What Is Spina Bifida?
An Essay on the Birth Defect and the Deception Sold to Prevent It
Author’s Note
Spina bifida is a birth defect the mainstream declares mostly solved. The compound added to enriched flour in 1998, credited with a roughly thirty percent decline in cases, is the current answer to what causes the defect and how to prevent it.
The essay that follows examines that answer against the field’s own literature. It also examines what the same literature says about what actually damages the neural tube during the four to seven days it is closing. The answers are documented. They are not disputed within the birth defects field. They are simply not the answers that shape what a mother is told.
The Admission Inside the Canon
In 1990 and 1991, six anencephalic births occurred in six weeks at a single hospital in Cameron County, Texas, on the Mexico border. Anencephaly is the failure of the skull and brain to form during the first month of embryonic development. Infants born with the condition do not survive.
The regional rate of neural tube defects was running at 27 per 10,000 live births, three to four times the American prevalence. The affected population was overwhelmingly Mexican-American women eating a diet built around corn tortillas. Twenty-three studies over the next twenty years established the cause: fumonisin, a mycotoxin contaminating the corn supply the year of the outbreak. The public health response was to expand folic acid outreach to the population that had been poisoned.
That move, from documented mass poisoning to folate-deficient population vulnerable to environmental exposures, is the move the folic acid narrative performs everywhere it appears. It also runs through the field’s own numbers.
Gary Shaw is not a fringe figure. He is a senior investigator at Stanford’s School of Medicine and one of the most prolific researchers in the birth defects literature. In 2016 his group published an analysis of more than 1.3 million California births spanning 1989 through 2010, examining neural tube defect rates before and after the United States mandated folic acid fortification of enriched grain products in January 1998. Reporting on his own institution’s data to Stanford Medicine’s news office, Shaw said the decline in neural tube defects began “probably in the late 1960s or early 1970s.”¹ Fortification did not begin the decline. When the policy took effect, the pre-existing rate of decrease (approximately 8.7 cases per 100,000 births per year) did not accelerate. It slowed.
This is not a critical position argued from outside the field. It is one of the field’s most senior investigators, reporting on his own dataset, saying the decline was already happening when the policy later credited with the decline had not yet been enacted.
The paper Blom, Shaw, den Heijer, and Finnell published in Nature Reviews Neuroscience in 2006 carried the title “Neural tube defects and folate: case far from closed.” Inside, some of the most prominent researchers in the field wrote that the mechanism by which folic acid produces its supposed benefit “is far from clear.”² A 2009 paper by Heseker, Mason, Selhub, Rosenberg, and Jacques in the British Journal of Nutrition was titled “Not all cases of neural-tube defect can be prevented by increasing the intake of folic acid.”³ Roy Pitkin’s 2007 review in the American Journal of Clinical Nutrition, written to defend the folate hypothesis, was forced to concede that following folic acid recommendations did not produce the expected reduction in NTD births.⁴
The parent of a child born with spina bifida knows the condition is real. The lower back with the visible sac, the paralysis below the lesion, the surgery within days of birth, the years of orthopedic and urological care that follow: all of that is real. What is not real is the story the parent has been told about why it happened.
The story runs like this: the condition is a birth defect caused, above all, by insufficient folic acid intake before conception; mandatory food fortification and prenatal supplementation have solved most of the problem; the remaining cases reflect individual susceptibility, sometimes genetic. Each of those positions is false, and the establishment’s own literature has been documenting it for two decades.
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In Print
Two of my books are now available as paperbacks. The Unvaccinated: What a Forbidden Comparison Reveals About the True Cost of Vaccination is, as far as I know, the only book of its kind — the completely unvaccinated as a comparison group, laid out across twenty chapters and five appendices. Alongside it is Medicalized Motherhood: From First Pill to Permanent Patient, which follows a woman through 123 documented interventions from teenage pill to postpartum discharge. Both are printed to order through Lulu, shipped worldwide, USD $19.99 each. A physical book reaches the person a Substack post never will — the sceptical relative, the friend who won’t click a link but might open a book, the visitor whose eye lands on a coffee table. Buy one to keep, and one to give away.
What Spina Bifida Is
The neural tube is the embryonic structure from which the brain and spinal cord form. In humans it develops during the third and fourth weeks after conception. Around day twenty-one after fertilization the neural plate begins to fold in on itself along the length of the developing embryo. Between days twenty-two and twenty-eight the folds close, producing a tube that runs from the cranial end (which becomes the brain) to the caudal end (which becomes the base of the spine). The vertebrae, the meninges, and the surrounding tissues form later around this tube.
When closure fails, the results depend on the location. Failure at the cranial end produces anencephaly: the top of the skull and the forebrain do not form, and the infant does not survive. Failure in the middle produces encephalocele: brain tissue protrudes through an opening in the skull. Failure at the caudal end produces spina bifida: a section of the vertebral column does not close, and the spinal cord and its coverings are exposed or protrude through the gap. In the most common form (myelomeningocele), the sac visible on the newborn’s back contains both meninges and neural tissue. Below the level of the lesion, motor and sensory function is impaired or absent, along with bladder and bowel control.
Two facts about the timing carry the entire essay.
First, the neural tube closes between days twenty-one and twenty-eight after fertilization. Most women do not know they are pregnant during this window. Whatever exposures, deficiencies, or drug regimens act during those days act on a mother who does not yet know she is a mother.
Second, whatever damaged the closing tube damaged it once, and the resulting deformity is permanent. Spina bifida is not progressive. It is a fixed structural consequence of something that happened in a narrow four-to-seven-day window. The relevant question is not what accumulates over years. The relevant question is what interfered with closure during those specific days.
The mainstream establishment has an answer: folate deficiency in the mother, corrected by folic acid supplementation and food fortification. The sections that follow examine that answer against the field’s own numbers, then against the compound actually being sold, and then against the drugs, injections, and toxic exposures the folic acid story functions to conceal.
