Climbing Everest and Its Effect on Everything

Mount Everest in Utero: How Fetal Oxygen, Maternal Stress and Birth Shape the Face, Airway and Brain

Insights from the Myofocus Education Seminar

I recently spent four days helping teach a seminar with the Myofocus Education team, and several ideas from that week are still turning over in my mind. This month's blog pulls a few of them together. It ranges across maternal health, child development and adult airway health, and I hope it prompts you to think differently about how the brain and airway are shaped long before a child takes their first breath.

Oral Myotherapy, Tongue Tie and the Developing Airway

The seminar focused on oral myotherapy and tongue tie, which gave me the chance to teach on my favourite territory: mouth breathing, and the way primitive reflexes influence craniofacial development and long-term health. Our final guest lecturer on day four was Dr. Jeevanan Jahendran, an ear, nose and throat specialist, a genuinely original thinker and an all-round great human.

Mouth Breathing and Retained Primitive Reflexes

Primitive reflexes such as the Moro reflex, the Asymmetric Tonic Neck Reflex (ATNR) and the Tonic Labyrinthine Reflex (TLR) are essential for survival and for the earliest stages of development. Problems arise when they persist past the age at which they should integrate. Retained reflexes can disrupt craniofacial growth and set up lasting health issues.

Mouth breathing is a clear example. It changes the growth pattern of the face and can contribute to long face syndrome, dental malocclusion and a range of airway-related problems. Addressing retained reflexes, including through oral myotherapy, can therefore have far-reaching benefits for overall development and health.

Dr. Jahendran on the Aerodigestive Tract

Dr. Jahendran's lecture on the aerodigestive tract was a highlight. He traced the close relationship between the respiratory and digestive systems and showed how dysfunction in one drives dysfunction in the other. His central message was that breathing technique and respiratory health directly affect digestion and general wellbeing, and that these systems need to be assessed together, not in isolation.

Fetal Oxygen Supply: "Mount Everest in Utero"

As much as I enjoyed the aerodigestive material, what really lit me up was being introduced to a 1954 paper by Nicholson J. Eastman MD titled Mount Everest in Utero. It is a phenomenal piece of work that has largely disappeared down the memory hole. A great deal of mid-20th-century physiology has been forgotten, and much of it was never taught in our degrees. It certainly wasn't in mine.

The Fetus Lives in a Low-Oxygen World

The partial pressure of oxygen delivered across the placenta is dramatically lower than the roughly 100 mmHg leaving the heart. At around 39–40 mmHg, the oxygen pressure in the umbilical cord is equivalent to standing at about 33,000 feet, roughly a quarter of a mile above the summit of Everest, an altitude at which an adult would die without supplemental oxygen.

So how does the fetus survive? It cannot increase oxygen delivery to itself, so it regulates oxygen consumption at the tissue level instead. As another paper put it, fetal arterial PO2 levels really are close to those on Everest, yet the fetus is well oxygenated for its needs.

The "Valley of the Shadow of Birth"

During birth itself, the fetus is exposed to a profound degree of hypoxia and, in the vast majority of cases, comes through it well. The insult is severe enough that perinatal physiologists have called the process the "Valley of the Shadow of Birth".

Two things can go wrong at this transition. A sudden further drop in oxygen (from trauma or poor breathing) causes hypoxic injury, while the abrupt exposure to high oxygen after birth, relative to the low-oxygen environment the baby has just left, produces hyperoxia. Both drive oxidative stress and free-radical damage, and oxidative stress biomarkers have been shown to correlate with clinical outcomes in the child.

Maternal Stress and Fetal Blood Supply

Now roll back to around five weeks of pregnancy and consider the mother's system in relation to fetal blood supply and primitive reflexes. When the mother's system perceives a threat, a survival response called the fear paralysis reflex activates and diverts blood away from the uterine region towards her own body. This temporarily lowers the oxygen supply to the developing fetus.

Occasionally, that's no problem. But imagine a chronically high-stress environment, or smoking. Excess adrenaline can inhibit fibroblast growth or push fibroblasts to differentiate into myofibroblasts, which produce strong contracture. That has real implications for tongue and oral fascial restriction.

Cortisol, WNT Signalling and Facial Development

Under chronic stress, excess cortisol suppresses the WNT signalling pathway, which I discuss in my book First Principles. WNT signalling is fundamental to bone and facial connective tissue development, and its suppression increases FGF23 production. Cortisol excess also drives high inflammation and type-3 immunity.

Hypoxia itself can be viewed as chronic stress for the fetus, and it has been shown to disrupt folate metabolism, creating or exposing defects in DHFR and MTHFR function. In a rat model of folate- and B12-deficient mothers, neonatal hypoxia raised homocysteine levels, mainly by reducing homocysteine trans-sulphuration in the developing animals on a methyl-deficient diet, potentially amplifying the well-documented harms of high homocysteine.

[Image: folate metabolism pathway — credit MDPI]

Defects in folate metabolism during the critical facial development window at 5–12 weeks cause a significant loss of cells expressing the genes essential for facial structure, including the WNTs and FGFs (fibroblast growth factors). This profoundly affects the shape and size of the developing face and leads to facial maldevelopment after birth, with consequences that persist through life.

The chain, then, looks like this: hypoxia alters facial growth, fascial fibroblast function and MTHFR/DHFR metabolism in the growing child, and all three contribute to tongue fascial restriction and maldevelopment of the cartilaginous structures of the face.

How Birth Method Affects the Newborn

What follows is not intended as judgement of anyone's birth choices. It's meant to raise questions about the direction our society is heading, as I did in First Principles.

