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Nitrous Oxide, vitamin B12 and Autism

Usage of nitrous in labour should be banned.

“Nitrous Oxide in Labour: The Unexamined Use of a Schedule 6 Poison on a Defenceless Foetus During Peak Neurodevelopmental Vulnerability”

Say NO to Nitrous Oxide

Vitamin B12 Distribution in the body, a two pool system

Vitamin B12 in the body is distributed in two major pools, (i) the intracephalic area and the (ii) extracephalic area. The intracephalic area (the brain) is loaded in utero and once a baby is born there is almost no exchange of vitamin B12 into or out of the cephalic area. Hence, damage by agents such as Nitrous oxide, leads to permanent and irreversible damage of the brain, which lasts a life time, effectively making a :"dead pool" of B12..

Nitrous Oxide and Birth of the birth of the Child

Pain control during labour, and the birth of the child can be controlled by the use of Nitrous oxide and can be either given ad lib or via the control of an anesthetist. The use of nitrous oxide during labour has increased from 1% of births in 1980 to up to 50% in 2025.Nitrous oxide, Nitrous oxide has three well‑established psychoactive properties, (i) it alters consciousness and perception,(ii) It produces dissociation, euphoria, and anxiolysis, and (iii) It impairs judgement, coordination, and memory formation. These properties are used to alter the pain threshold of the mother, who is informed that it is "safe and will not harm her unborn child". Nitrous oxide, though, also has another, non-reversible activity, it permanently inactivates one of the most crucial enzymes in the body, methionine synthase. As such it is one of the three causes of vitamin B12 deficiency mediated, developmental delay.

The concept that autism, or developmental delay can be assessed at birth by the anaesthetist is fanciful at best. Hence, neonatal development ex utero starts once the baby is born, hence it would be impossible to gauge whether the child has been affected by nitrous oxide or not, as there would be no development that would be assessable in the first hour, day or even week after birth. In addition, the assessment of autism, is a behavioural assessment carried out by a trained psychiatrist (under the GSM-5 criteria), and would definitely fall outside the remit, or experience of an anaesthetist.

The concept that the foetus would not be affected by nitrous is equally as fanciful and is based on the illogical assumption that nitrous oxide can in some way ONLY affect the NMDA receptors of the mother, and in no way affect the interaction of nitrous oxide with Co(I)B12 within methionine synthase, and thereby not affect methionine synthase activity of the foetus. In addition, the effect on the foetus is not only likely to be more than that on the mother, it most assuredly would be. Hence, the duality of nitrous oxide activity would mean that as the mother is receiving pain relief and euphoria from the reaction of nitrous oxide with the NMDA receptor, the foetal methionine synthase would, in a time and dose dependent fashion, be progressively inactivated with every breath of nitrous oxide that the mother takes. In addition, that whilst the nitrous oxide can be expelled rapidly by the lungs of the mother, no such process occurs in the foetus, rather, the accumulated nitrous oxide in the foetus would act as a delayed release depot for transplacentally acquired nitrous oxide, resulting from the mother’s repeated inhalation. .

It is not scientifically defensible to infer long‑term neurodevelopmental safety of fetal nitrous oxide exposure from normal neonatal appearance or short‑term postnatal observations. Autism, developmental delay, and other neurodevelopmental conditions are behavioural diagnoses made months to years after birth using structured criteria and specialist assessment. They cannot be identified in the first hour, day, or even week of life, and their assessment lies entirely outside the remit and expertise of the anaesthetist.

Consequently, reassurance based on a normal neonatal examination provides no meaningful evidence regarding the absence of long‑term neurodevelopmental effects of nitrous oxide exposure in utero.

Equally problematic is the implicit assumption—sometimes stated, sometimes simply presumed—that nitrous oxide can act selectively on maternal NMDA receptors without materially affecting the fetus. This assumption is not supported by basic physiology or biochemistry. Nitrous oxide is a small, inert gas that crosses the placenta freely. The same molecule that produces maternal analgesia and euphoria via NMDA receptor antagonism is also known to irreversibly inactivate methionine synthase by oxidising the Co(I) form of methylcobalamin, and forming NO-Co(III)B12, which totally inactivates methionine synthase..

Fetal methionine synthase activity is lower at baseline and more vulnerable to inhibition than maternal enzyme at the same exposure. Thus, while the mother experiences transient, reversible analgesia as her brain nitrous oxide concentration rises and falls with each inhalation, the foetus is subjected to a cumulative, time‑dependent inactivation of methionine synthase throughout the exposure period.

Although nitrous oxide is rapidly eliminated via the maternal lungs once administration ceases, the fetus has no independent route of excretion. Fetal elimination depends entirely on placental transfer back into the maternal circulation. During ongoing maternal use, this results in a state of continuous fetal exposure, even as maternal brain concentrations fluctuate in a wave‑like pattern.

Taken together, these considerations make it untenable to claim that the fetus is unaffected by nitrous oxide, or that normal short‑term neonatal observations can be taken as evidence of long‑term neurodevelopmental safety. Any assertion to the contrary rests on assumptions that are physiologically implausible and inconsistent with established biochemical mechanisms."

The problem with nitrous oxide though is that it is toxic to the foetus,

1. The foetus is exposed to a psychoactive agent without benefit The mother receives analgesia and altered perception. The foetus receives only biochemical disruption, and the inevitable and continuing inactivation of methionine synthase..

2. The foetus is exposed at a time when psychoactive effects are maximally harmful. During late gestation, the brain is undergoing: (i) neuronal migration, (ii) dendritic arborisation, (iii) synaptic wiring (iv) methylation‑dependent gene regulation

A psychoactive agent that alters neurotransmission or methylation at this stage is not benign.

3. The Schedule 6 classification implicitly recognizes nitrous as both toxic and psychoactive, The warnings required on consumer products explicitly reference: (i) inhalation risks,  (ii) neurological effects, (iii) altered mental state (iv) harm to minors

Yet obstetric practice exposes the foetus — a minor — to the same substance that is both toxic and psychoactive at 50% concentration to an adult.

Nitrous oxide has never been properly evaluated for use in pregnancy. Its current use is a historical artefact, not an evidence‑based practice. The Schedule 6 classification now makes this regulatory gap untenable

Do not for one minute believe that the anaesthetic profession has the mother and baby's best interests at heart. If they did they would advise against any use of nitrous oxide.

Vitamin B12 deficiency and Nitrous oxide and anaesthetics. 

Methionine synthase binds to MethylCo(III)B12 which subsequently acts as a Methyl Donor to convert Homocysteine to Methionine, and the resultant Co(I)B12 can act as an acceptor for incoming methyl groups such as those on 5-methyltetrahydrofolate.

MethylCo(III)B12 + Homocysteine [Methionine Synthase] <=> Co(I)B12 + Methionine

Co(I)B12 + 5MTHF [Methionine Synthase] <=> MethylCo(III)B12 + THF

During the methylation reaction of MethylCo(III)B12 + Homocysteine [Methionine Synthase], the product, Co(I)B12 + Methionine is formed. In the absence of 5MTHF, the Co(I)B12 is oxidized to Co(II)B12.This can them be rescued by Methionine Synthase reductase (MTRR) with FMN/FAD/NAD as co-factors. This donor/acceptor function can be dramatically reduced through exposure to nitrous oxide either as an anaesthetic or though inhalation from a "Nang" or "whippit", which can then have disastrous affects on the function of vitamin B12, and its role in methylation. Hence, in the absence of sufficient 5MTHF Co(I)B12 will build up. Co(I)B12 then is reduced to Co(II)B12 and in FMN/FAD absence intracellular Co(I)B12 and Co(II)B12 and can readily react with nitrous oxide to form NO-Co(III)B12, which is inactive, yet will “clog up” methylation by Methionine synthase, and irreversibly inactivate the enzyme, hence explaining the toxicity of nitrous oxide. The NO-Co(III)cobalamin has an extremely long half-life and is resistant to loss of the NO moiety, meaning that the child may be "stuck" with it for life time.