The Category Cannot Survive Its Own Numbers
Nicolaes Tulp coined the term spina bifida in a book of medical observations published in 1641.⁵ Caspar Bauhin described what he called a “tumor” of the lower spine in 1592; Pieter van Foreest described the condition in the late 1500s. Isolated archaeological depictions exist in pre-Columbian Meso-American cultures, but for most of European recorded medicine before the early modern period, a condition producing an unmistakable visible deformity of the lower back was either extraordinarily rare, or unrecorded, or both.
By the 1950s the picture had changed. A 2018 review published in the Annals of the New York Academy of Sciences noted birth prevalence rates above four per 1,000 births in poor working-class populations in mid-twentieth-century Britain.⁶ In some regions the rate approached the general prevalence of Down syndrome. Diet was poor. Industrial and pharmaceutical exposure was expanding sharply across the population.
Then, in the late 1960s and early 1970s, rates began to fall.
Shaw’s California data show the decline running at approximately 8.7 cases per 100,000 births per year through the 1990s.¹ Comparable declines were reported in the United Kingdom and Europe. An international assessment led by Botto in 2006 examined trends across a range of countries and concluded that through the middle of 1996, no change in the time trend could be attributed to the introduction of national folate supplementation policies.⁷ The decline was in progress before folic acid intervention could plausibly have caused it. Something else was working.
Part of what was working was prenatal screening. Maternal serum alpha-fetoprotein testing for neural tube defects expanded through the late 1970s and 1980s. Ultrasound examination of the fetal spine became routine over the same period. By the time Velie and Shaw examined California data for 1989 through 1991, 30% of spina bifida pregnancies and 52% of anencephaly pregnancies were being terminated after prenatal diagnosis and never appeared in live-birth statistics.⁸ A substantial fraction of the pre-fortification decline reflected pregnancies detected prenatally and ended before delivery, not pregnancies in which the defect had been prevented.
Mandatory fortification in the United States took effect in January 1998. The Centers for Disease Control claims a 28% reduction in NTDs following fortification.⁹ The Arizona Birth Defects Monitoring Program, examining state data from 1995 through 2009, reported a 15% reduction: roughly half the CDC figure.¹⁰ A 2008 CDC analysis of 21 surveillance systems examining 1999 through 2004 reported that the spina bifida decline had slowed to a statistically insignificant 3%. The anencephaly decline (20%) continued.¹¹
A 2021 study by Allen and colleagues in Prenatal Diagnosis, examining England and Wales from 2007 through 2017, made the accounting explicit. Live births affected by neural tube defects were decreasing. Terminations of NTD-affected pregnancies were increasing every year.¹² The apparent public health victory was, in substantial part, a screening artifact. The pregnancies were still occurring. The babies were not being born.
The claim that folic acid fortification solved most of the spina bifida problem depends on ignoring four facts in the establishment’s own record. The decline began roughly a quarter century before fortification. The CDC’s headline figure of 28% diverges from state-level analyses reporting reductions half that size or smaller. The spina bifida decline stalled at a statistically insignificant 3% in the 2003-2004 follow-up. And a substantial and growing fraction of the “prevented” cases were terminated pregnancies rather than prevented conditions. Each of these points appears in the establishment’s own literature. The public health message is what remains after they have been removed.
The Chemical Sold as Folate
Folic acid is a laboratory-synthesized compound developed in the early 1940s. Lucy Wills, working in Bombay in the early 1930s, had identified a factor in yeast and liver extracts that reversed a form of anemia in pregnant women.¹³ Wills was not administering folic acid. She was administering food. The compound eventually named folic acid and marketed under that name (pteroylmonoglutamic acid) is a synthetic approximation of a natural family of related compounds found in leafy vegetables, liver, legumes, and eggs. The synthetic version is more chemically stable, cheaper to manufacture, and easier to standardize for pharmaceutical use. Those are the properties that made it the industrial choice.
The natural compounds, collectively called folates, exist in food as reduced and methylated forms. These are molecules the body absorbs and uses directly. When a person eats leafy greens or liver, the folate goes straight into cellular metabolism. Folic acid, the industrial substitute, is not one of those forms. Before the body can use it, an enzyme called dihydrofolate reductase must first convert it. That enzyme’s capacity in the human liver is limited. When intake exceeds the enzyme’s throughput (around 200 to 400 micrograms per day), the excess folic acid circulates in the bloodstream unmetabolized.¹⁴ Whether unmetabolized folic acid causes harm is a question the establishment has not been eager to investigate. Morris and colleagues, examining NHANES data in 2007, reported that elderly Americans with high serum folate and low cobalamin showed the worst cognitive performance in the sample.¹⁵ The finding has not received the attention that a finding in the opposite direction would have received.
The methylenetetrahydrofolate reductase (MTHFR) enzyme handles part of the body’s folate processing. Roughly 40% of the population carries variants that reduce this enzyme’s activity, and the establishment calls these variants a defect. On the reading offered here they are the opposite. Four in ten people carry the biological signature of resistance to a laboratory chemical developed in the 1940s and inserted into flour, cereal, prenatal tablets, and infant formula, and the resistance itself is called the problem.
Joel Fuhrman noted in a 2017 article that folic acid and dietary folate are chemically different substances, and that pregnancy is not the only time women should focus on folate.¹⁶ The natural folate story is unremarkable. Leafy vegetables, liver, legumes, eggs, and grain prepared traditionally through sprouting or fermentation deliver folate in usable forms alongside the cofactors, minerals, and lipids the body needs to process it. Weston Price documented multiple traditional populations whose diets were rich in these foods and whose birth defects and reproductive failures were essentially unknown.¹⁷ None of those populations took supplements.
Shaw’s own group made the whole-food point concrete. In a 2009 study published in Epidemiology using serum samples from more than 180,000 California pregnancies drawn from a folate-fortified population, women in the lowest decile of choline intake had 2.4 times the NTD risk of women in the middle range, while women in the highest decile had roughly one-seventh the risk.¹⁸ Choline is not folate. It is concentrated in egg yolks, liver, red meat, and dairy. It is not added to fortified flour. It has not been made the target of any public health fortification program. In a population where every serving of bread and cereal was already fortified with folic acid, a whole-food nutrient outside the fortification program predicted NTD risk more powerfully than the fortification itself. The finding, from the same investigators who authored the folic acid research, has not become the organizing question of the field.
