Pb toxicity alters neurotransmitter function, leading to altered brain function and development (Gundacker, et al; 2021)
• Pb (lead) toxicity late in pregnancy is associated with causing lower MDI scores during infancy (Shah, et al; 2016)
• Pb (lead) toxicity is associated with lower fetal cortisol levels during the 2nd trimester (Tamayo et al., (2016), and this association is related to reduced sensory abilities (Cai et al., 2019)
• Pb (lead) toxicity is known to be toxic to the hippocampus of the brain (Gundacker, et al; 2021)
• Elevated maternal blood Pb (lead) levels are associated with decreased DNA methylation of the fetus Pilsner et al. (2009),(Wu, et al; 2017)
• Pb (lead) toxicity adversely effects an important neurotrophic molecule, BDNF (brain derived neurotrophic factor). Reduced BDNF is thought to be strongly etiological in developmental delays (Gundacker, et al; 2021).
• Low levels of Pb exposure has been shown to inhibit neural cell adhesion molecule, which impairs neurite growth in utero (Hu, et al; 2008)

Pb (lead) Protection: Calcium, Selenium, NAC, Chlorella, Curcumin

• Pb (lead) can displace and interfere with nutrient minerals, calcium, magnesium and iron (Rahman, et al; 2019)
• Lactating mothers with a high Pb (lead) burden (n=617) were assigned either 1,200mg of calcium daily or placebo for 6 months. The calcium supplemented group experienced a 15-20% reduction in blood Pb levels (Hernandez-Avila, et al; 2003). Diets deficient in calcium can result in the increased absorption of Pb (lead), by means of up-regulation of 1,25 dihydroxyVitaminD and the associated Ca2 protein, both of which can take up Pb for transport (Rahman, et al; 2019)
• An experimental animal study found melatonin counters the toxic effects of Pb on developing rat brain, including restoration of glutathione and SOD, while improving Pb-induced histological damage to Pirkinje cells (Bazrgar, et al; 2015)
• Few human studies evaluating the effects and mechanisms of selenium on Pb toxicity have been done to date. However, several preclinical studies in rodent, chicken and in vitro models have been done, which show the importance of selenium and selenoproteins in the protection against Pb toxicity. For example, Pb toxicity induces mitochondrial dysfunction in the kidney of the chicken. This toxic effect is reduced with selenium supplementation (Jin et al., 2017).
• Curcumin and Nanocurcumin have shown the ability to detoxify Pb (Pal, et al; 2015)
• The fresh water algae chlorella is known to facilitate Pb excretion (Dhandhayuthapani, 2022)
• NAC (n-acetyl cysteine) is a precursor to the antioxidant glutathione. NAC has had mixed effects on preeclampsia. In an Egyptian study involving 115 preeclamptic women (compared to 25 non-eclamptic pregnant women), significant associations were found with preeclampsia, blood Pb levels as well as proteinuria. NAC at a dosage of 400mg daily was initiated for greater than 1 month. Sequential follow-up revealed significant reductions in both systolic and diastolic blood pressure, significant reductions in Pb levels, as well as significant reductions in proteinuria (Motawei, et al; 2018). While other preeclampsia research found no obvious benefit to NAC by itself, it should be pointed out that no study has yet to investigate the combination of synergistic nutrients for Pb detoxification. From a clinical point of view, if Pb toxicity has been identified, the combined use of nutrients and antioxidants should be considered for greatest effect: NAC, Calcium, Melatonin, Magnesium, Selenium.

