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The Link Between Nitrous Oxide Use and Vitamin B12 Deficiency

Nitrous oxide, also known as laughing gas, is an anesthetic that was first used in 1844 for dental surgery. It is still used in pediatrics and dentistry, in which nitrous oxide mixed with oxygen is delivered under controlled conditions, but increasingly the drug is used to get a “quick high.” Precise prevalence figures for this anesthetic are not known, although in the Global Drug Survey 10% of all respondents and 15% of Canadian respondents indicated they had used it in the previous year.

Scientists last year described a rare medical case where, due to regular intake of laughing gas, the patient lost the ability to walk. The man inhaled the drug every day for two months. This led to severe vitamin B12 deficiency. Treatment and complete cessation of drug use helped restore lost functions.

Now, scientists have confirmed this link: Regular consumption of nitrous oxide causes vitamin B12 deficiency. Study published V Canadian Medical Association Journal (CMAJ).

Doctors have found that nitrous oxide blocks the work of vitamin B12 (cobalamin). It chemically inactivates and leads to accumulation of its inactive form. Because of this, methionine synthase and methylmalonyl-CoA mutase (MCM) stop working – important enzymes, cofactor which is vitamin B12. With a deficiency of cobalamin, there is a violation of the formation of phospholipids, which are critical for the conductivity of nerve cells, and a violation of DNA synthesis.

Interaction between nitrous oxide and metabolic functions of vitamin B12 / ©CMAJ

Other hypotheses to explain the neurotoxicity of nitrous oxide involve the action of N-methyl-D-aspartate (NMDA) receptor antagonists, cytokine dysregulation, and growth factors that regulate myelin integrity and hypoxia resulting from long-term and heavy use of nitrous oxide.

The three most common sequelae were myelopathy (usually in the form of subacute combined degeneration of the cervical spine), neuropathy affecting the motor nerves, and encephalopathy, which is less common, easily overlooked, and often presents for the first time with psychiatric symptoms.

Moreover, for patients in whom nitrous oxide affected the brain, all these pathologies often occur. They usually present bilaterally. paresthesia, weakness and gait disturbances. A decreased or increased level of reflexes may be present, depending on whether the peripheral nerves or the spinal cord are more involved.

Less often, but still there are problems with the bladder: urinary retention or incontinence, strong urge to urinate. Ataxia is also detected ( violation of the coordination of movements of various muscles), Romberg’s symptom ( instability, staggering), Lermitte’s symptom (sensation of the passage of electric current through the spine when the head is tilted forward) and Babinski’s reflex (pathological foot extensor reflex). Neurological symptoms often develop acutely or subacutely after several weeks or months of nitrous oxide use.

Because nitrous oxide inactivates vitamin B12, it can also cause hematological problems. For example, megaloblastic macrocytic anemia occurs in 35–50% of chronic users. Less common are leukopenia and thrombocytopenia.

“Nitrous oxide toxicity should be considered in the differential diagnosis in all patients with signs and symptoms of peripheral neuropathy, myelopathy, or encephalopathy, especially at a young age. To confirm the diagnosis, it is important to know the history of nitrous oxide exposure and, in particular, heavy use, which underlines the importance of taking a detailed history of drug and substance use,” the authors noted.

Previously, scientists have discovered microorganisms that consume laughing gas as food and thereby fight global warming.

2023-08-21 11:37:25

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