The industrial food supply has been stripped of these compounds. Refined grain lost most of its folate through milling. Cooked liver, cooked greens, and pastured eggs have been displaced by cereal, refined seed oils, and industrial dairy. The observed low serum folate the fortification program was ostensibly correcting was itself the consequence of a food supply engineered to be nutritionally impoverished. The response was not to restore the food. The response was to insert a stable synthetic compound into the flour and call the problem addressed.
The compound sold as folic acid is a real chemical. Some of its effects in some populations are real. What is not real is the framing that treats it as folate itself, as a substitute for the whole-food matrix in which folate occurs, or as anything other than the industrial compound it is.
The Drugs That Cause What Folic Acid Is Sold to Prevent
If the compound sold as folic acid is not what causes or cures spina bifida, the question becomes what does. The clearest answers sit inside the labels of drugs prescribed to the mother.
Sodium valproate was approved as an antiseizure medication in Europe in 1967 and in the United States in 1978. Within a few years, cases of infants born with spina bifida to mothers taking the drug began appearing in the literature. Robert and Guibaud published the first cluster in the Lancet in 1982.¹⁹ The French case-control analysis calculated an odds ratio of 20.6 for the association between valproate exposure and spina bifida.²⁰ Cohort studies pooled by Wyszynski and colleagues reported a risk approximately twenty times that of the general population.²¹
The current MotherToBaby fact sheet, published by the Organization of Teratology Information Specialists and hosted on the National Library of Medicine’s NCBI platform, states the risk plainly. Valproate exposure carries approximately a 1 to 2% risk of a neural tube defect in the resulting infant, against a background rate of about 0.07% in the general population.²² Approximately 7% of infants exposed to valproate in the first trimester show some major congenital anomaly.²³ Roughly 70% of the anomalies produced are neural tube defects.
Carbamazepine, marketed as Tegretol, is another antiseizure drug that Rosa documented in the New England Journal of Medicine in 1991 as causing spina bifida. His analysis of Food and Drug Administration adverse event reports and cohort studies concluded that in utero exposure to carbamazepine without concurrent valproate carried a 1% risk of the defect.²⁴
Both drugs are also prescribed for what the establishment calls bipolar disorder, migraine, and neuropathic pain. Both are recommended for continuation through pregnancy in women taking them for epilepsy, on the grounds that seizure control is essential and the alternative drugs are not clearly safer. The medical literature acknowledges the teratogenic effects openly. The Food and Drug Administration lists spina bifida among the risks in the drug labels. The response is to recommend that women taking these drugs also take folic acid, on the theory that the drug’s teratogenic mechanism operates through a disturbance of folate metabolism that supplementation can counter.
The establishment has been documenting since the early 1980s that its own antiseizure drugs cause the birth defect its public health apparatus attributes primarily to maternal folate deficiency. Both facts appear in the same medical literature. They are not reconciled with each other. The drug-caused cases are separated out as a distinct risk category, and the mainstream causal story about folic acid deficiency continues to be delivered to women as though the drug-caused cases did not exist.
The drug-caused cases are not marginal. Van Gelder and colleagues, in a 2010 review in Human Reproduction Update, noted that the human teratogenic risks of more than 90% of prescription drugs approved in the United States during the preceding decades were undetermined.²⁵ Prescription drug use during pregnancy is common. The recognized teratogenic drugs (methotrexate as a folate antagonist, isotretinoin as a retinoid, warfarin as an anticoagulant, thalidomide historically, valproate and carbamazepine as antiseizure agents) are the visible portion of a much larger iceberg. The unrecognized teratogens are not being tested for the effects they may be producing.
Mark Yerby’s 2003 paper in Epilepsia, cited in Dawn Lester’s chapter on birth defects, put the situation as directly as the establishment permits: most antiepileptic drugs have been associated with birth defect risk, and valproate and carbamazepine specifically are associated with neural tube defects.²⁶ The paper’s title reveals the clinical stalemate: Clinical care of pregnant women with epilepsy: neural tube defects and folic acid supplementation. The proposed response is to keep the pregnant woman on the drug that causes the defect and to give her a synthetic compound to try to offset the drug’s effect.
The Injections in the Same Window
Modern obstetric practice delivers to women of childbearing age an expanding schedule of injections: Tdap during pregnancy, influenza in any trimester, hepatitis B, human papillomavirus before conception, and since 2020 the COVID-19 injections at any point. Tdap is officially recommended at 27 weeks or later. The Boostrix Pregnancy Registry reports that 63% of registered exposed pregnancies received the injection during the first trimester, regardless of the third-trimester recommendation.²⁷ The neural tube closes between days twenty-one and twenty-eight after fertilization. A substantial fraction of these injections operates in or immediately before that closure window.
The establishment has been running trials on the practice. The results are in its own literature.
Florea and colleagues published the largest such trial in Infectious Diseases and Therapy in 2023. Their cohort study compared 16,350 Boostrix-exposed live-born infants against 16,088 unvaccinated controls in Kaiser Permanente Southern California.²⁸ Of the fourteen congenital anomaly body systems evaluated, eight showed statistically significant elevated adjusted risk ratios in the Tdap-exposed group: eye, ear/face/neck, respiratory, upper gastrointestinal, genital, renal, musculoskeletal, and integument. The adjusted risk ratios ranged from 1.17 to 2.02, or 17% to 102% higher rates than the unvaccinated controls. The study was funded by GlaxoSmithKline, the manufacturer of Boostrix. The authors concluded that Boostrix during the third trimester of pregnancy was safe. Their argument was that maternal vaccination after 20 weeks of gestation is unlikely to fall within the risk window for congenital anomalies, and that the elevated rates they had documented reflected background rates rising over time and improved diagnostic identification rather than the vaccine. The elevated rates were left in the paper. The recommendation to vaccinate all pregnant women with Tdap was not modified.
