Nutrients in Food and their bodily purpose XXIV (Pregnancy: Nature vs Nurture vs Nutrition)

By on March 23rd, 2022 in Articles, Nutrients

Introduction

The general consensus was that neonates were basically oblivious to their environment throughout pregnancy and the first year of life, but the groundbreaking book ‘The secret life of the unborn child’ by Thomas Verny MD published in 1981, changed all that.  How wrong we all were.

Life does not begin at birth, Life begins at conception, or at least at completion of the first tremester when the complete unborn child is built. 

Within the first trimester is the time that ‘the baby is under construction’, which are the words of Dr Verny, and by the end of the second trimester the unborn is a sensitive, feeling, aware, remembering small human.  During the second and third trimesters, nature focuses on growth of the fully constructed baby.

In 1983 Dr Verny founded an organisation known as APPPAH – Association for Prenatal and Perinatal Psychology and Health.

The first trimester is absolutely, unequivocally, crucial in terms of the availability of adequate nutrients for both mother and baby. Ideally, at least 1 year before conception, both mother and father should be taking all 90 essential nutrients to ensure a healthy pregnancy and a healthy newborn.

You might argue that most pregnancies produce healthy babies without taking any nutrients except the ones that conventional medicine are aware of such as folate acid. The only reason now that they consider folate acid as being important is because Dr Joel Wallach had to sue the FDA eight times before they recognised the importance of folate acid for the mother to be.

Baby under construction

As I mentioned in the introduction, the first 3 months is where the new human is being developed when Mum, through the placenta link, provides the building materials ( nutrients ), while in the uterus the fetus is continually downloading genetic information required for the on-going construction.  

It is a most fundamental instinct to survive in all living organisms, but if there is choice to be made between mother and neonate in terms of health, nature will prioritize the well being of the neonate since reproduction is profoundly important in nature.

If nutrients are not in abundance, the body will extract the nutrients from the mother wherever it can find them, which are essential for the unborn child’s needs for survival.  In some circumstances, the body simply runs out of certain nutrients required for the construction process of the baby and malformation or birth defects occurs.

Dr Wallach likens the baby under construction to a car assembly plant, where you can imagine, that when the partially assembled car arrives at the light assembly area and the engineers are away having a work brake, when the engineers return several cars have already passed without light fixtures.  Quality control will flag the problem at the end of the assembly line and correct it, or reject the assembly altogether. Within natures assembly line, interruption and/or interference in the construction process is far more complicated, and cannot be corrected once the first trimester is completed.

The March of Dimes Association, a non profit US organization that was founded by President Roosevelt in 1938, was originally set up as the National foundation for infantile paralysis, to combat polio, the prevention of birth defects, and infant mortality.  Roosevelt had a personal vested interest in these matters since he contracted a paralytic illness in 1921 when he was 39, whose doctor’s probably misdiagnosed as Polio. His condition is thought to have been Guillain Barre syndrome, an autoimmune condition, where the immune system attacks and damages the peripheral nervous system, a condition that is curable by dietary nutrition.

Back to Basics

We all inherit 46 chromosomes, 23 from mother and 23 from father.  The 23 chromosomes are made up of 1-22, called autosomes ( a non sex chromosome) and chromosome 23 are sex chromosomes known as XY on the male side and XX on the female side. The Y chromosome on the male side is more than 50% smaller than the X chromosome. The Y chromosome carries only 40-50 genes, and 50% of these are male specific, required for reproductive purposes.

An example of a male Y chromosome gene is the SRY gene that expresses proteins that masculinises the embryo, which gets deleted if the embryo develops through the default female pathway.

The X chromosomes are larger, typically supporting around 1300 genes in both male and female. According to geneticist Mary Lyon (1925-2014), although the female human species contain two X Chromosomes, one is irreversibly inactivated for a lifetime, and X chromosome cellular expression can derive either from the father or the mother, randomly. Generally, it is a 50-50 split between both parents from their respective X chromosomes. Regardless of this phenomena, epigenetic mechanisms still apply, subject to environmental stimuli which includes toxicity, nutrient deficiency and nurturing.  