Data from the Australian Institute of Health and Welfare shows a steady shift away from non-instrumental vaginal birth towards caesarean section over the past decade. In 2020:

• 50% of women had a non-instrumental vaginal birth (down from 56% in 2010)
• 7.4% had a vaginal birth assisted by vacuum (8.1% in 2010)
• 5.2% had a vaginal birth assisted by forceps (4.0% in 2010)
• 37% had a caesarean section (up from 32% in 2010)

Why the Hours of Labour Matter

The concern here is stress on the child and the possibility of altered oxygen supply at a critical juncture. Birth normally takes time, and that time allows the baby to adjust to an oxygen-rich world. Eastman observed that the fetus lives in a continuous state of cyanosis, so pronounced that it is obvious at any caesarean section and, if seen in a person after birth, would indicate someone gasping for air and close to death.

The activation of the Moro, ATNR, TLR and Galant reflexes during the hours of a natural vaginal delivery prepares the child for that high-oxygen environment. A sudden exit through a surgical opening skips that preparatory phase and reflex activation, and could be considered unrestrained hyperoxia, with the oxidative stress and inflammation to brain tissue discussed above.

Uterine Contractions and Oxytocin Induction

Before birth the fetus appears to thrive on its normally low oxygen supply. But variations in uterine contractility and placental behaviour can push that meagre supply even lower, and this the fetus can only tolerate for a few minutes. Eastman noted that an average contraction of around ninety seconds produces temporary fetal anoxia, visible as the characteristic slowing of the fetal heartbeat. If a contraction lasts five minutes, which can happen with injudicious use of oxytocic drugs during induction, the fetus is at well-known risk of dying from anoxia.

Synthetic Oxytocin and Neurodevelopmental Outcomes

Oxytocin induction appears to have increased in recent years. A 2021 study of Danish and Finnish children reported oxytocin use in 31% and 46% of deliveries respectively. The authors noted a correlation, not yet established as causation, between synthetic oxytocin in birth and both ADHD and autism spectrum disorder (ASD).

Another paper concluded that it is premature to say perinatal oxytocin increases neurodevelopmental risk. I have a couple of issues with that. First, the conclusion rests on classifying observational studies as low quality, despite pooled cohorts of more than 500,000 children for ADHD and 800,000 for ASD. Second, when you dig into the data, children exposed to oxytocin induction scored 0.45 of a standard deviation lower on receptive vocabulary (IQ) testing and 0.14 standard deviation units lower on problem-solving z-scores than unexposed children.

Other findings point the same way. One study showed increased problem behaviour after oxytocin-induced birth. A 2011 study found increased ADHD risk with Pitocin induction, though other groups did not replicate it. For ASD, multiple papers reported a relative risk above one, yet the authors judged heterogeneity between study groups too high to draw a conclusion or recommend any change to obstetric practice. Another group found more ADHD in induced children but attributed it entirely to families sharing similar diagnosis rates, as though ADHD were simply genetic. That has been stubbornly difficult to prove. There is no single gene for ADHD or ASD.

As the father of a child with ASD who was induced with synthetic oxytocin, I'll admit to a bias in the opposite direction from those researchers.

Anoxia at Birth: What Eastman's Guinea Pigs Showed

What if the neurodevelopmental changes trace back to where Eastman started in 1954: that oxytocin can cause anoxia, which at the time was mainly linked to cerebral palsy? He described experiments in which guinea pigs were asphyxiated at birth to simulate infants born anoxic. Many showed obvious brain damage and neurological abnormalities as neonates. Most of those visible defects resolved and the animals appeared normal, yet permanent impairment of learning ability remained. As adults they learned more slowly and forgot more quickly than controls. The highest brain centres were the most permanently affected, a pattern that closely resembles what we see in ASD.

Dose, Duration and Reperfusion

Perhaps the dose and duration of synthetic oxytocin exposure is what matters. A high dose over a longer period may push the child further into anoxia and generate greater oxidative stress in vulnerable neuronal pools. A lower dose may instead drive acidification, alter methylation and fibroblast differentiation, and change connective tissue development in the newborn. And if an anoxic child with low Apgar scores is then reperfused with high-dose oxygen shortly after birth, that too has a documented history of neuronal injury.

Building a Mother-Flourishing, Child-Flourishing Environment

There are no definitive answers to these questions, which brings us back to "first do no harm" and, if in doubt, don't. For me it points to a societal need for an environment where mothers and children flourish: better nourishment, less physiological stress and a lower drive towards birth intervention, whether elective or inductive.

"More research is needed" applies, but with better questions. The lens has to shift from "the system is fine, don't rock it" to "how do we create beautiful, healthy children?", with systems that encourage health rather than simply a live birth. Something is driving the rise in developmental disorders in our kids.

Conclusion

Frederick Douglass put it best in 1855: "It is easier to build strong children than to repair broken men." Let's think big together and make the world better for our children, and for theirs.

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References

1. Eastman NJ. Mount Everest in Utero. 1954.
2. Study on fetal arterial PO2 levels.
3. Perinatal physiology literature on hypoxia during birth ("Valley of the Shadow of Birth").
4. Study on oxidative stress and free-radical conditions in neonates.
5. Literature on maternal stress and primitive reflexes.
6. Wustenberg S. First Principles (cortisol and the WNT signalling pathway).
7. Rat model study of folate- and B12-deficient mothers and neonatal hypoxia.
8. Study on folate metabolism defects during facial development.
9. Australian Institute of Health and Welfare, birth statistics 2010–2020.
10. Eastman NJ on fetal cyanosis and oxytocic drug risk.
11. 2021 Danish and Finnish cohort study on oxytocin induction, ADHD and ASD.
12. Review concluding perinatal oxytocin neurodevelopmental risk is "premature".
13. 2011 study on Pitocin induction and ADHD.
14. Douglass F. 1855.