Traversa and colleagues, publishing in the British Medical Journal in 2014, analyzed adverse maternal, fetal, and neonatal outcomes in a cohort of Italian pregnancies following the 2009 A/H1N1 pandemic influenza vaccination.²⁹ Vaccinated women showed elevated adjusted odds ratios of 1.26 for gestational diabetes and 1.19 for eclampsia. This finding closes a loop the mainstream literature keeps open. Maternal diabetes, including gestational diabetes, is an accepted risk factor for neural tube defects in the establishment’s own guidelines. If vaccination during or before pregnancy raises gestational diabetes rates, and gestational diabetes raises neural tube defect rates, the vaccine is producing the risk factor the mainstream already concedes as causal. The story does not need to argue for a novel mechanism. It only needs to name the chain.
The mechanism by which injected material reaches embryonic tissue is documented. The Tdap vaccines currently administered to pregnant women in the United States contain 0.3 to 0.33 milligrams of aluminum per dose in the form of aluminum hydroxide or aluminum phosphate adjuvant.³⁰ A study reproduced by Forrest Maready in Crooked followed sheep receiving aluminum-containing injections. The sheep developed weight loss, paralysis, and death.³¹ When researchers biopsied the injection site, they found the tissue saturated with white blood cells that had absorbed the aluminum. The same aluminum-loaded white blood cells were then found in the sheep’s lymph nodes and spinal cord tissue. The aluminum had been transported from the injection site by cellular carriers into the central nervous system. A 1921 paper by Dollken had already documented that aluminum exposure produces degeneration of the nerve cells and fibers of the cord and medulla in animals.³² A century of evidence establishes that injected aluminum reaches nervous tissue and damages it.
The Brazilian episode of 2014-2015 played out the same pattern at scale. In October 2014, the Brazilian Health Ministry’s Immunization Division issued a technical bulletin recommending Tdap for all pregnant women, including up to three doses during pregnancy for those not previously vaccinated. Doctors in the poorer regions of northeastern Brazil, where public health clinics were most active, followed the bulletin closely. Thirteen months later, in late 2015, a cluster of infants born with abnormally small heads (microcephaly) appeared in the same regions.³³ The World Health Organization declared the cause to be the Zika virus, transmitted by mosquito. Prior to the outbreak, Zika had been considered by the establishment a mild illness with no known connection to congenital malformation. The geographical concentration of microcephaly cases matched the population where the vaccination bulletin had been followed most closely.
The Brazilian pattern is the Cameron County pattern. A malformation appears after an injection or exposure program. An alternative cause is announced. The injection program continues. The exposure is not investigated.
Paul Patterson, a neuroscientist at the California Institute of Technology, studied what mainstream neuroscience labels “maternal immune activation.” His animal work documented that a large inflammatory response in a pregnant animal produces significant neurodevelopmental damage in the offspring. In an interview recorded by J. B. Handley in How to End the Autism Epidemic, Patterson issued the warning his findings implied. Vaccination is by design a provocation of the same inflammatory response. Universal maternal vaccination should not be promoted.³⁴ In terrain terms: the pregnant body’s response to the injection reaches the developing embryo and damages what is under development at the time. The neural tube, under development between days twenty-one and twenty-eight, is precisely such a structure.
In March 2026, the University of Minnesota’s Center for Infectious Disease Research and Policy announced that its Vaccine Integrity Project would independently review the safety of Tdap in pregnancy. Among the outcomes the review will assess, the announcement listed “congenital anomalies, such as spina bifida.”³⁵ The establishment has begun to concede that the question is worth asking. The essay has been asking it throughout.
What the Adjacent Fields Have Named
The birth defects literature has documented additional causes that the folic acid conversation has walled off.
Paul Winchester, a neonatologist at Indiana University, examined every live birth in the United States between 1996 and 2002 (approximately 30.1 million births) against monthly measurements of pesticides and nitrates in surface water published by the United States Geological Survey. He reported the results in Acta Paediatrica in 2009. Agrichemical concentrations in surface water peaked between April and July. Total birth defects, and eleven of twenty-two birth defect subcategories, were more likely to occur in live births conceived in April through July. Winchester named spina bifida directly as one of the defects showing this seasonal association.³⁶
The Yang analysis, published in 2014, went further by identifying specific pesticide classes associated with specific defects. Hydroxy benzonitrile herbicides were associated with spina bifida. Petroleum derivatives were associated with anencephaly. Dithiocarbamates were associated with cleft lip.³⁷
The Argentine research by Andrés Carrasco, reported internationally in 2010, found that glyphosate (the herbicide Monsanto sold as Roundup) produced birth defects in amphibian and chicken embryos at concentrations far below those used in agricultural application.³⁸ Glyphosate is the most widely used herbicide in the world. Its use expanded dramatically after the 1996 introduction of Roundup Ready crops. Residues appear in the food and water supply routinely.
Electromagnetic exposure at power-frequency levels is a documented reproductive harm. Nordstrom’s 1983 investigation of Swedish high-voltage switchyard workers found chromosomal abnormalities in the workers’ sperm and elevated birth defects in their children.³⁹ The BioInitiative Report’s 2012 review cited multiple lines of evidence connecting exposure to 50/60 Hz magnetic fields to increased birth defect risk, among other reproductive harms.⁴⁰
Alcohol is teratogenic and its role in fetal damage is uncontroversial. Grandjean and Landrigan, publishing in Lancet Neurology in 2014, named fluoride, manganese, chlorpyrifos, DDT, tetrachloroethylene, and the polybrominated diphenyl ethers as documented developmental neurotoxicants.⁴¹ Their paper has been cited more than three thousand times. Its findings have not become the organizing question of the birth defects field.
These exposures act on the embryo during the same narrow developmental window in which the neural tube is closing. Each has been documented in peer-reviewed literature. None of them appears prominently in the CDC’s public-facing “planning for pregnancy” materials, which focus on folic acid intake, weight, and blood sugar control.