The X Chromosome gene expression also applies to genetic imprinting ( those 100 or so genes that escape gene reprogramming  (total gene reset for the new life) of the foetus. There are still unanswered questions, however. Is the body’s choice on which X chromosome is inactivated, random or is there intelligence involved, and why have two X chromosomes when one is always shut down permanently. Why does the body build an additional chromosome 21 making 3 chromosomes in a trisomy format that is evident in the birth defect ‘ Down’s Syndrome’. Why does the body build polyps or ovarian cysts because of iodine deficiency or estrogen dominance. These are areas that need to be researched, not developing epigenetic cancer drugs which will never work even if they spent the next 100 years doing further research.

Natures assembly line I

Despite 80 years or so into birth defects research, 70%, according to the conventional medical world are unknown.  They reference one birth defect called Fragile X syndrome, which the scientific community all state that it is s genetic defect in a gene that call the FMR ( Fragile X Mental Retardation ), because it is transcriptionally silenced and is unable to make a protein. Statistics report 1 in 7000 males and 1 in 11,000 females. As a result, children of around 3-4 years old are suddenly affected by intellectual deficits in the form of learning impairments or cognitive disability with autistic behavior, such as aggression and social anxiety, and in some cases epilepsy and seizures.

According to most scientific papers it is genetics and environmental stimuli that cause Fragile X syndrome , however, as a result of preconceptual/prenatal screening for Fragile X syndrome amongst 40,000 women, ( Berkenstadt et al 2007) no difference in carrier frequency was seen between women with and without family history of mental retardation and developmental abnormalities which questions the validity of a Autosomal Recessive Gene Theory (genetic transmission).   

Reading the scientific literature in terms of epilepsy, they describe it as a generic term encompassing multiple syndromes, with distinct symptoms, etiology, prognosis and treatments, again, travelling the road of genetic anomalies affecting GABA receptor plasticity ( Gamma Aminobutyric Acid, an inhibitory neurotransmitter used within the central nervous system) and  E/I balance (Excitatory/Inhibitory). Postulating that an altered E/I Balance is the underlying mechanism of epileptogenesis and seizure generation, resulting in a disturbance in homeostatic plasticity. This all sounds very scientific and it is probably what is going on, but what causes it ?…TOXICITY.   If you have witnessed an epilepsy patient experiencing an epileptic seizure, it is quite an unpleasant. But why is this epileptic seizure occurring ?…The brain is attempting to electrically burn out the toxins that have reached overload levels..like a ‘Reset switch’.

Toxicity

I would also surmise that it may well be the same reason that during the first trimester of a pregnancy a toxic load suffered by the fetus could result in causing the Fragile X syndrome to trigger, altering the normal histone acetylation ( gene is readable) to a methylated state ( gene is not accessible and silenced).   

Developmental anomalies which are associated with this condition include an elongated face, a prominent forehead, protruding jaw and large ears, and connective tissue anomalies such as hyperextensible finger and thumb, joints, hand calluses, velvet like skin, flat feet and mitral valve prolapse ( leaflets of the mitral valve bulge into the heart’s left atrium like a parachute when the heart is contracting).

All of these anomalies could arise from toxic interference on other chromosomes other than X where some of the genes responsible for facial development are known to reside e.g  Chromosome 3 position 3q25.33 is involved in Centroid size, face height and width, chromosome 1 position 1q31,3 and chromosome 7 position 7q21.3 is involved with chin prominence. So where does this toxicity come from ?.  

Environments in the home, at work, and lifestyle can all contribute adversely to the developing fetus by smoke, alcohol, drugs, allergens, paint fumes, solvents (e.g Naphthalene a volatile polycyclic aromatic hydrocarbon), pesticides, heavy metals, cleaning products, beauty and body products.