Mercury: Preeclampsia & Developmental Toxicity

• Mercury is a developmental neurotoxin
• Methylmercury crosses the placental barrier and accumulates more in the fetus than in the mother (Rahimzadeh, et al; 2014)
• Elevated blood mercury levels are associated with both moderate to severe preeclampsia, and higher mercury levels are associated with lower birth weight (Wang, et al; 2022). Importantly, low birth weight is associated with several adverse developmental outcomes
• Fetuses and neonates are more susceptible to the toxic effects of mercury, due to premature cysteine conjugation and lower circulating levels of albumin (Dorea, 2015)
• Selenium is necessary as an antioxidant cofactor in mercury detoxification, via glutathione peroxidase, and other endogenous antioxidant systems
• The Fresh water algae, chlorella pyrenoidosa has been studied in pregnant mice to significantly reduce the transfer of methylmercury from mother to fetus (Uchikawa, et al; 2011). Of note, additional studies in pregnant women have found this same form of chlorella able to reduce dioxin transfer in breast milk, while beneficially raising IgA levels (Nakano, et al; 2007)
• Melatonin reduces the toxic effects of toxic elements, including mercury (Sener, et al; 2003)

Cadmium & Preeclampsia

Cadmium is a considerable developmental toxic metal. Analysis of 1,274 pregnant women in the U.S. were screened for a variety of metals and minerals. 9% of these women developed preeclampsia. This cohort identified lower manganese levels or higher cadmium levels as being a significant risk factor for preeclampsia (Liu, Zhang, et al; 2019). How cadmium influences preeclampsia and pregnancy:

• Higher cadmium levels are associated with lower birth weight (Wang, et al; 2018)
• Cadmium is toxic to the endothelium (Prozialek, et al; 2006)
• Cadmium increases the stress response in the placenta, as evidenced by increased glucocorticoids (Wang, et al; 2014)
• Cadmium adversely affects thyroid receptor function, and this effect has been observed to adversely alter blood vessel formation in the placenta (Liu, et al; 2022)
• Cadmium adversely affects the immune system, and has been shown to generate autoimmune angiotensin II type 1-receptor-agonistic autoantibodies (AT1-AA), and activation of complement C5 and C5a. This mechanism has been identified as a molecular pathway involved in preeclampsia (Zhang, et al; 2016)
• Cadmium disrupts DNA synthesis, and induces abnormal expression of miRNA’s and TGFß signaling (Brooks, Martin, et al; 2016)
• Cadmium increases the inflammatory cytokine, IL-6, which is associated with preeclampsia and endothelial dysfunction (Panigua, et al; 2019)
• Cadmium disrupts HIF1a and TGFß pathways in maturing trophoblast cells (Adebambo, et al; 2018)
• Cadmium toxicity in the umbilicus is associated with poor developmental outcomes after birth (Chandravanshi, et al; 2021)

Zinc, NAC & Selenium Are Critical to Prevent Toxic Effects of Cadmium

• Zinc sufficiency is necessary for the function of metallothionein, an antioxidant capable of binding 7 atoms of cadmium
• Zinc is critical to prevent or reverse endothelial cell damage induced by cadmium (Kaji, et al; 1993)
• Zinc and Selenium restore organ histology following cadmium poisoning (Jihen, et al; 2008)
• Zinc supplementation restores glutathione peroxidase following cadmium toxicity (Sidorczuk, et al; 2012)
• NAC (n-acetyl cysteine) protects kidneys from cadmium toxicity, partly by increasing glutathione and SOD and reducing lipid peroxides (Kaplan, et al; 2007)
• Co-administration of NAC, Taurine and Melatonin have shown beneficial effects at preventing cadmium-induced brain toxicity in an experimental study (Gulyasar, et al; 2010)

Albumin, Free Fatty Acids, Oxidative Stress & Preeclampsia

Free fatty acids (FFA’s) serve as primary cellular metabolic fuel, consumed in the mitochondria, and transported in blood primarily by serum albumin. High levels of circulating FFA’s are found in preeclampsia, and this is likely a product of the increased oxidative stress condition. When an excess of FFA’s is found in the blood, this causes an acidic shift of the serum albumin transport protein (Vigne, et al; 1997). An increase in albumin bound FFA’s can lead to major pro-thrombotic conditions, as well increases in the amount of oxidized albumin, leading to severe oxidative stress.

Albumin is a negative acute phase protein, it may decrease in oxidative stress and inflammatory conditions. Importantly, albumin’s free cysteine, Cys34 is critical in this protein’s thiol functions. The increased oxidation of albumin impairs its ability to act in metal scavenging and antioxidant functions.