The Fumonisins Case
The Cameron County cluster prompted an investigation. Missmer and colleagues, working with Katherine Hendricks at the Texas Department of State Health Services, published the mechanistic study in Environmental Health Perspectives in 2006. Their case-control analysis linked NTD risk to maternal exposure to fumonisins, mycotoxins produced by the fungus Fusarium verticillioides that contaminates corn. The exposure was measured directly using a sphinganine-to-sphingosine ratio in maternal serum, a validated biomarker of fumonisin exposure. Moderate consumption of tortillas during the first trimester was associated with elevated NTD odds ratios after adjustment for confounders.⁴²
The corn supply that crop year was heavily contaminated, coinciding with fumonisin-attributed livestock epizootics in Texas. Mexican-American women in the border region who consumed that corn as their staple food were exposed to fumonisin doses far above background.
Twenty years and twenty-three studies later, Suarez and colleagues published a review in Birth Defects Research summarizing what had been learned. The conclusion, as expressed in the abstract, treated fumonisins as one of “several insults” that a “folic acid deficit population” was vulnerable to.⁴³
A population poisoned by mycotoxin-contaminated corn was reframed as a folate-deficient population vulnerable to environmental exposures. The dietary exposure that doubled the NTD rate in the affected community was included in the list of contributing factors but positioned behind the folic acid recommendation. Twenty-three studies established the toxicological mechanism. The public health response was to expand folic acid outreach to Mexican-American women along the border.
The interpretive move on display is the one introduced at the opening of this essay and repeated at Brazil. The primary cause is toxic. It is documented. The story presented to the population blames the mother’s diet for lacking the industrial supplement.
The Sequence Reversed
The establishment story runs like this. The cause of spina bifida is largely unknown but appears to reflect a combination of genetic susceptibility, maternal factors including folate status and diabetes, and a scattering of environmental exposures the field is still investigating. Prevention consists of periconception folic acid supplementation, food fortification, and management of maternal weight and blood sugar. Where the intervention succeeds, credit goes to the folic acid. Where it fails, the case joins the residual category of individual susceptibility.
Reversing the arrow produces a coherent picture.
The neural tube closes between days twenty-one and twenty-eight after fertilization. During that window, damage to the developing embryo interferes with closure. The damage comes from documented sources. Antiseizure drugs (valproate, carbamazepine), folate antagonists (methotrexate, aminopterin), retinoids (isotretinoin), anticoagulants (warfarin), alcohol, agrichemicals present in surface water and food, mycotoxins in contaminated grain, industrial solvents, electromagnetic exposure at power-frequency levels, and hyperthermia have all been documented to damage embryonic development. The periconceptional and prenatal injections routinely delivered to women of childbearing age have been documented in the establishment’s own trials to produce elevated congenital malformation rates across multiple body systems. The aluminum they contain has been documented to reach spinal cord tissue via cellular transport. The neural tube itself has not been isolated in the published trials, but the mechanism and the timing converge on it, and the establishment has begun to acknowledge the question. A mother whose diet has been stripped of the whole-food matrix (green leaves, organ meat, eggs, properly prepared grain) that supplies natural folate, choline, and the other cofactors involved in tube closure carries a depleted terrain that magnifies the damage the toxic exposures cause. The industrial compound sold as folic acid was engineered as a cheap and stable substitute for the natural matrix. It restores serum folate readings. It does not restore the matrix. Its independent effect on neural tube defects is smaller than the establishment claims, and its causal story does not survive the field’s own data.
The condition was rare in traditional populations. It became measurable in Europe during the pharmaceutical and industrial era. It has been managed since 1998 through a program that credits a synthetic supplement with a decline that was already in progress before the supplement was introduced, and that counts as prevented the cases now identified prenatally and terminated before delivery.
The primary causes are the exposures the folic acid story functions to obscure. The condition is preventable. The prevention is not what the mother is told.
How To Explain It To A 6 Year Old
Before a baby is born, the baby grows inside its mother. This takes about nine months. Most of the important building happens in the first two months, before the mother even knows the baby is there.
In the very first month, the baby’s body has to build a long tube inside it. This tube will become the baby’s brain at the top and the baby’s spinal cord all the way down. The spinal cord is the bundle of nerves that lets the brain talk to the arms and legs. Without it, the arms and legs cannot move.
The tube starts as a flat sheet. Then the sheet has to fold up, like folding a piece of paper into a straw. The folding takes about a week, from day twenty-one to day twenty-eight after the baby starts growing. During that week, the tube has to close all the way along its length. If any part of the tube does not close, that part will not work properly for the rest of the baby’s life.
Sometimes the tube does not close near the bottom, at the baby’s lower back. This is called spina bifida. The baby is born with a bump on the back where the tube did not close. The nerves in that part of the spine did not form right. The baby may not be able to walk. The baby may need many operations. The baby will need care for a lifetime.
Doctors are supposed to tell mothers what makes the tube fail to close. Here is what mothers are told: it happened because the mother did not take enough of a pill called folic acid. The pill is added to bread and cereal so that every mother gets some. Doctors say this pill solves most of the problem.
Here is what mothers are not told.
The pill was invented in a laboratory in the 1940s. It is not the same thing that is in leafy green vegetables or in liver. It is a copy that the body has trouble with. About four out of every ten people cannot use it properly.
The number of babies born with spina bifida was already going down before the pill was added to the bread. It went down for reasons no one is sure about. When the pill was added, the going-down did not speed up. In many places it slowed down.
Some medicines that mothers take, especially medicines for seizures, cause spina bifida directly. The medicines are called valproate and carbamazepine. Mothers who take these medicines are about twenty times more likely to have a baby with spina bifida than mothers who do not. The doctors know this. The medicines are still prescribed. Mothers are told to take extra folic acid to try to make it safer.