Evidence suggests that even postnatally, during breastfeeding, these products can still influence the levels of toxicity within the neonate. These Endocrine disruptor chemicals (EDC)  can also interfere with a women’s reproductive health as stated in an NCBI report by Caserta D et al 2013 stating that once analysis samples were taken of EDC serum levels and nuclear receptor expressions*, the % of patients with detectable bisphenol A (BPA) was significantly higher in the infertile patients

*Nuclear receptors are cellular proteins that sense steroid and thyroid hormones that in conjunction with other proteins regulate specific gene expression that control the development, homeostasis and metabolism of the organism. The mechanism of action of Nuclear receptors only occurs when bound with a lipophilic (fat based) ligands which could be endogenous hormones, vitamins A and D and xenobiotic endocrine disruptors

Wickstrom R in 2007 stated that prenatal exposure to tobacco smoke is a major risk factor for the newborn, even mortality risk for the neonate.  The toxic chemicals interferes with normal neurotransmitter function, potentially invoking neurodevelopmental abnormalities. In a study conducted in 2009 by CP Klingenberg, they suggested that prenatal alcohol exposure alters facial symmetry. By analyzing 17 facial ‘landmarks’ using geometric morphometrics, Klingenberg and colleagues were able to show significant directional asymmetry of facial shape in terms of a shift of ‘landmarks’ to the right and a displacement around the eyes to the left due to fetal alcohol exposure. The relevance of these studies demonstrate that air borne inhaled toxins can affect epigenetic gene expression.

Summing up

Since other chromosomes are involved with Fragile X syndrome, other than the X chromosome and the FMR gene, it does not make sense that the lack of 1 protein can cause this flurry of physiological/cognitive problems such as  intellectual deficits in the form of learning impairments or cognitive disability with autistic behavior , epilepsy and seizures, and developmental anomalies. These developmental anomalies are not a result of dysfunction on the X chromosome since other chromosomes are affected as well.  Why does this birth defect only show itself after 3 years or so after the child is born, It is feasible that the physical deficits would be noticed within the first year. Rather than a genetic flaw, it is more likely that toxicity and even nutrient deficiency as well is the major causative reason..

Duchenne muscular dystrophy (DMD)

Let us explore how conventional allopathic medicine describe this condition. According to the Muscular dystrophy association DMD is a GENETIC disorder characterized by progressive muscular degeneration and weakness and is one of 9 types of muscular dystrophy.

In the early stages of the condition it is the shoulder, upper arm, hips and thigh muscles that are affected, causing difficulty in rising from the floor, climbing stairs, maintaining balance and raising the arms. By the early teens the heart and respiratory muscles are affected.

A milder form of DMD is called Becker Muscular dystrophy. The medical establishment have had 150 years or so to figure out what really causes this condition ever since Guillaume Duchenne a French neurologist first described it, and then in 1986 it was decided that it was a genetic defect….surprise surprise..if we can’t figure out what is causing it, then either/and call it a syndrome caused by a mutant gene.   The ‘defective gene’ was tracked down to a gene located on the X chromosome (position Xp21) that expresses the building of a protein called Dystrophin.

Dystrophin is a rod shaped cytoplasmic protein and part of a protein complex that acts as a shock absorber to muscle fibres when it connects the cytoskeleton ( the outer skin infrastructure of a cell that provides its shape and mechanical resistance to deformation) of a muscle fiber to the surrounding extracellular matrix through to the cellular membrane. It is one of the longest genes ( 2.3 megabases ) that takes 16 hours to transcribe the mRNA of 14 kilobases.

Analysis

According to Wikipedia Keshan’s disease is a form of cardiomyopathy where parts of the heart muscle thicken and fibrosis occurs. The celebrated Dr Joel Wallace and his wife Dr Ma Lan performed 1700 autopsies on children in the Chinese province of Keshan who had died from Hypertrophic cardiomyopathy.  Many of these children had cystic fibrosis as well.

Dr Wallace is also an experienced veterinarian, explains that in animals such as pigs can perish from a disease called ‘Mulberry heart disease’, in sheep ‘Stiff lambs disease’, and in calves ‘White muscle disease’, but all these animals diseases are a form of cardiomyopathy which can lead to a heart attack.

We have already mentioned muscular dystrophy of which they are 9 variations including DMD and the milder form Becker Muscular dystrophy.  