Co(I)B12 + Nitrous Oxide <=> NO-Co(III)B12

Normally, in the absence of incoming folate, Co(I)B12 is reduced to Co(II)B12 and MethylCo(III)B12 is formed by the action of MTRR and SAM. If this does not occur, methionine synthase releases Co(II)B12 and thereby frees up the binding site for MethylCo(III)B12. The Co(II)B12 then is secreted into serum and so contributes to the elevated serum B12 levels. Unless functional B12 markers, such as MMA and homocysteine are measured it is not possible to tell if the vitamin B12 is functionally active or inactive. Hence Paradoxical B12 deficiency will result. Thus, poisoning with nitrous oxide is very different to functional B12 deficiency due to folate, or functional B2 deficiency, in that whilst Co(II)B12 or Co(I)B12 can be converted to MethylCo(III)B12, thereby restoring activity of the [MethylCo(III)B12-methionine synthase] complex, NO-Co(III)B12 cannot be displaced and thereby regenerate the activity of the enzyme.

Higher levels of Co(I)B12 are present in functional B2 deficiency, such as occurs in Iodine, Selenium and/or Molybdenum deficiency, due to lack of activity of the FAD/NADH-dependent MTHFR enzyme, particularly in those with mutations in the MTHFR protein, or in those with a diet low in folate, thereby making those individuals more susceptible to the action of nitrous oxide. The inactive NO-Co(III)B12 would be indistinguishable from inactive Co(II)B12, and when measured in the current total serum B12 and the inappropriately named active B12 tests, as they do not distinguish which analogue of cobalamin is being measured, cyanocobalamin, hydroxycobalamin, methylcobalamin, adenosylcobalamin, Co(II)cobalamin, Co(I)cobalamin, glutathionyl-Co(III)cobalamin or cysteinyl(III)cobalamin, to name but a few. An indication of the extent of damage that nitrous can do to the nervous system can be gleaned from those who use Nangs, and their devastating neurological consequences. Reports of side-effects include “subacute-onset, progressive distal lower limb sensory symptoms and unsteadiness”, “subacute combined degeneration of the cord”” ataxia and progressive paresis”, depression, development of diseases of the brain, spine and nerves. The severity of these reactions has led the UK government to consider criminalizing the use of Nitrous Oxide. Curiously, this suggest has not been carried through and currently nitrous oxide is used over 70% of births in the UK Genetically, Nitrous oxide sensitivity should be higher in those with MTRR +/+ mutations, as is found for the following SNPs, MTRRG12099A, MTRRA66G, and in MTHFR mutations A1298C, and rs13306571..

N2O irreversibly inactivates methionine synthase in everyone

Nitrous oxide was commonly used as an anaesthetic gas, yet as long ago as 1956 (Lassen et al, 1956) it was realized that the activity of vitamin B12 was destroyed by nitrous oxide use and could cause megaloblastic anemia. In 1968, Banks and co-workers demonstrated that nitrous oxide could react with the cobalt in vitamin B12 and lead to the inactive NO-Co(III)B12 complex. The destruction of the activity of vitamin B12 is dependent upon the time and dose of administration of nitrous, with over 50% of individuals producing signs of megaloblastic depression of bone marrow function (Nunn and Chanarin, 1978). As early as 1978 (Amess et al, 1987) the use of nitrous oxide for anaesthesia was found to be contra-indicated, yet to this day it is still used, and many individuals report signs of B12 deficiency following use. Unbelievably, despite numerous publications showing poor outcomes of nitrous oxide use in pregnancy, and several demonstrating an association between nitrous and autism, and over 200 publications, demonstrating inactivation of vitamin B12 with subsequent sequelae, clinicians in the US, UK and Australia claim "“ Initiation and management of nitrous oxide by registered nurses is a safe and cost-effective option for labor pain.”. In the UK, up to 77% of patients use inhaled nitrous for labour analgesia(See PDF).  One of the problems with Nitrous inactivation of vitamin B12 activity is that the levels of B12 in serum still remain high, yet paradoxically the B12 is inactive - as per the discussion on paradoxical vitamin B12 deficiency. Unbelievably, nitrous oxide is still used as an anaesthetic to this day in the USA ,UK and Australia, both on mothers during pregnancy, and also on young children. Evidence suggests that this alone is responsible for many cases of autism (Xin et al, 2024). It has been known for over 40 years that the use of nitrous oxide in anaesthesia (laughing gas) or in recreational abuse, can cause vitamin B12 deficiency (Shah and Murphy, 2019: Tani etal, 2019; Oussalah etal, 2019; Chi, 2018; Stockton etal, 2017; Massey etal, 2016: Garakani etal, 2014; Safari etal, 2013; Chiang etal, 2013; Krajewski etal, 2007; Cohen etal, 2007; Jameson etal, 1999; Smith, 2001: Deleu etal, 2001; Mayall, 1999; Horne and Holloway, 1997: Kinsella and Green 1995; Carmel etal, 1993; Koblin etal,1990; O'Leary etal, 1985; van der Westhuyzen and Metz, 1984; 1982; Lumb etal, 1982; Kondo etal, 1981: Seteinberg etal, 1981; McKenna etal, 1980; Linnell  etal, 1978; Deacon  etal, 1978). Post surgical complications of the use of Nitrous include peripheral neuropathy  (Neuveu etal, 2019: Egan, 2018: Kaski etal, 2017; Richardson 2010),  metabolic encephalopathy (Vive etal, 2019), myeloneuropathy (Edigin etal, 2019; Friedlander and Davies, 2018; Alt etal, 2011; Waklawik etal, 2003; Sesso etal, 1999: Nestor and Stark, 1996), neuropathy (Gullestrup etal, 2019; Conaerts etal, 2017:Middleton and Roffers, 2018), pancytopenia (Norris and Mallia, 2019), Myopathy  (Williamson etal, 2019), myelopathy (Dong etal, 2019; Mancke etal, 2016;  Probasco etal, 2011: Hathout and El-Saden, 2011; Pema et al, 1998), severe neuropsychiatric symptoms (Lundin etal, 2019), combined degeneration of the spinal chord (Lan etal, 2019; Patel etal, 2018; Anderson etal, 2018; Antonucci, 2018; Keddie etal, 2018; El-sadawi etal, 2018; Yuan etal 2017: Buizert etal, 2017; Chen and Huang, 2016; Pugliese etal, 2015: Chaugny etal, 2014; Cheng  etal, 2013; Lin etal, 2011; Wijesekera, etal, 2009; Renaud etal, 2009: Wu etal, 2007; Ahn and Brown, 2005 Ilniczky etal, 2003: Beltramello etal, 1998: Rosener and DIchgans, 1996), neurotoxicity (Johnsonn etal, 2018), neuronopathy  (Morris etal, 2015), polyneuropathy (Alarcia etal, 1999), psychosis (Sethi et, al, 2006), dementia (El Otmani etal, 2007), ataxia (Miller etal, 2004), megaloblastic anemia (Barbosa etal, 2000), neurological impairment (McNeeely etal, 2000), neurologic decompensation (Felmet etal, 2000), neurologic degeneration (Flippo and Holder, 1993), spastic paraparesis (Lee etal, 1999). Curiously, Nitrous is still recommended by the American Association of Anesthesiologists, NSW Department of Health, and the Association of Anesthesiologists, the New Zealand College of Midwives..  In fact, several countries with high standards of healthcare, such as Canada, Sweden, Australia, Finland, and the United Kingdom, use a blend of 50% oxygen and 50% nitrous oxide to treat pain during labour. Whilst they do not express concerns about potential damage to the newborn, they do, however, express concerns about the potential effect on Global warming, which is of greater concern than the effect on the neonatal brain!!  The rational appears to be due to the replacement of epidural medication, with its risk on the spine, with the nitrous oxide. This attitude typifies the medical profession, treat the problem now, worry about the side effects later. We have contacted numerous hospitals, the Royal Children's Hospital Melbourne, Mayo Clinic Kopabirth, NZ College of Midwives, midwife associations, The America Pregnancy Association, Queensland Government, The Royal Australian and New Zealand College of Gynecology ("Excellence in women's health"), Doctors for the Environment and anaesthesiologists expressing our concerns yet not one has "returned our call". Atrocious!! Interestingly, the increase in the use of Nitrous from around 1% of births in 1980, in 2011-2014 when it is was 12% to 35=55% of births in 2024, has paralleled the rise in the rate of autism from <0.1% to now ~ 3%. In response to concerns about health, Dr Vitoria Eley of Queensland Department of Health "Great to see you engaging with the anaesthesia literature"..Queensland Government "Nitrous Oxide : Gas is safe for your baby..." Estimates suggest that if a woman chooses nitrous oxide, she has an 8-10% chance of having a baby who subsequently is diagnosed with autism, and a 25% chance of the child having ADHD or OCD. Use of Nitrous is so frequent that hospitals are using scrubbers to try to remove this greenhouse gas (Khan-Perez et al, 2022). Despite the well known dangers of Nitrous, institutions such as RANZCOG are still recommending the use of Nitrous to pregnant women. The American College of Obstetricians and Gynecologists have disregarded all the publications on the dangers and nitrous and have take the view that have decided that since there are no studies on the use of Nitrous and the neonate, that they will disregard the literature and instead of erring on the side of caution have dispelled the possibility of harm (Home | ACOG). "The use of N2O has increased in labor and delivery units across the United States since 2011. Despite inferior analgesic properties compared to epidural analgesia, N2O offers a safe alternative for many parturients who want a greater sense of control and mobility. Broughton etal, 2020). What is worse is that for many mothers, they receive information in baby classes, taught by nurses that claim nitrous to be safe.