Some shots that mothers get during pregnancy also raise the chance of babies being born with things wrong with them. A big study on the shot for whooping cough looked at over sixteen thousand babies whose mothers got the shot and compared them with over sixteen thousand babies whose mothers did not. The babies of the mothers who got the shot had more problems in eight parts of the body. The doctors who did the study said the shot was still safe. The shot is still given to every pregnant mother.
Chemicals that farmers spray on crops end up in the water. Babies conceived in the spring, when the chemicals are highest, are more likely to be born with spina bifida. A doctor in Indiana named Paul Winchester looked at thirty million American babies and found this pattern clearly.
A mother who was told her baby’s spine did not close because she did not take enough of the pill was not told the true story. The true story is that many things damage the baby’s spine while it is closing. Some of the things are medicines. Some are shots. Some are farm chemicals. Some are toxins in food. The pill was offered as the answer so that the questions about the medicines, the shots, and the chemicals would not be asked.
The spine closes in a week. What is happening to the mother’s food and water and medicine and shots during that week is the thing that matters. That is what mothers were supposed to be told.
References
Stanford Medicine News Center. (2016, May 18). Less decline than expected in rate of brain, spine defects after folic acid fortification program. Reporting on research led by Gary M. Shaw and colleagues, published in Birth Defects Research Part A: Clinical and Molecular Teratology, analyzing 1.3 million California births from 1989 through 2010.
Blom, H. J., Shaw, G. M., den Heijer, M., & Finnell, R. H. (2006). Neural tube defects and folate: case far from closed. Nature Reviews Neuroscience, 7(9), 724-731.
Heseker, H. B., Mason, J. B., Selhub, J., Rosenberg, I. H., & Jacques, P. F. (2009). Not all cases of neural-tube defect can be prevented by increasing the intake of folic acid. British Journal of Nutrition, 102(2), 173-180.
Pitkin, R. M. (2007). Folate and neural tube defects. American Journal of Clinical Nutrition, 85(1), 285S-288S.
Smith, G. K. (2001). The history of spina bifida, hydrocephalus, paraplegia, and incontinence. Pediatric Surgery International, 17(5-6), 424-432. See also: Tulp, N. (1641). Observationum medicarum libri tres. Amsterdam.
Blencowe, H., Kancherla, V., Moorthie, S., Darlison, M. W., & Modell, B. (2018). Estimates of global and regional prevalence of neural tube defects for 2015: A systematic analysis. Annals of the New York Academy of Sciences, 1414(1), 31-46.
Botto, L. D., Lisi, A., Bower, C., et al. (2006). Trends of selected malformations in relation to folic acid recommendations and fortification: An international assessment. Birth Defects Research Part A: Clinical and Molecular Teratology, 76(10), 693-705.
Velie, E. M., & Shaw, G. M. (1996). Impact of prenatal diagnosis and elective termination on prevalence and risk estimates of neural tube defects in California, 1989-1991. American Journal of Epidemiology, 144(5), 473-479.
Williams, J., Mai, C. T., Mulinare, J., et al. (2015). Updated estimates of neural tube defects prevented by mandatory folic acid fortification: United States, 1995-2011. MMWR Morbidity and Mortality Weekly Report, 64(1), 1-5.
Arizona Birth Defects Monitoring Program. (2012, January 9). Facts about Spina Bifida, 1995-2009 ABDMP Data Collection. Arizona Department of Health Services.
Boulet, S. L., Yang, Q., Mai, C., et al. (2008). Trends in the postfortification prevalence of spina bifida and anencephaly in the United States. Birth Defects Research Part A: Clinical and Molecular Teratology, 82(7), 527-532.
Allen, C., Dey, T., Peacock, D., Impey, L., & Kilby, M. D. (2021). Trends in termination of pregnancy for neural tube defects in England and Wales from 2007 to 2017: Observational prospective study. Prenatal Diagnosis, 41(9), 1176-1182.
Wills, L. (1931). Treatment of “pernicious anaemia of pregnancy” and “tropical anaemia” with special reference to yeast extract as a curative agent. British Medical Journal, 1(3676), 1059-1064.
Bailey, S. W., & Ayling, J. E. (2009). The extremely slow and variable activity of dihydrofolate reductase in human liver and its implications for high folic acid intake. Proceedings of the National Academy of Sciences, 106(36), 15424-15429.
Morris, M. S., Jacques, P. F., Rosenberg, I. H., & Selhub, J. (2007). Folate and vitamin B-12 status in relation to anemia, macrocytosis, and cognitive impairment in older Americans in the age of folic acid fortification. American Journal of Clinical Nutrition, 85(1), 193-200.
Fuhrman, J. (2017, March). Why you need folate and not folic acid. DrFuhrman.com.
Price, W. A. (1939/2009). Nutrition and Physical Degeneration. Price-Pottenger Nutrition Foundation.
Shaw, G. M., Finnell, R. H., Blom, H. J., Carmichael, S. L., Vollset, S. E., Yang, W., & Ueland, P. M. (2009). Choline and risk of neural tube defects in a folate-fortified population. Epidemiology, 20(5), 714-719. See also: Shaw, G. M., Carmichael, S. L., Yang, W., Selvin, S., & Schaffer, D. M. (2004). Periconceptional dietary intake of choline and betaine and neural tube defects in offspring. American Journal of Epidemiology, 160(2), 102-109.
Robert, E., & Guibaud, P. (1982). Maternal valproic acid and congenital neural tube defects. Lancet, 2(8304), 937.
As reported in: Ornoy, A. (2009). Valproic acid in pregnancy: How much are we endangering the embryo and fetus? Reproductive Toxicology, 28(1), 1-10.
Wyszynski, D. F., Nambisan, M., Surve, T., et al. (2005). Increased rate of major malformations in offspring exposed to valproate during pregnancy. Neurology, 64(6), 961-965.
MotherToBaby / Organization of Teratology Information Specialists. (2024). Valproic Acid Fact Sheet. National Center for Biotechnology Information, NCBI Bookshelf NBK583009.