Lou Gehrig was a famous baseball player for the NY Yankees between 1923-1939, and died at 38 in 1941. He retired from baseball when he was 36 because of a neuromuscular problem called Amyotrophic Lateral Sclerosis (ALS) diagnosed by the Mayo clinic with a grim prognosis that his life expectancy was less than 3 years, since the disease causes increasing paralysis and difficulty in swallowing and talking and the motor function of the central nervous system ultimately gets destroyed.

ALS is a generic way the body breaks down, caused by inflammation and fibrosis ( the thickening and scarring of connective tissue ). arthritis, multiple sclerosis, Parkinsons, Bell’s Palsy or whatever ‘flavor’ of degenerative disease. Sclerosis simply means the hardening of nerve fibres which is the same thing as fibrosis.

This hardening of the nerve fibres is the body’s protective response to inflammation….I repeat THIS HARDENING OF CONNECTIVE TISSUE IS THE BODY’S PROTECTIVE RESPONSE TO INFLAMMATION.  In all of these conditions there are common denominators in the etiology ( cause ) and pathology ( diagnosis using body fluids) of visceral lesions ( viscera meaning the internal organs of the body) leading to all of these health issues and that is nutrient deficiency with a specific emphasis on Selenium deficiency.  Selenium is crucial for the body as is all of the required 90 essential nutrients.

The Importance of Selenium

  1. The turnover of cells within the human organism takes up to 7 years (the white blood cells that line the small and large intestines to assimilate nutrients and attack invaders) so exposure to radiation, toxic chemicals, starvation etc can deplete nutrients (especially selenium that has cancer prevention properties). Selenium builds amino acids allowing the body to make 20 million new cells each day. In essence if the body is deficient in selenium for example anytime during that 7 year replacement cycle, cancer could potentially ignite in the body.
  2. Selenomethionine is a naturally occurring amino acid found in brazil nuts and is used in all DNA to messenger RNA starting points referred to as the initiation codons.  To have enough dietary selenium cuts the risk in DNA damage Even the National institute of health suggests that dietary selenium diminishes cellular changes that lead to prostate cancer  (although prostate cancer is generally caused by a hormonal imbalance, specifically excess estrogen )
  3. The tumor suppressing protein P53 found on chromosome 17 is a selenium based gene that suppresses the formation of tumors (if you are not familiar with basic cell structure we have 46 chromosomes in each cell -these chromosomes are inherited by our parents 23 from each and on each chromosome there are approximately 1000 or so genes that express the functioning of the body). In the bodies daily production of some 20-25 million cells the body does make mistakes but there are mechanisms to correct them, however if there is not enough P53 operative these mistakes are not corrected and can potentially proliferate in a cancer like fashion.
  4. Selenium is essential for various physiological levels such as the production of Glutathione peroxidase a family of enzyme that protects us from oxidative damage by preventing the accumulation of hydrogen peroxide and lipid hydroperoxides which are oxidized fatty deposits (seen on the skin and are called liver spots which is a misnomer since the medical term is Lipofuscin. These oxygen radicals can attack anything, proteins, DNA etc which is why we need to consume enough ( not excessive amounts) antioxidants to assist the body in reducing this problem
  5. As we know today there are 25 selenoenzymes (selenium triggered) including Glutathione peroxidase as discussed above. Another enzyme is thioredoxin reductase that assist in the electron transfer within the cell but can become oxidized and cause havoc within the cell, so with the help of selenium the oxidized state is minimized.  In fact this enzyme is essential for cell growth and survival.
  6. The eye is normally rich in selenium so deficiency can affect vision
  7. The manufacture of dentine for teeth is dependent on selenium
  8. The thyroid gland that controls our metabolism requires iodine from our food to make 2 hormones Triiodothyronine (known as T3 ) and Thyroxine (know as T4); approximately 20% of T3 is made and is the active form and T4 80% the storage form and the body converts T4 to T3 as required since T3 is 4 times stronger than T4.  The thyroid gland is controlled by the pituitary gland and the pituitary gland is controlled by the Hypothalamus. This conversion needs the presence of selenium. It is important to mention that if your iodine is low then selenium supplementation will only exacerbate the problem and vice versa so it is important that you have adequate iodine levels. ( A whole food supplement containing kelp every day would be advisable ). It is important to note that thyroid problems can emanate from the thyroid itself, the pituitary gland or the hypothalamus and doctors will check the T4 and/or the T3 levels in the blood and may prescribe drugs which may not help if the problem is coming from somewhere else..they are not going to check your selenium levels in your blood so it is best just to put the fuel that your body needs for optimum function and in the case of the thyroid appropriate levels of iodine and selenium.
  9. The heart in order for its contractile function to work efficiently it requires selenium (cardiomyopathy and Keshan’s disease as described above are generally caused by selenium deficiency).  Additionally, there exists in the heart approx 7 strains of cardiophilia viruses which are normally dormant and benign but under certain circumstances including selenium deficiency they can be activated, become virulent and can cause major problems.
  10. From the above you can appreciate that selenium is a natural antiviral agent and has been used to help patients suffering from the AIDS virus.
  11. The liver is normally rich in selenium and if deficient can cause necrosis in some cases.
  12. A condition known as lymphedema which is swelling of the lymphatic system caused by cancer treatment for breast cancer or the removal of lymph nodes.  This is a horrible condition where women can very easily get infections of the lymph system since the system contains a blockage that by conventional medicine can’t alleviate, and women are subjected to long term antibiotics to prevent infection.  Selenium supplementation can help and in some cases reverse the condition quite rapidly.
  13. Selenium is used to treat pancreatitis and septicemia.
  14. Cystic Fibrosis is a selenium deficiency condition as proven by Joel Wallach in 1977