When one examines the age ranges for both ASD and for AD, it is clear that there is some event that occurred, or some change that has occurred, since 1980, that has started the dramatic increase in the rate of autism. All of the children that we have data for who have ASD or ADHD, are functionally deficient in vitamin B12, with normal to elevated serum vitamin B12, and standard markers MMA, HVA, VMA, QA, KA, 5HIAA, pyroglutamic acid and phosphoric acid.

N2O inhibition of methionine synthase is rapid, potent, and irreversible inactivation in all if exposed for long enough, and harmful in a substantial proportion of patients that are not identified before exposure

A Schedule 6 Toxin in the Delivery Suite: Dose‑Dependent Methionine Synthase Inactivation in the Near‑Term Foetal Brain

There are several groups who have shown the deleterious effects of nitrous on the brain. Thus Selzer (2003) demonstrated increased susceptibly of those with MTHFR mutations to Nitrous Oxide, and Kalikiri and co-workers (2004) found a dramatic change in MMA and homocysteine levels in nitrous, as too Baum (2007). The study findings of a mechanistic link between nitric oxide levels and  are significant (Jackson, 2023). Prolonged misuse of nitrous oxide for recreational purposes can lead to spinal cord demyelination and loss of the ability to walk, neurologists have warned. 

Potential signs of deficiency in folate, or functional B12 would be any orofacial defects such as Cleft palate, tongue tie, difficulty feeding.

The extent of damage to the brain will be dependent upon how long the child was exposed to nitrous oxide, and at what stage their development was at. Hence areas of the brain that were most active at the time of exposure are most likely to be affected the most. At time of birth this would be cerebellum, followed after birth by the subcortical areas and then the cerebral cortex. Of note, Human foetal/neonatal and geriatric kinetics of inactivation and reactivation are unknown in any tissue.

N2O is the only inhaled anesthetic that will kill everyone who breathes it at clinical concentrations for 5-7 day

A Schedule 6 Toxin in the Delivery Suite: Direct Fetal Exposure via Maternal Inhalation — the Only Available Biological Delivery Route

Identification of Nitrous oxide intoxication 

Developmental delay, due to nitrous oxide intoxication is not detectable for months after the birth. Hence, statements, such "As does not harm the baby" have little to no verification. Whilst there is a scintilla of evidence about brain damage with nitrous oxide it would not be prudent to continue the practise, particularly since the association of increased use of nitrous parallels the increased rate of autism.

Deleterious consequences of nitrous are long-lasting, not “short acting”

Symptoms include Complete Regression into autism, The loss of developmental skills such as: Expressive and receptive language, Gross motor skills, Fine motor skills, reduced Cognitive skills, Overall neurological deterioration (skill loss may be permanent in some children). Examination of serum B12 will reveal normal to elevated serum B12, BUT, metabolic analysis by urinary OAT, or serum MMA and/or homocysteine, will reveal higher than normal levels, which are indicative of Paradoxical B12 deficiency (https://b12oils.com/paradoxical.htm ).Standard modes of identificaion of absolute vitamin B12 deficiency will miss paradoxical B12 deficiency. The so-called ACTIVE B12 test, a complete and utter waste of money, will generate a false result, as the transcobalamin will have inactive B12 in its binding site, and so come up as positive in the in appropriately named active B12 test.

Nitrous oxide intoxication and the mother

Evidence is mounting that whilst the mother may not show signs of nitrous intoxication at the time of birth, many show evidence of vitamin B12 deficiency later, with serum levels of vitamin B12 being raised. In these individuals markers of methyl B12 deficiency would be elevated homocysteine, as well as HVA, VMA, QA, KA, 5HIAA, pyroglutamic acid and phosphoric acid. Whilst the levels may be lower than in the child, the levels will persist and are unable to be changed by repeated high dosages of vitamin B12. Further, there is evidence that the inactive NO-Co(III)B12 may then be used to load the brain of subsequent children, who will then show signs of B12 deficiency at birth, regardless of whether nitrous oxide is delivered or not. Currently there have been no successful examples of dislodging NO-Co(III)B12 from the mother, who may subsequently suffer conditions such as Chronic Fatigue Syndrome, or early onset dementia. Hence even single usage of nitrous oxide during labour may have long lasting deleterious effects upon the mother and subsequent children. At this time the medical profession has shown a "No Mia Culpa" attitude, denying all knowledge of the risk of nitrous oxide and definitely not accepting any blame for the damage it has caused. This is totally contra to the Hippocratic Oath and its intension to "Do no harm". It is recommended that every mother who has had nitrous oxide during labour be tested for functional B12 deficiency, and that this be resolved before any attempt is made to have another child.

When Analgesia for the Mother Becomes Toxic Exposure for the Foetus: Rethinking Nitrous Oxide as a Schedule 6 Poison in Labour

Treatment of Nitrous oxide intoxication 

Treatment of Nitrous oxide inhalation is possible if it is done early, however, treatment has to be quick, or permanent damage is done. Successful treatment, though appears to occur mainly in those who had an absolute B12 deficiency,. Hence if the body normally has 300-350 pmol/ml transcobalamin-bound vitamin B12, but in deficiency it has less than 200 pmol/ml, then administering excess vitamin B12 will cause a reduced but functional sufficiency of vitamin B12. These people can be "rescued" by the addition of high doses of vitamin B12, incoming B12 will still show a response. However, in individuals with a saturated transport system and a deficiency in functional B2, and particularly in those with MTHFR and MTRR mutations, nitrous intoxication will affect all the B12, and so addition of excess B12 will not be effective. This has been noted by various workers, who have claimed some success in treatment of some of the individuals who had nitrous, but not all (Brunt et al, 2024; Boulin et al, 2025; Einsiedler et al, 2022; Zheng et al, 2020; Xiang et al, 2021) This, though, is not what happens following exposure during labour, and so the potential for treatment is lost, particularly given that diagnosis of neurological damage is not done until many months or even years later. There is hope though, but it depends upon making sure that you get any deficiencies such as functional B2 and B12 deficiencies right first, and then slowly let nature take its course. In those who are severely affected this may take years!!