Tomson, T., Marson, A., Boon, P., et al. (2015). Valproate in the treatment of epilepsy in girls and women of childbearing potential. Epilepsia, 56(7), 1006-1019.
Rosa, F. W. (1991). Spina bifida in infants of women treated with carbamazepine during pregnancy. New England Journal of Medicine, 324(10), 674-677.
Van Gelder, M. M. H. J., van Rooij, I. A. L. M., Miller, R. K., Zielhuis, G. A., de Jong-van den Berg, L. T. W., & Roeleveld, N. (2010). Teratogenic mechanisms of medical drugs. Human Reproduction Update, 16(4), 378-394.
Yerby, M. S. (2003). Clinical care of pregnant women with epilepsy: neural tube defects and folic acid supplementation. Epilepsia, 44(Suppl 3), 33-40.
Boostrix Pregnancy Registry (US), GlaxoSmithKline. Study protocol NCT02096276. Registry data reported 63% of registered exposed pregnancies received Tdap in the first trimester and 37% in the second or third trimester. See also: Kuznetsova, A., et al. (2022) summary of Boostrix pregnancy registry findings.
Florea, A., Sy, L. S., Ackerson, B. K., Qian, L., Luo, Y., Becerra-Culqui, T., Lee, G. S., Tian, Y., Zheng, C., Bathala, R., Tartof, S. Y., Campora, L., Ceregido, M. A., Kuznetsova, A., Poirrier, J. E., Rosillon, D., Valdes, L., Cheuvart, B., Mesaros, N., Meyer, N., Guignard, A., & Tseng, H. F. (2023). Investigating Tetanus, Diphtheria, Acellular Pertussis Vaccination During Pregnancy and Risk of Congenital Anomalies. Infectious Diseases and Therapy, 12(2), 411-423.
Traversa, G., Del Manso, M., Bianchi, F., et al. (2014). Evaluation of safety of A/H1N1 pandemic vaccination during pregnancy: cohort study. BMJ, 348, g3009. Adjusted odds ratios of 1.26 for gestational diabetes and 1.19 for eclampsia among vaccinated women.
Boostrix (GlaxoSmithKline) US prescribing information and CDC vaccine information: US formulation contains 0.3 mg aluminum per dose (as aluminum hydroxide); non-US formulation contains 0.5 mg. Adacel (Sanofi Pasteur) prescribing information: contains 0.33 mg aluminum per dose (as aluminum phosphate adjuvant).
Maready, F. (2018). Crooked: Man-Made Disease Explained. Feels Like Fire. See chapters on aluminum transport, the sheep study, and the Brazilian microcephaly episode.
Dollken, A. (1921). Description of aluminum-induced degeneration of nerve cells and fibers in the spinal cord and medulla, as cited in Maready (2018).
Brazilian Ministry of Health, Immunization Division. (2014, October). Technical Bulletin recommending Tdap for pregnant women. As documented in Maready (2018); see also PBS Frontline coverage of the microcephaly cluster in northeastern Brazil.
Handley, J. B. (2018). How to End the Autism Epidemic. Chelsea Green Publishing. Contains the Patterson interview and warning against universal maternal vaccination on the basis of inflammatory response findings in pregnant animals.
University of Minnesota Center for Infectious Disease Research and Policy (CIDRAP). (2026, March 4). Vaccine Integrity Project kicks off evidence review of Tdap vaccine in pregnancy. Announcement of independent review including congenital anomaly outcomes such as spina bifida.
Winchester, P. D., Huskins, J., & Ying, J. (2009). Agrichemicals in surface water and birth defects in the United States. Acta Paediatrica, 98(4), 664-669.
Yang, W., Carmichael, S. L., Roberts, E. M., Kegley, S. E., Padula, A. M., English, P. B., & Shaw, G. M. (2014). Residential agricultural pesticide exposures and risk of neural tube defects and orofacial clefts among offspring in the San Joaquin Valley of California. American Journal of Epidemiology, 179(6), 740-748.
Paganelli, A., Gnazzo, V., Acosta, H., López, S. L., & Carrasco, A. E. (2010). Glyphosate-based herbicides produce teratogenic effects on vertebrates by impairing retinoic acid signaling. Chemical Research in Toxicology, 23(10), 1586-1595. See also: Engdahl, F. W. (2010, October). Study shows Monsanto Roundup herbicide link to birth defects. Global Research.
Nordstrom, S., Birke, E., & Gustavsson, L. (1983). Reproductive hazards among workers at high voltage substations. Bioelectromagnetics, 4(1), 91-101. See also: Becker, R. O. (1990). Cross Currents: The Perils of Electropollution. Jeremy P. Tarcher.
BioInitiative Working Group. (2012). BioInitiative Report: A Rationale for Biologically-Based Exposure Standards for Low-Intensity Electromagnetic Radiation. See especially Section 18: Electromagnetic Field Exposure Effects (ELF-EMF and RFR) on Fertility and Reproduction.
Grandjean, P., & Landrigan, P. J. (2014). Neurobehavioural effects of developmental toxicity. Lancet Neurology, 13(3), 330-338.
Missmer, S. A., Suarez, L., Felkner, M., Wang, E., Merrill, A. H., Rothman, K. J., & Hendricks, K. A. (2006). Exposure to fumonisins and the occurrence of neural tube defects along the Texas-Mexico border. Environmental Health Perspectives, 114(2), 237-241.
Suarez, L., Felkner, M., Brender, J. D., Canfield, M., Zhu, H., & Hendricks, K. A. (2012). Neural tube defects on the Texas-Mexico border: What we’ve learned in the 20 years since the Brownsville cluster. Birth Defects Research Part A: Clinical and Molecular Teratology, 94(11), 882-892.
Additional Sources
Lester, D., & Parker, D. (2019). What Really Makes You Ill? Why Everything You Thought You Knew About Disease Is Wrong. See especially the chapters on birth defects, teratogens, and pharmaceutical drugs.
Geehr, E. (2024). Unavoidably Unsafe. On the establishment’s own signals of congenital anomaly, obstetric complication, and adverse birth outcome following vaccination during pregnancy.