During pregnancy, a selenium deficiency can result in miscarriage, low birth weight, infant mortality, cystic fibrosis, muscular dystrophy and liver cirrhosis.

In the growing child, selenium deficiency can result in crib death ( Sudden infant death syndrome or SIDS), growth retardation, muscular dystrophy including DMD and Becker’s version, Scoliosis ( spine is malformed ), Cardiomyopathy ( muscular dystrophy of the heart muscle- Keshan’s disease), Adrenoleukodystrophy ( brain disorder caused by damage of the myelin protective sheath for neurons).  

Interestingly, Wikipedia mentions Adrenoleukodystrophy linkages to the X chromosome as in DMD. We should be aware that selenium is involved in structural development in the body and is used as a scaffolding piece to maintain integrity of the DNA double helix and it and other minerals are used in the nucleotide rungs of the DNA ‘ladder’ structure.

We also know that nutrients play an essential role in epigenetic switching of gene expression, so it is quite feasible that anomalies observed in particular gene silencing (extraordinary methylation) is also caused by nutrient deficiency. Note that Selenium deficiency is linked to cancer caused by a dysfunction of the selenium based tumor suppressor gene P53 on chromosome 17, and initiation codon malfunction in DNA and RNA.

Conclusions

In this article we have focused more on the physiological aspects that can affect the unborn child, the neonate and the young child.  

Dr Wallach, having conducted many autopsies on children who perished from Keshan’s disease, 90% of which can lead to heart cardiomyopathy, various forms of muscular dystrophy and fibrosis are in fact not due to genetic transmission, but a simple nutrient deficiency, as proven in some instances by Dr Wallach.

In the next article we will highlight other potential birth defects and the crucial nurturing of the child during pregnancy. One could consider nurturing as a psychological nutrient.

I have chosen a short paragraph from Dr Thomas Verny’s  wonderful, way ahead of its time, monograph ‘The secret world of the unborn child’:

‘Nature has gone to great lengths to design a bonding system that fits the newborn’s needs in very precise ways.  She not only dramatically alters the behaviour of an adult woman who has already lived 20-25 years or more, she alters it in exactly the ways and for the length of time that suits the baby best. To thrive emotionally,Intellectually and physically an infant needs the special kind of loving contact and care that only bonding fully develops in his mother’.

