Vitamin B12 and MND/ALS: Hope, science, and the impact of our genes.

research2693
Oct 28
6 min read

When the first symptoms of motor neurone disease (MND) appear — a weak hand, a twitching muscle, a stumble that feels “off” — life can suddenly divide into before and after.

MND can feel merciless, but science continues to search for signs of hope. One such sign comes from a nutrient most people associate with energy and tiredness: Vitamin B12.

An old vitamin with a new story

Vitamin B12 is not just another supplement. It acts like the body’s electrician, wiring and protecting the nervous system. Without it, the insulation around nerves (called myelin) begins to break down. Electrical signals then misfire, disrupting communication between the brain and body (Surendran et al., 2018).

Japanese researchers have explored an intriguing question: could large doses of Vitamin B12 protect motor neurones in MND? Their clinical trial tested ultra-high-dose methylcobalamin (50 mg injected twice weekly) in people newly diagnosed with amyotrophic lateral sclerosis (ALS), the most common form of MND. Participants who began treatment within one year of symptom onset experienced a 43% slower rate of functional decline compared with placebo (Oki et al., 2022).

In 2024, Japan’s Pharmaceuticals and Medical Devices Agency (PMDA) approved methylcobalamin for “slowing the progression of functional impairment in patients with ALS” (PMDA, 2024).

Although the official indication did not specify early-stage ALS, improvement was seen in participants treated within one year of symptom onset. This highlights that earlier intervention appears to provide the greatest benefit.

It represents a remarkable shift: a vitamin once used primarily for anaemia now showing pharmacological promise in a neurodegenerative condition.

How could vitamin B12 protect motor neurones?

Think of each motor neurone as a long electrical cable running from your spine to your muscles. It requires insulation, continuous maintenance, and a reliable energy source to function effectively.

Vitamin B12 supports all three of these processes. It helps to produce and repair myelin, fuels mitochondrial energy, and recycles homocysteine — a by-product that can damage cells if it accumulates (Surendran et al., 2018).

Laboratory studies show that high-dose B12 can slow neuronal damage and improve survival (Kaji et al., 2019). The JETALS human trial confirmed that when used pharmacologically, rather than simply as a nutrient, B12 can influence the pace of disease (Oki et al., 2022).

However, “slower decline” does not mean reversal. High-dose B12 may help protect remaining neurones rather than restore those already lost.

The genetic puzzle behind B12

Not everyone processes vitamin B12 in the same way. The body’s ability to absorb and activate it depends partly on genetic SNPs — the tiny differences in our DNA that make each of us unique.

One example is the FUT2 gene, which influences how sugars coat the gut lining and support beneficial bacteria. Certain variants, known as non-secretors, are linked to lower blood B12 levels (Hazra et al., 2008), as though some of the “docking stations” for absorption are missing.

Another gene, TCN2, produces the protein that transports B12 through the bloodstream. A common variation changes its shape slightly, meaning less B12 reaches cells even when blood levels appear normal (Miller et al., 2009).

Other genes, including MTR and MTRR, act like recyclers, keeping B12 active in the methylation cycle and preventing homocysteine from rising (Surendran et al., 2018).

When these genes function less efficiently, the body’s demand for B12 increases. Although research has not yet confirmed whether these variants predict who will respond best to high-dose B12, they help explain why the same nutrient can behave differently in different people.

When chemistry gets complicated: The mercury question

Some people worry that methylcobalamin — one form of vitamin B12 — might interact with mercury in the body and increase its toxicity. The concern makes sense: in nature, certain bacteria can convert mercury into methylmercury, a more harmful form that builds up in some fish (Cossa et al., 2022).

However, this process only occurs in bacteria, not humans. Those bacteria possess two genes, hgcA and hgcB, which allow them to add a methyl group to mercury (Parks et al., 2013). Human cells do not have these genes, so this transformation cannot occur in our bodies (Podar et al., 2015; Ruggiero et al., 2021).

In people, mercury is detoxified through a completely different process. The body binds it to glutathione — a natural antioxidant — and excretes it through the liver and kidneys (Clarkson & Magos, 2006; Cossa et al., 2022).

Even though methylcobalamin carries a methyl group, it cannot transfer it to mercury. Think of it as a key designed for a different lock — mercury simply is not that lock.

For people with higher mercury exposure, such as those who eat large predatory fish or have older dental fillings, some clinicians may prefer to use hydroxocobalamin, a non-methylated form of B12 that the body activates as needed (Podar et al., 2015). This is a precautionary choice rather than a sign that methyl-B12 is unsafe.