Thomas, P. (2022). Vax Facts. Includes the MTHFR polymorphism discussion, the folic acid versus methylfolate distinction, and the Tdap aluminum content.
Cowan, T. S. (2018). Vaccines, Autoimmunity, and the Changing Nature of Childhood Illness. Chelsea Green Publishing.
Cowan, T. S. Substack essays on the industrial synthesis of the compounds sold as cholecalciferol, ascorbic acid, and related “vitamins.”
Bieler, H. G. (1965). Food Is Your Best Medicine. Random House. On the toxic background theory of diabetes and metabolic disorder.
Shelton, H. M. (1934). The Hygienic System: Orthopathy. Self-published. On the acute-to-chronic suppression cascade central to the terrain framework.
Firstenberg, A. (2017). The Invisible Rainbow: A History of Electricity and Life. Chelsea Green Publishing.
Roytas, D. (2024). Can You Catch a Cold? Untold History and Science of the Common Cold.
Bailey, M., & Bailey, S. (2023). The Final Pandemic: An Antidote to Medical Tyranny.
Purdey, M. (2007). Animal Pharm: One Farmer’s Struggle to Discover the Truth about Mad Cow Disease. Chelsea Green Publishing. On the toxic causation of neurological disease.
Fraser, H. (2011). The Peanut Allergy Epidemic: What’s Causing It and How to Stop It. Skyhorse Publishing. On the pattern of blaming mothers and genetics for what injection sensitization produced.
Humphries, S., & Bystrianyk, R. (2013). Dissolving Illusions: Disease, Vaccines, and the Forgotten History. On the historical pattern of vaccine damage attributed to other causes.
Hendricks, K. (1999). Fumonisins and neural tube defects in South Texas. Epidemiology, 10(2), 198-200. (Original description of the Cameron County cluster.)
Closing Author’s Note
Spina bifida is preventable. It is not preventable through folic acid supplementation, which is the establishment’s answer and which does not withstand its own literature. It is preventable by removing what damages the neural tube during the first month after conception.
The condition became measurable in Europe with the industrial and pharmaceutical era, rose through the twentieth century, and began to fall in the late 1960s, before any folic acid intervention could account for the fall. The further decline after 1998 was substantially driven by expanded prenatal screening and termination. The public health apparatus took credit.
The drugs that most reliably cause spina bifida are prescribed by the same medical system that recommends folic acid to prevent it. Valproate carries a twenty-fold increased risk of neural tube defects. The response has been not to withdraw the drug but to prescribe folic acid alongside it. The women told to take the supplement are being asked to correct with one industrial chemical the damage caused by another industrial chemical their physicians are still prescribing.
The prenatal injections are on the same page. Florea’s establishment-published, industry-funded study of more than 32,000 pregnancies documented elevated congenital malformation rates across eight body systems, including musculoskeletal, following Tdap in pregnancy. The authors declared the vaccine safe. The University of Minnesota’s Vaccine Integrity Project announced in March 2026 that it would independently review the same practice, explicitly listing spina bifida among the outcomes it will assess. The question the essay has been asking is being asked now inside the field.
The agrichemicals that damage the closing neural tube are documented in Paul Winchester’s analysis of every United States birth over a seven-year period. The mycotoxins that doubled the neural tube defect rate along the Texas-Mexico border are documented in twenty-three studies. Choline, concentrated in egg yolks, liver, and pastured meat, is documented by Shaw’s own group as reducing NTD risk seven-fold at the highest intake decile compared to the lowest. None of these findings figures prominently in the preconception counseling most women receive.
The message worth carrying is not the one currently delivered. Whole food, organ meat, leafy vegetables, eggs, properly prepared grain, and avoidance of the documented teratogens (antiseizure drugs, retinoids, alcohol, agricultural chemicals in food and water, the periconceptional and prenatal injection schedule, and unexamined pharmaceutical exposures during the first month after conception) address the causes the folic acid narrative was constructed to obscure. Traditional populations that ate that way and were not injected did not have this condition at the rates observable in the industrial world.
An obstetrician’s office. A young woman sits across from her physician. She has been on valproate for six years, prescribed to her at nineteen for chronic migraines. Her doctor knows the drug carries a twenty-fold increased risk of the birth defect they are about to discuss preventing. He hands her a prescription for prenatal vitamins, a small pamphlet about the importance of folic acid, and a schedule of injections to receive through the pregnancy that has already begun. The pamphlet does not name the drug she is holding. The schedule does not name what has been documented about the shots on it. Neither does he. She goes home. Between days twenty-one and twenty-eight after conception, before she knows she is pregnant, the drug she is still taking and the injections she is about to receive will operate on the tube that is trying to close in her body.
The compound sold as folic acid is the smoke. The fire has other names: valproate, carbamazepine, methotrexate, isotretinoin, glyphosate, atrazine, fumonisin, aluminum adjuvants, the injection schedule that reaches into the neural tube closure window, and the industrial food supply that no longer delivers folate in its natural form. This essay was written to name what has been named around spina bifida and never at it.
Truth Be Told: I’ve Accepted an Invitation to Speak on The Unvaccinated
On September 17th, I’ll be giving a one-hour presentation titled The Unvaccinated as part of a six-hour livestream called Truth Be Told. This is the first time I have accepted an invitation to an event, and I have been honoured with the opening act. The livestream begins at 12pm EST.
Vaccination is the subject closest to my heart, and this is another opportunity to spread the word. The format will preserve the pen name.
Tickets are here.
The code UNBEKOMING is $5 off and applies automatically at that link. Replay available afterwards. Hope you can make it.
Every time I think I can’t consider western medicine any more evil, I read another of your articles. Thank you for the very important work you publish (faster than I can keep up).
When I was a young woman I was told by the doctor that, if I wanted to get pregnant, I should not take any meds. This is less than 50 years ago, in Europe. Obviously this knowledge has disappeared. Why do doctors nowadays no longer know this? Have they not learned from the disastrous use of meds in pregnant women?