Check out other Articles in this series:

Nutrients in Food and their bodily purpose I (Phenols)

Nutrients in Food and their bodily purpose II (Lignans, Triterpenes, Phytosterols, Carotenoids & Fats)

Nutrients in Food and their bodily purpose III (Phenolic acids, sulphur, sulphides,sulphoxides )

Nutrients in Food and their bodily purpose IV (Glucosinolates, Sulforaphane, Indole-3-Carbinol)

Nutrients in Food and their bodily purpose V (Lipid distribution, absorbed fats, Criciferous Veg)

Nutrients in Food and their bodily purpose VI (Nutrients required for Liver Detox)

Nutrients in Food and their bodily purpose VII (Seeds & the Omega Fatty Acids)

Nutrients in Food and their bodily purpose VIII (Nutrients required for cellular energy production)

Nutrients in Food and their bodily purpose IX (Water I Properties and Body fluids)

Nutrients in Food and their bodily purpose X (Water II Cellular Hydration)

Nutrients in Food and their bodily purpose XI (Water III Fluid filtration, reabsorption, excretion)

Nutrients in Food and their bodily purpose XII (Water IV Blood pressure, Blood volume regulation)

Nutrients in Food and their bodily purpose XIII (Water V Body Fluid Dysfunction

Nutrients in Food and their bodily purpose XIV (Dental Nutrients)

Nutrients in Food and their bodily purpose XV (Nutrients involved in Methylation I)

Nutrients in Food and their bodily purpose XVI (Nutrients involved in Methylation II)

Nutrients in Food and their bodily purpose XVII (Nutrients involved in Methylation III)

Nutrients in Food and their bodily purpose XVIII (Nutrients involved in Methylation IV)

Nutrients in Food and their bodily purpose XIX (Methylation V and the Microbiota I)

Nutrients in Food and their bodily purpose XX (Methylation VI and the Microbiota II)

Nutrients in Food and their bodily purpose XXI (Superfoods: Wheatgrass)

Nutrients in Food and their bodily purpose XXII (Superfoods: Adaptogens)

Nutrients in Food and their bodily purpose XXIII (A look into our nutritional past Sir Robert McCarrison)

References/Acknowledgments :

  1. Epilepsy, E/I Balance and GABAa Receptor plasticity Jean Marc Fritschy 2008 NCBI PubMed
  2. Diseases of Faulty nutrition Seleneriverpress
  3. Nuclearreceptors,Chromosome3,Dystrophin,Cytoskeleton, Adrenoleukodystrophy, Keshan’s disease  Wikipedia,
  4. Mitral valve prolapse Mayo Clinic
  5. Genetic testing for FMR1 Mutations including Fragile X Syndrome  Blue cross/Blue shield of north carolina Corporate medical policy
  6. Identifying the causes of birth defects March of Dimes
  7. Of Men and Mice : Modelling the fragile X syndrome Regina Dahlhaus 2018 NCBI PubMed
  8. The influence of endocrine disruptors in a selected population of infertile women  Caserta D et al 2013 NCBI PubMed
  9. Effects of nicotine during pregnancy: human and experimental evidence Wickstrom R 2007 NCBI PubMed
  10. Facial genetics Stephen Richmond et al 2018 NCBI Pubmed
  11. 5 face shaping genes identified Trevor Stokes Live Sciences 2012
  12. The FMR1 gene and Fragile X-Associated Tremor/Ataxia syndrome Brouwer et al 2009 NCBI PubMed
  13. Preconceptional and prenatal screening for fragile X syndrome: experience with 40,000 tests Berkenstadt et al 2007 NCBI PubMed
  14. Prenatal alcohol exposure alters the patterns of facial asymmetry CP Klingenberg et al 2012 NCBI PubMed
  15. Rare earths.Forbidden cures Dr Joel Wallach & Dr Ma Lan book 1994-2011
  16. Epigenetics -The death of the genetic theory of disease transmission Dr Joel Wallach, Dr Ma Lan, Dr Gerhard Schrauzer book 2014
  17. The 90 essential nutrients – Sodium, Selenium, Molybdenum, Sulphur extremehealthacademy.com – Eric Malouin
  18. The secret life of the unborn child book 1981 Thomas Verny MD

Author: Eric Malouin