The evidence shows that methylcobalamin does not make mercury more toxic. Understanding the real chemistry helps replace fear with confidence.

Keeping perspective

It can be tempting to see vitamin B12 as the missing piece, but science teaches humility.

The strongest evidence currently applies to early-stage ALS, where high-dose injections appear most effective (Oki et al., 2022). Beyond that, research continues to evolve. Genetic studies (Hazra et al., 2008; Miller et al., 2009) and findings on detoxification pathways add depth, though not certainty.

Progress in medicine does not always come from new drugs; sometimes it comes from seeing an old molecule in a new light. Vitamin B12 is not a miracle cure, but it reminds us that the body holds extraordinary capacity for repair when given the right support.

Where You Nutrition Clinic fits

At You Nutrition Clinic, our practitioner Kerry combines nutrigenomics data, functional health markers, and the latest nutritional science to build a personalised understanding of each client’s unique biology - including B12 metabolism.

For someone living with MND/ALS, this may include exploring how genes influence B12 pathways, how diet affects inflammation and detoxification, and how subtle imbalances can be supported through nutrition and lifestyle.

If you would like to explore your own B12 pathways and other genetic profile, contact Kerry at You Nutrition Clinic for a personalised nutrigenomic consultation.

💬 Stay Connected

If you’d like to learn more about the clinic or connect with our practitioners, visit You Nutrition Clinic — where education, science, and personalised nutrition come together.

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References

Clarkson, T. W., & Magos, L. (2006). The toxicology of mercury and its chemical compounds. Critical Reviews in Toxicology, 36(8), 609–662. https://doi.org/10.1080/10408440600845619

Cossa, D., Heimbürger-Boavida, L. E., Liss, P. S., Mason, R. P., & Sonke, J. E. (2022). Mercury biogeochemical cycling in the ocean and policy implications. Nature Reviews Earth & Environment, 3(1), 42–58. https://doi.org/10.1038/s43017-021-00228-5

Hazra, A., Kraft, P., Selhub, J., Giovannucci, E. L., Thomas, G., Hoover, R. N., Chanock, S. J., & Hunter, D. J. (2008). Common variants of FUT2 are associated with plasma vitamin B12 levels. Nature Genetics, 40(10), 1160–1162. https://doi.org/10.1038/ng.210

Japan Pharmaceuticals and Medical Devices Agency (PMDA). (2024). Review report: Methylcobalamin injection for amyotrophic lateral sclerosis (ALS). Tokyo, Japan.

Kaji, R., Imai, T., Iwasaki, Y., et al. (2019). Ultra-high-dose methylcobalamin in amyotrophic lateral sclerosis: A long-term outcome study. Journal of Neurology, Neurosurgery & Psychiatry, 90(4), 451–457. https://doi.org/10.1136/jnnp-2018-318402

Miller, J. W., Ramos, M. I., Garrod, M. G., Flynn, M. A., Green, R., & Allen, L. H. (2009). Transcobalamin C776G genotype modifies the association between vitamin B12 and homocysteine in older adults. The Journal of Nutrition, 139(10), 1937–1942. https://doi.org/10.3945/jn.109.111922

Oki, R., Izumi, Y., Fujita, K., et al. (2022). Efficacy and safety of ultra-high-dose methylcobalamin in early-stage amyotrophic lateral sclerosis: A randomized clinical trial. JAMA Neurology, 79(6), 562–571. https://doi.org/10.1001/jamaneurol.2022.0901

Parks, J. M., Johs, A., Podar, M., Bridou, R., Hurt, R. A., Smith, S. D., Tomanicek, S. J., Qian, Y., Brown, S. D., Brandt, C. C., & Liang, L. (2013). The genetic basis for bacterial mercury methylation. Science, 339(6125), 1332–1335. https://doi.org/10.1126/science.1230667

Podar, M., Gilmour, C. C., Brandt, C. C., Smit, E., Johs, A., Hurt, R. A., Brown, S. D., & Parks, J. M. (2015). Global prevalence and distribution of genes and microorganisms involved in mercury methylation. Science Advances, 1(9), e1500675. https://doi.org/10.1126/sciadv.1500675

Ruggiero, L., Goni, F., & Arnaldi, P. (2021). Methylmercury exposure and detoxification in humans: Mechanisms, genetics, and clinical implications. Toxicology Letters, 348, 35–48. https://doi.org/10.1016/j.toxlet.2021.05.008

Surendran, S., Adaikalakoteswari, A., Saravanan, P., & Shenoy, A. (2018). An update on vitamin B12-related gene polymorphisms and B12 status. Genes & Nutrition, 13(2). https://doi.org/10.1186/s12263-018-0591-9