To some extent, increasing dietary protein and certain amino acids can increase albumin levels (tryptophan, BCAA’s). The degree of hypoalbuminemia has been shown to relate to the degree of preeclampsia (Ghazali, et al). High levels of Ischemia Modified Albumin (IMA) have been shown to correlate with preeclampsia (Ustun, et al; 2010). When this form of albumin appears, it is linked to ischemia risk, and is caused by elevations in free fatty acids, and is characterized by low binding affinities for Zinc and Cobalt.

Chlorella As A Special Mention For Pregnancy

Chlorella in pregnancy has not yet been studied in preeclampsia. However, it lowers toxic elements that are associated with pregnancy (Pb, Hg), reduces methylmercury transfer to fetus (mouse study: Uchikawa, et al; 2011), reduces proteinuria and edema in pregnant women, which are both common findings in preeclampsia (Nakano, et al; 2010). Chlorella reduces signs of pregnancy induced hypertension (PIH), and is associated with improved hematological parameters when supplemented during pregnancy (Nakano, et al; 2010). Chlorella contains naturally occurring antioxidants, including beta carotene, and lutein, both of which have been shown to be low in preeclampsia (Cohen, et al; 2015), (Cohen, et al; 2015), as well as Vitamin E, which has also been found low in preeclampsia (Mikhail, et al; 1994), (Shaban, et al; 2004).

Moreover, chlorella pyrenoidosa lowers dioxins in breast milk by around 30% and has been shown to beneficially raise maternal IgA levels in milk (Nakano, et al; 2007). Chlorella reduces lipid peroxide levels in humans with NAFLD (Mameghani, et al 2013). Some women with preeclampsia have NAFLD.

There are 2 forms of chlorella. Both are similar: chlorella vulgaris and chlorella pyrenoidosa. Both bind toxic substances, and contain very similar nutritional properties. According to most research, chlorella pyrenoidosa has been the form used to reduce dioxin, methylmercury transfer in utero, and to raise IgA levels. Importantly, the form of chlorella used should be tested to have very low toxic contaminants. This is because it is an algae, and can bioaccumulate many toxic compounds that are present in the growing medium.

Genetic Risk Factors for Preeclampsia

Genetics can play a role in the predisposition to preeclampsia. The following genes are associated in some studies with preeclampsia risk. The Metabolic Healing Nutrigenomics report enables both healthcare practitioners and consumers to evaluate their genetics through the use of their raw data file from 23andme or AncestryDNA.

ACE – Angiotensin converting enzyme is centrally involved in blood pressure regulation. Genetic polymorphisms in ACE (rs4343) are associated with preeclampsia (Do, et al; 2018)

AGT – Angiotensinogen is involved in blood pressure regulation. The AGT polymorphisms (rs699 and rs4762) are associated with different forms of hypertension, including preeclampsia (Procopciuc, et al; 2011)

MTHFR C677T – Meta analysis research investigating the relationship between this notorious genetic polymorphism found a relationship with preeclampsia, especially in Asians and caucasians (Wu, et al; 2015). The MTHFR polymorphism impairs the utilization of folate, and is associated with higher levels of homocysteine, which can impair endothelial function and lead to hypertension (Wu, et al; 2014).

Leiden Factor 5 (LF5) – Is centrally involved in blood clotting. The polymorphism of this gene is associated with preeclampsia, and severe preeclampsia, according to meta analysis (Wang, et al; 2015)

Prothrombin F2 – Is centrally involved in blood clotting. This polymorphism is strongly associated with preeclampsia, according to meta analysis research (Wang, et al; 2015)

ApoE – In some populations, the ApoE 2 genotype is inversely associated with preeclampsia risk (Ahmadi, et al; 2012). ApoE affects blood lipid concentrations, its metabolism, influences Alzheimer’s risk and may influence the toxicity and detoxification capacities of heavy metals.