Treatment should ensure that any Iodine, Selenium and/or Molybdenum deficiency is resolved. This is to ensure maximal activity of what little active methionine synthase enzyme there still is. A constant supply of methylCo(III)B12 is required to try to load the brain with as much methylCo(III)B12 as possible, so that any new methionine synthase that is synthesized has the active from of B12 around during synthesis. To further optimize the activity of residual methionine synthase, it is desirable to provide a constant supply of 5MTHF. This, though, is not so straight forwards. If one was to over-supplement with 5MTHF, the material will not be trapped within the cells as trapping of folate within the cell requires polyglutamination, and in order for that to occur, folate has to be within the folate cycle, and this can only occur by providing folate (folic acid), as 5MTHF has to be processed by methionine synthase before it is converted to Tetrahydrofolate, and given that methionine synthase activity is extremely low in nitrous oxide affected children, this method will be very inefficient. Further, supplying high dose 5MTHF will raise measured serum folate levels (of unknown identity), which is diagnostic of functional methionine synthase deficiency, but which is poorly understood by pathology labs and particularly by clinicians. Instead, it would be better to supply folic acid, which enters the folate cycle and is quickly converted to dihydrofolate, and then tetrahydrofolate, which is the normal analogue of folate that cycles within the cell. The THF can then contribute to various reactions within the folate cycle, it will be polyglutaminated and so stay within the cycle, and will provide a ready supply of THF for conversion to 5,10-methylene-THF, which will be processed by MTHFR to keep supplying 5MTHF for reaction with methionine synthase. The presence of the polyglutaminated "tail" will ensure that the THF is always available for modification, rather than being rapidly lost from the cell. Whilst folinic acid could potentially be used, it is much more expensive and does not provide any advantage to the child and has mainly been used as a folate derivative in persons being treated with methotrexate.

Say NO to the use of Nitrous.

Markers of functional B12 deficiency due to Nitrous oxide intoxication 

Markers of functional B12 deficiency would be very similar to those observed with with functional B2/B12 deficiency, and would include

  • Elevated or normal serum vitamin B12

  • Elevated MMA and homocysteine

  • Elevated neurotransmitter metabolites, HVA, VMA, QA, KA, 5HIAA

  • Elevated pyroglutamic acid

  • Reduced SAM:SAH ratio

  • Reduced GSH:GSSG ratio

  • Low serum creatinine

The most distinguishing features of Nitrous oxide toxicity is the

  • Lack of correlation between MMA and markers of Methyl B12 deficiency.

  • The ratio between MMA and HVA is less than 0.4 MMA;HVA.

  • Inability to resolve the methyl B12 deficiency markers by fixing the functional B2 markers.

Comparison of Methyl deficiency markers against MMA.

Neurotypical (left) vs ASD (right)

Comparison of MMA vs the methyl B12 deficiency markers HVA, VMA and QA in normal individuals reveals a close linear correlation. In comparison there was little correlation between HVA, VMA and QA and MMA in the ASD example. Data was collected over a 4 year period of treatment with Adenosyl/Methyl B12. In that period MMA levels decreased in both groups, and methyl deficiency markers reduced in the control, however, there was no evidence of change of Methyl B12 deficiency markers in the ASD individual.

Comparison of HVA to MMA between Nitrous affected autism child (left panel) and B12 deficient neurotypical individual (right panel) shows a considerable difference in the ratio of HVA:MMA. Hence, in the NT individual, HVA generally has a close relationship to MMA, with 2:1 being the highest ratio, , but in the nitrous oxide exposed child, the ratio of HVA:MMA varies considerable from 5:1 to 1.3: 1 with many data points >3:1. In addition, despite MMA being less than 1.0, in the nitrous affected child HVA has persisted above 3.0. In contrast the NT individual HVA was below 2.0 for most oft he data, and reached 1.2.

The data is commensurate with what is known about nitrous poisoning in babies. Hence, " babies affected by nitrous have a life long mental and often physical disability, requiring constant care, and repetitive medical and educational costs, often costing over $50,000 per year".

A Schedule 6 Poison in the Birth Room: The Fetus as the Involuntary End‑User of Maternal Nitrous Oxide

Effect of Nitrous on the brain 

Nitrous mainly affects areas of the brain involved in neurotransmission, sensory processing and cognitive function. Exposure to nitrous during delivery affects those areas under-rapid development and synaptic formation. Areas to be affected would be the Frontal Cortex, which affects executive functioning and decision making. Nitrous acts as an NMDA receptor antagonist and affects glutamatergic signaling, affecting attention, impulse control and higher cognitive functions. Nitrous affects dopaminergic functioning thereby causing movement disorders, and difficulties in co-ordination. Nitrous also affects the cerebellum, potentially affecting motor development and causing difficulties with balance. Nitrous also has been linked to subacute spinal degeneration, thereby resulting in neuropathy, weakness and altered reflexes.

Usage of nitrous in labour should be totally banned.

When a Schedule 6 Toxin Reaches the Foetal Brain: Maternal Inhalation as the Unintended Delivery Pathway

Thalidomide similarities 

In many ways the Nitrous "story" is similar to the Thalidomide story. Hence the drug was tested on women who were not pregnant, and was found to be safe. However, when it was administered as as a sedative and a treatment for morning sickness, with disastrous consequences. Potentially, though Nitrous is worse. Hence many of the thalidomide babies had limb deformities, they were otherwise OK. In contrast, babies that are affected by nitrous have a life long mental and often physical disability, requiring constant care, and repetitive medical and educational costs, often costing over $50,000 per annum.

Prevention of Nitrous oxide intoxication 

Obviously prevention involves total avoidance of nitrous oxide during pregnancy. This appears to be totally ignored by the medical profession. In Australia for instance, 80% of women in labour receive pain relief of which 52% use nitrous oxide. It is little wonder that the rates of autism and ADHD have sky-rocketed in the past 30 years. See Nitrous). Every mother that we have spoken to (9 at present), who had nitrous and who subsequently had a child diagnosed with autism, was told that nitrous oxide was safe. Further, and perhaps more worryingly, every web-site for obstetric nurses and maternal health care has also said the same. we have contacted many, and not one has replied. Comments from mothers include "however after my very long use of nitrous in labour (6 hours of more), my son later developed autism". "I had nitrous oxide as advised during my first birth.... My child has ASD". "I had it with both kids. Was low in B12 when pregnant with my second child (diagnosed ASD)". "I had nitrous oxide during labour with both my children, both autistic".

In what is arguably one of the best examples of cognitive dissonance, the Anaesthetic Society of Australia has  Not only failed to acknowledge the plethora of references describing the inactivation of the essential enzyme, methionine synthase by nitrous oxide, as well as the categorization of nitrous oxide as a Schedule 6 toxin, and the more recent publications on the linkage of the use of nitrous oxide to the subsequent development of autism in the babies born to mothers treated with nitrous oxide during labour, and the recent death of a young child by  nitrous oxide intoxication, and the multitude of examples of degeneration of the spine in recreational nitrous oxide users, rather it has failed to modify its practise of using nitrous oxide by proclaiming  that it will continue to use nitrous oxide until a clinical trial demonstrates that it harms the foetus during delivery.This "no mia culpa" attitude flies in the face of the Hippocratic oath, and more specifically ignores two of the major tenets of the oath (i) Non-maleficence, the avoidance of causing harm to patients, and (2) Prohibition of certain acts, which forbids administering poison... Hence administration of a Schedule 6 toxin to a minor (the foetus), subsequently resulting in brain damage and developmental delay of the soon to be born child.

Treatment of Nitrous oxide intoxication 

Treatment of nitrous oxide intoxication should begin as soon as possible by injection of large amounts of Methyl B12. If treatment is delayed, the RnB protocol (https://b12oils.com/rnbautism.htm ) should be used to ensure correction of functional B2 deficiency, and also high dose Adenosyl/Methyl B12, in the hope that the toxic NO-Co(III)B12 can be displaced. The longer the nitrous exposure and the longer the time until treatment is commenced, the less success there will be. For this reason, Prevention is Better than cure. The problem with treatment is that all forms of vitamin B12 in the body are bound up by B12 binding proteins, such as Haptocorrin, and Transcobalamin. The affinity (or binding strength) of these proteins are so high, that it is almost impossible to displace the bound vitamin B12 (of any analogue) with free vitamin B12. In addition, it has not been possible to displace the NO-Co(III)B12 with free MethylCo(III)B12. This effectively means that until the Methionine synthase is degraded, there is no possibility of fixing the Methyl Co(III)B12 deficiency. In addition, there is almost no transport of vitamin B12 into the brain, once the child is born, thus making displacement almost impossible.

Usage of nitrous in labour should be totally banned.

Further Comments.

Nitrous oxide (N2O) primarily affects brain regions involved in neurotransmission, sensory processing, and cognitive function. If exposure occurs during delivery, the areas most vulnerable would likely be those undergoing rapid development and synaptic formation. Based on current research, the following brain regions may be impacted:

1. Frontal Cortex (Executive Function & Decision-Making)

2. Basal Ganglia (Motor Control & Coordination)

3. Cerebellum (Balance & Motor Learning)

4. Default Mode Network (Self-Referential Thinking & Sensory Processing)

5. Spinal Cord (Peripheral Nervous System & Reflexes)

While these effects are hypothetical in the context of neonatal exposure, further research is needed to determine whether maternal NO use during labor has measurable impacts on newborn neurodevelopment. nitrous oxide (N2O) exposure can influence neuronal stem cell viability, but its effects depend on concentration and duration of exposure. Research suggests that nitric oxide (NO), a related molecule, plays a complex role in neural stem cell fate—sometimes promoting proliferation and other times inhibiting neurogenesis.

 

Effects of Nitrous Oxide on Neuronal Stem Cells

1. Neurogenesis inhibition

  • Studies indicate that NO exposure can divert neural stem cells away from neurogenesis, instead favouring astroglial differentiation
  • This shift could impact brain development and repair mechanisms
  • This could result in neuropathy, weakness, and altered reflexes.

2. Stem cell viability and Proliferation

  • Some research suggests that NO can stimulate neural stem cell proliferation, bypassing traditional growth factor pathways.
  • However, excessive NO production can lead to oxidative stress, DNA damage, and apoptosis

3. Potential implication for nitrous oxide exposure

  • If N₂O exposure mimics high NO levels, it could alter neural stem cell fate, potentially affecting brain development.
  • his raises questions about prenatal exposure and its impact on neurodevelopmental disorders.

The brain has a remarkable ability to recover and adapt, but the extent of recovery after nitrous oxide exposure during birth depends on several factors, including duration of exposure, severity of B12 inactivation, and individual metabolic resilience.

 

Potential for Recovery

Neuroplasticity & Repair Mechanisms:

Vitamin B12 Restoration:

Severity of Initial Damage:

Research Insights

Some studies suggest that early intervention can improve outcomes, but long-term effects of neonatal nitrous oxide exposure remain an area of ongoing investigation. These studies aim to correct functional B12 deficiency first before expecting significant neurological recovery, particularly in children. Since B12 is essential for methylation, DNA synthesis, and myelin formation, its absence or dysfunction can severely impact brain development and repair processes.

Why Fixing B12 Deficiency is Crucial for Recovery
  1. Methylation Restores Neurological Pathways:
    • B12-dependent methylation is essential for gene expression and neurotransmitter synthesis.
    • Without sufficient B12, key pathways involved in neural plasticity remain impaired.
  2. Myelin Repair Requires Functional B12:
    • B12 plays a crucial role in myelin maintenance, and its deficiency can lead to subacute combined degeneration.
    • Neurological recovery depends on remyelination, which cannot proceed until B12 function is restored.
  3. Developmental Delay Can Be Reversible if Addressed Early:
    • Studies suggest that early B12 correction can significantly improve cognitive function and motor skills in children.
    • However, prolonged deficiency may cause permanent impairments.
  4. Oxidative Stress & Cellular Energy Production:
    • B12 is critical for mitochondrial function, ensuring efficient energy production for neuronal repair.
    • Functional B12 deficiency contributes to oxidative stress, further damaging brain cells.

If a child has experienced prenatal or early-life nitrous oxide exposure, addressing B12 status as early as possible could maximize their potential for recovery.

Further: The partitioning of inhaled nitrous oxide (N2O) into fetal blood and brain compared to the mother's brain depends on several factors, including placental transfer, fetal circulation, and tissue solubility. In this regard, the brain of a neonate is around 12% total weight of the child, whilst that of an adult is around 2%, hence the effect on the neonate is likely to be 6 times higher than the mother.

1. Placental Transfer of N2O

2. Partitioning into Foetal Brain vs. Maternal Brain

3. Potential Effects on Fetal Brain Development

 Comparison of Nangs to Nitrous Oxide gas.

  1. Nangs are essentially small metal cylindrical bulbs that are filled with 8 gm of nitrous oxide gas. By comparison a full cylinder of nitrous oxide has a pressure of 745 psi and contains the equivalent of 1500 L of gas at atmospheric pressure and room temp. For recreational abuse some use 50-100 nangs per day, This is equivalent to 400-800 gm nitrous, whereas nitrous at room temp is 1.226kg/cubic meter.
  2. Nitrous preferentially reacts with Co(I)B12 in Methionine synthase, as it is only reduced to Co(II)B12 in MMA-CoA mutase.

 

Usage of nitrous in labour should be totally banned.

Comparison of Thalidomide to Nitrous Oxide gas.

  1. Potentially the damage caused by Nitrous oxide administration during Labour would be equal or greater to that seen following administration of Thalidomide to the mothers during pregnancy. One major difference, however, is that the toxic nature of Nitrous oxide to vitamin B12, has been established for years, and yet knowingly or unknowlingly the Medical profession has used nitrous "ad lib" during labour. and room temp. For recreational abuse some use 50-100 nangs per day, This is equivalent to 400-800 gm nitrous, whereas nitrous at room temp is 1.226kg/cubic meter.

    Recommendations to cease use of Nitrous Oxide

    In recent years, there have been recommendations to eliminate nitrous oxide from medical use due to its toxicity, possible increase in morbidity and mortality, and adverse environmental effects. (Dimic et al, 2023) . Of these reasons, the most pressing appears to be that nitrous is the fifth largest contributor to green-house gas emissions, rather than to damage to the brain of a child (Natale et al, 2026).

    Since October 2022 in Australia, nitrous oxide has been classified as a Schedule 6 poison, prohibited from supply to anyone under 16 due to its neurotoxic potential. Yet in obstetric practice, the same substance is administered in 50% concentration to pregnant women, resulting in involuntary foetal exposure at levels vastly exceeding occupational safety limits. The foetus — a minor under 16, unable to consent, and receiving no therapeutic benefit — is exposed to a Schedule 6 toxin at the moment of peak neurodevelopmental vulnerability. This appears inconsistent with both the intent and the letter of the Schedule 6 protections

    Further to this, the clinician or associated health care worker, due to their actions in supplying a Schedule 6 poison to a person under 16 would be legally liable for any damage that this incurs.

     Nitrous oxide, No Laughing Matter.

    During labour, the delivery of Nitrous oxide, occurs through an exquisitely maintained Pharmaceutical window with the mother carefully ensuring that levels of nitrous never drop below the minimum effective concentration of this Schedule 6 toxin. By comparison, the Pharmaceutical Industry has yet to design such a perfect delivery system as that of the mother receiving nitrous from her health professional.

    With every breath she takes, she ensures that she continuously bathes the brain of her foetus in the highly toxic, Schedule 6 toxin, nitrous oxide (One should be aware that it is illegal to give a Schedule 6 toxin to persons under the age of 16. Such a person would be the foetus, within the mother’s womb). Her search for pain relief means that the nitrous is continuously delivered at a concentration above the minimum toxic range, in an optimal delivery device, the mother. Unknowingly, the mother repeatedly breathes in a soothing gas containing 500,000 ppm of nitrous oxide, a mixture that is 20,000 times the safe upper environmental exposure limit, and delivers the nitrous, via the placenta to the soon to be delivered foetus.

    The brain of the foetus, though, is not the brain of the mother. In contrast to the mother’s highly developed brain, for the foetal brain, it is the start of its neurodevelopmental journey. During the 3rd trimester of pregnancy, it is primed for its peak of differentiation and synaptogenesis. With every breath of euphoria generating feeling of the mother, more and more damage is being inflicted on the foetal brain, ensuring that it becomes progressively less capable of developing normally and so ensures that if its development does proceed, it will be greatly delayed.

    In a scene akin to some gruesome horror movie, the mother repeatedly inhales mind-altering drugs in some attempt to alleviate the pain of childbirth, and with every breath, unknowingly, ensures the gradual destruction of the future cognitive and developmental capabilities of her soon to be born child.

    Meanwhile, trapped within in the womb, continually flooded with toxic nitrous oxide, the foetus cannot speak up to halt the intoxication, and for many, they never will be able to speak. Whilst it is highly unlikely that any mother would deliberately bathe the brain of her unborn child in toxic levels of a Schedule 6 toxin, this has effectively and irreversibly been what she has done.

    Little wonder, that some two to three years later, when her child fails to achieve its milestones and potential in life, she will not know or realize that she, and that she alone, is the reason for the child’s failure to develop. Something that will haunt her for the rest of her life.

    At that time, the people who advised her that nitrous oxide was perfectly safe for her and her unborn child will be long gone and will be adopting a “no mia culpa” attitude, denying any culpability for the regressed child.

    Little did she know, that the advice from those doctors, nurses and mid-wives, at the very time when she should have been able to depend upon them, and whom she trusted implicitly, was incorrect. Little did she know, that one decision on that day would completely change her life from one of joy and amazement and love of her child, to one of constant care, heartbreak, frustration and depression. A life, in which many times she will consider giving up her child to care by someone else, and in some instances even cause her and her family to commit murder and suicide. No, Nitrous is definitely no laughing matter, and should be avoided at all costs during those final hours of the foetus’ life, a life that was until that moment completely under her control.

    Class Action against Nitrous Oxide

    There is currently a class action for injured patients, families, and healthcare workers filed against providers and equipment manufacturers https://cassaction101.com/lawsuits/nitrous-oxide-lawsuit/

    Even if you signed a consent form during labour, you may file a nitrous oxide lawsuit, if the healthcare providers were negligent or failed to inform you of specific risks - such as permanent or delayed developmental due to inactivation of vitamin B12 through administration of nitrous oxide during labour. We have yet to find any hospital or Mid-wife institution that states how dangerous nitrous oxide can be.

    Hospital Negligence     https://monacosolicitors.com.au/service/hospital-negligence-lawyers/  https://monacosolicitors.com.au/service/birth-injury-lawyers/

    Nitrous use in the US

    In many ways, the current use of nitrous oxide in the US can be blamed upon the extensive work by Judith Bishop

    Today it is used by 60%to 75% of laboring women in countries such as the United Kingdom, Canada, Sweden, and New Zealand. The United States, however, was a late adapter. In 1999, in the United States this was all to change when Judith Rooks,CNM, MPH, FACNM, came into the picture

    The Campaign.

    In a campaign only rivalled by that of the tobacco industry, Judith Rooks, efforts were able to raise the use of nitrous oxide in labour from 1% to over 50% and also successfully raise the incidence of autism from 0.1% to 8% in the children from mothers who used nitrous. Rooks’ work single-handedly resulted in the destruction of the brains of millions of children. A spectacular success. Unfortunately, whilst the needs of the mother for pain relief were, little regards was taken to the outcomes of the brain’s of the children, who were then subjected to developmental delay and a life-time of care. At least the mothers had no pain at the time of birth, to the great relief of the anaesthetists and nurses who were pushing the use of nitrous oxide. Curiously, later when the “fruits of their labour” were revealed, these anaesthetists and nurses were nowhere to be found and denied that their insistence in the technique and their strong reassurance that it would do no harm to mother or baby. No mia culpa. Whilst the action of nitrous oxide as an NMDA receptor antagonist was not determined until 1998 (some 64 years after it was first used in labour) (Jevtović-Todorović, V., Todorovć, S., Mennerick, S. et al. Nitrous oxide (laughing gas) is an NMDA antagonist, neuroprotectant and neurotoxin. Nat Med 4, 460–463 (1998). https://doi.org/10.1038/nm0498-460),

    The action of nitrous oxide on vitamin B12 had been known since 1979 (Nunn, 1979l) with many clinical examples of toxicity known following that date (Vishnubhat et al, 1991; Cheng etal, 2013). In this regard, Rook’s work was arguably worse than that of the tobacco companies work on addiction and the use of cigarettes. When they started their campaign, the link to cancer was not known, whereas in Rook’s case, the action of nitrous oxide on vitamin B12 was well known. As is often the case, however, the medical profession with their accomplices totally ignored the science. In many regards, Judith Rooks could be regarded as the mother of modern autism in the US  Whilst it is assumed that many a mother who received pain relief as a result of her efforts, one can but wonder as to whether they would look equally as favourably on the 8% of children with autism and the 22% of children with AHDH, as a result of her efforts.

    Institutions contacted with no response..

    https://www.thewomens.org.au/

    Royal Children's Hospital Patient.info@rch.org.au

    Australian Medical Association ama@ama.com.au

    Autism Speaks, Autism CRC,

    Australian Society of Anaesthetists, Dr Simon Martel, Specialist Anaesthetist, Australian Society of Anaesthetists  contact@drmartel.com, Dr Suzanne Bowersbower@asa.org.au Bernard Rupasinghe - Policy and Public Affairs Manager. "Your views have been duly noted, and we value contributions from all members of the public on issues related to anaesthesia and patient care. Please be assured that your correspondence has been received and recorded. Should you wish to pursue this matter further, you may wish to to direct your concerns to the appropriate government authorities......" In other words, business as usual, we will not be changing our current treatments. Calculations on nitrous use in labour suggest that one four hour session with nitrous oxide is equivalent to 30 years of maximal work-related tolerated dose of 25 ppm!

    Clinical Excellence Queensland - Healthcare Improvement Unit. Basically have failed to realize the known toxicity of nitrous oxide, rather "Any consideration of changes to clinical guidance would occur only where the required evidentiary thresholds are met, including high-quality epidemiological evidence, prospective clinical studies, reproducible biochemical and mechanistic validated and demonstrated clinical causation rather than correlation" Response This is despite the warning on the https://health.qld.gov.au about Occupational health and safety for nitrous oxide "Prolonged occupational exposure may cause health issues for clinicians (eg reduced fertility, disrupted vitamin B12 synthesis)!! Curiously their recommendations are NOT for short duration, hence "Greater user satisfaction and more effective pain relief at 120 minutes when compared to opioid.." The response is typical of the medical fraternity, who somehow has the belief that despite their one in-house Occupational Health and Safety warnings about the use of nitrous oxide, and over 130 scientific publications on inactivation of vitamin B12 with nitrous oxide, and despite setting upper limits for nitrous oxide exposure to 25 ppm, allow the pregnant woman to imbibe 500,000 ppm nitrous oxide ad lib for hours, and then is of the illogical belief that it will do no harm to the foetus, which is continually bathed in a Schedule 6 toxin.

    Healthdirect Australia Clinical Governance Team "At present, specialist colleges and professional bodies in Australia continue to list nitrous oxide as an accepted option for pain relief in labour for most women when used in recommended doses and with appropriate monitoring."

    secretariat@oaa-anaes.ac.uk 14/05/2026 "Thank you for your information. We continue to review the international evidence base, and so we are grateful for your contribution. We will keep this on file and continue to consider any emerging evidence and developments in this area. At this stage, however, we do not feel there is sufficient evidence to change our current recommendations"

    Mayo Clinic OPX@mayo.edu 14/05/2026 Lily, Patient experience representative "Thank you for reaching out and sharing your concern with the Office of Patient Experience. We truly appreciate you bringing this to our attention. It is always our steadfast goal to provide excellent care and services to all our patients. Please be assured that your concerns will be thoughtfully shared with leadership for internal review and to inform our continuous process improvement efforts. Mayo Clinic values patient input and regularly partners with local teams and leadership to enhance the patient experience, including facility improvements, through a collaborative review process."

    Minister.Jammat@dpc.wa.gov.au, Minister.sanderson@dpc.wa.gov.au, Dr  Katherine Isoardi katherine.isoardi@health.qld.gov.au , Dr Froessler bernd.froessler@sa.gov.au; Minister of Health

    Curtin Education zoe.bradfield@curtin.edu.au

    NSW Health jan.fizzell@health.nsw.gov.au

    NSW Nurses & Midwives Association https://www.nswnma.asn.au gensec@nswnma.asn.au

    QLD Nurses & Midwives Union memberconnect@qnmu.org.au

    VIC Nurses and Midwives Association records@anmfvic.asn.au

    Clinical Practice Guidelines : Nitrous Oxide - oxygen mix

    Curiously the Australian Journal of General Practice warns: Nitrous oxide exerts its neurotoxicity through vitamin B12 inactivation, which disrupts myelin sheath maintenance, leading to peripheral and central nervous system demyelination. See Nitrous) Yet despite this both the Royal Women's Hospital  and Australian Institution of Health and Welfare, recommend Nitrous oxide, as too Mater Hospital. When contacted about the link to ASD and CFS in the mothers, Response from Bronwyn Jenner (General Manager/Director of Clinical Services) "I am writing to acknowledge the information you provided to the Mater regarding the use of nitrou oxide during labour. Thank you for taking the time to provide use with the information". This directly infers that either they did not have the information before, or they had it and were doing nothing about it. There are no warnings about nitrous on their web-site.

    Recommendations of Sydney Children's hospital

    Nitrous Oxide is known to interfere with Vitamin B12 and folate metabolism. • Megaloblastic bone marrow changes can be detected following exposures of several hours.

    Absolute contraindications • < 12 months or 10 kg. (one would presume that this would mean a child in the womb!!) Increased risk of nitrous oxide induced bone marrow suppression, neurotoxicity, or increased homocysteine level: methionine synthetase deficiency, homocystinuria and methylmalonic academia

    Recommendations from Royal Womens hospital - The gas given to women in labour is a mixture of nitrous oxide mixed with oxygen....There are no after effects for you or your baby. (Contacted)

    Mistaken beliefs

    Despite over 100 references on inactivation of vitamin B12 by nitrous oxide, there is the mistaken belief of some members of the anaesthetic association that "injury from a single episode of medical use is rare. The inactivation only affects the vitamin B12 at the time of exposure. Any new vitamin B12 and enzyme produced will not be affected, and so effects on vitamin B12 or methionine levels should be short lived". Clearly these individuals do not know that vitamin B12 loading of the brain predominantly happens in utero, and following this, transport into the brain is almost non-existent, hence new vitamin B12 will not even reach the brain.

    The future - it is not good

    If, as it is ascertained on this page, the increased use of nitrous oxide is responsible for the increased rate of autism, then for those who use nitrous oxide they have an 8% chance of having a child with autism, and a 22% chance of having a child with ADHD. Hardly something that should be ignored!!!! YET it has been by every Institution that we have contacted.

    Hazardous Chemical Information System.

    Recommends exposure to no more than 25 ppm. 50% nitrous is 20,000 times this amount! Upper limit 50 ppm. "This level was set to :prevent embryofetal toxicity in humans (resulting in an increased risk of spontaneous abortion) and significant decrements in human psychomotor and cognitive functions or other adverse health effects in exposed personnel".

    Queensland Health. "It is widely accepted the N2O has limited value in modern anaesthesia. Its declining use in anaesthesia is due partly to improved alternatives and partly to the growing environmental conscience of anaesthetists."

    Addendum on the use of Nitrous in Labour

    The recommended safety guidelines for exposure appear to have an upper limit of 25 ppm, but the pregnant woman receives a 50% mixture of Nitrous Oxide gas, which would be 500,000 ppm, so 20,000 times more than the upper recommended limit.

    The 25 ppm limit is an occupational exposure standard for ambient air in workplaces such as dental surgeries, operating theatres, and labour wards. It is designed to protect staff, not patients. This value appears consistently across authoritative sources:

    • Safe Work Australia lists a TWA (time‑weighted average) of 25 ppm for nitrous oxide.
    • NIOSH also recommends a REL of 25 ppm for waste anesthetic gas exposure.

    This means that over an 8‑hour shift, the average concentration of nitrous oxide in the room air should not exceed 25 ppm. In contrast, a labouring woman inhales a 50% nitrous oxide / 50% oxygen mixture from a demand‑valve mask. with  the inspired concentration is 500,000 ppm, thus the inhaled concentration is 20,000 times higher than the occupational exposure limit. The 500,000 ppm is the deliberate inspired concentration for the mother on demand. Mothers with a higher pain tolerance will inspire much less than those with a lower pain tolerance, The nitrous oxide, though is a dual action molecule, not only is it an NMDA receptor antagonist, it is also a neurotoxin and as time and dose increases more and more methionine synthase is inactivated as NO-Co(III)B12 is formed.

    In contrast to the mother, the fetus, is not a “patient” receiving analgesia, rather the fetus is an unintended recipient of a high‑dose anesthetic/neurotoxic gas with no therapeutic justification. A gas which NIOSH has explicitly stated that nitrous oxide exposure impairs cognitive and neuromotor performance.

    Further, in contrast to the mother, the fetus has: direct placental transfer of N2O, which has a higher brain‑to‑body ratio, immature detoxification systems, active neurodevelopmental processes, vulnerability to methionine synthase inhibition, and cannot readily expel the gas via its lungs.

     “Workplace safety authorities restrict nitrous oxide exposure for staff to 25 ppm, yet a labouring woman inhales 500,000 ppm — a concentration 20,000 times higher. The fetus, which receives no analgesic benefit and is uniquely vulnerable to methionine synthase inhibition, is exposed to the same concentration. This represents a profound inconsistency in safety standards.”

    Nitrous Oxide - A Schedule 6 poison

    Since 1 October, 2022, nitrous oxide for non-therapeutic use has been nationally classified as a Schedule 6 poison. In addition, as for ALL Schedule 6 poisons, nitrous oxide cannot be supplied to anyone under 16 years-of-age. In contrast, Nitrous oxide, used for therapeutic purposes, including for analgesia is nationally classified as a Schedule 4 medicine. This, though raises a new legal and ethical frame, in that there is a statutory principle "The protection of minors from involuntary exposure to a toxic inhalant." This effectively means that the Nitrous oxide, a Schedule 6 poison has been supplied to a minor without consent. The foetus is involuntarily exposed to the gas, from which it receives no therapeutic benefit. The nitrous has been supplied at 20,000 times higher than the occupational limit. The exposure is not incidental it has been knowingly, and clinically administered to the foetus. This exposue occurs during the period of highest neurodevelopmental vulnerability.

    The timing of nitrous exposure is critically important.

    The month before term is one of the most metabolically intense periods in human neurodevelopment, and the processes that dominate this window are precisely the ones most vulnerable to methyl‑B12 inhibition, methionine synthase blockade, and creatine‑dependent energy failure.

    Parts of the fetal brain that are most active in the month before term

    Late gestation (≈36–40 weeks) is dominated by three major neurodevelopmental processes:

    A. Rapid myelination (oligodendrocyte maturation)

    • Myelination accelerates sharply in the final month before birth.
    • Oligodendrocyte precursor cells differentiate and begin high‑rate lipid synthesis.
    • Myelin production is one of the most methylation‑intensive and creatine‑dependent processes in the body, with resultant high demand on Methionine synthase activity..

    In this regard Myelin synthesis requires:

    • S‑adenosylmethionine (SAM) for methylation of lipids
    • ATP‑intensive membrane production
    • Creatine‑phosphate buffering for high‑rate energy turnover

    Methionine synthase inhibition directly compromises all three.

    B. Synaptogenesis and dendritic arborisation

    This is the period when:

    • Synapse number explodes
    • Dendritic trees expand
    • Axonal pruning/refinement begins

    These processes require:

    • High methylation flux (DNA, RNA, protein methylation)
    • Creatine‑supported ATP buffering for vesicle cycling and cytoskeletal remodeling

    This is also when the cortex undergoes its final “wiring” phase.

    C. Growth of subcortical structures

    Particularly:

    • Basal ganglia
    • Thalamus
    • Cerebellum

    These regions are:

    • Highly metabolically active
    • Rich in mitochondria
    • Dependent on aconitase function (TCA cycle)
    • Sensitive to oxidative stress and B12‑dependent metabolism

    The cerebellum, in particular, undergoes a massive growth spurt in the last month before birth. Hence, these processes are more active as the foetus approaches term.

    Premature infants have less mature brains because these processes accelerate near term.

    The last 4–6 weeks include:

    • A doubling of cortical synapses
    • A surge in myelin‑related gene expression
    • Peak oligodendrocyte differentiation
    • Rapid cerebellar expansion
    • Finalisation of thalamocortical connectivity

     The closer to term, the more intense the neurodevelopmental activity — and the higher the metabolic and methylation demand.

    This means the fetus at 38–40 weeks is more vulnerable, not less.

    Higher neurodevelopment activity increases demand on methionine synthase

    A. Methylation demand skyrockets

    Late gestation requires:

    • DNA methylation for cell fate decisions
    • RNA methylation for translation control
    • Phospholipid methylation for myelin
    • Protein methylation for synaptic plasticity

    All of this depends on: Methionine synthase + SAM=> methylation + SAH

    Nitrous oxide irreversibly inactivates methyl‑B12, shutting down methionine synthase.

    B. Creatine synthesis depends on methylation

    Creatine synthesis requires:

    • Guanidinoacetate methyltransferase (GAMT)
    • One SAM molecule per creatine molecule

    So when methylation falters:

    • Creatine production drops
    • ATP buffering collapses
    • High‑energy tissues (brain, muscle, heart) suffer first

    This aligns with the observation that ASD children have lower serum creatinine.

    C. Aconitase and mitochondrial metabolism are also vulnerable

    Nitrous oxide exposure increases:Oxidative stress, Homocysteine, S‑nitrosylation

    Aconitase is exquisitely sensitive to these, impairing: :TCA cycle flux ATP generation, Neuronal energy stability

    The Foetus at term is under higher metabolic demand and therefore more vulnerable to nitrous oxide

    In the final month before birth, the fetal brain enters its most metabolically intense phase of development, characterised by rapid myelination, explosive synaptogenesis, and accelerated growth of the cerebellum, thalamus, and basal ganglia. These processes demand exceptionally high rates of methylation and creatine‑dependent energy buffering, both of which rely on uninterrupted methionine synthase activity. Nitrous oxide irreversibly inactivates methyl‑B12, shutting down methionine synthase at the very moment when the near‑term fetus requires maximal methylation flux to support membrane synthesis, dendritic arborisation, and neuronal energy stability. This creates a profound biological vulnerability: the fetus at term is not less sensitive to nitrous oxide but markedly more so, because its neurodevelopmental machinery is operating at peak intensity and therefore at peak dependence on the very pathways nitrous oxide disrupts. Perhaps one could not think of a more perfect time to inflict damage upon the child

    Rebuttal: Why Short‑Term Neonatal Assessment Cannot Be Used to Infer Long‑Term Neurodevelopmental Safety of Nitrous Oxide Exposure

    It is not scientifically defensible to infer long‑term neurodevelopmental safety of fetal nitrous oxide exposure from normal neonatal appearance or short‑term postnatal observations. Autism, developmental delay, and other neurodevelopmental conditions are behavioural diagnoses made months to years after birth using structured criteria and specialist assessment. They cannot be identified in the first hour, day, or even week of life, and their assessment lies entirely outside the remit and expertise of the anaesthetist.

    Consequently, reassurance based on a normal neonatal examination provides no meaningful evidence regarding the absence of long‑term neurodevelopmental effects of nitrous oxide exposure in utero.

    Equally problematic is the implicit assumption—sometimes stated, sometimes simply presumed—that nitrous oxide can act selectively on maternal NMDA receptors without materially affecting the fetus. This assumption is not supported by basic physiology or biochemistry. Nitrous oxide is a small, inert gas that crosses the placenta freely. The same molecule that produces maternal analgesia and euphoria via NMDA receptor antagonism is also known to irreversibly inactivate methionine synthase by oxidising the Co(I) form of methylcobalamin.

    Fetal methionine synthase activity is lower at baseline and more vulnerable to inhibition than maternal enzyme at the same exposure. Thus, while the mother experiences transient, reversible analgesia as her brain nitrous oxide concentration rises and falls with each inhalation, the fetus is subjected to a cumulative, time‑dependent inactivation of methionine synthase throughout the exposure period.

    Although nitrous oxide is rapidly eliminated via the maternal lungs once administration ceases, the fetus has no independent route of excretion. Fetal elimination depends entirely on placental transfer back into the maternal circulation. During ongoing maternal use, this results in a state of continuous fetal exposure, even as maternal brain concentrations fluctuate in a wave‑like pattern.

    Taken together, these considerations make it untenable to claim that the fetus is unaffected by nitrous oxide, or that normal short‑term neonatal observations can be taken as evidence of long‑term neurodevelopmental safety. Any assertion to the contrary rests on assumptions that are physiologically implausible and inconsistent with established biochemical mechanisms."

    The decision by the medical profession to ignore over 100 publications on the dangers of nitrous oxide, and its ability to irreversibly inactivate methionine synthase. And then openly advertise nitrous as being safe for mother and baby, has arguably been the most significant factor in the rapid increase in the rate of asd and adhd.

References

 

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