We’ve all heard the advice: eat your fruit and vegetables, get your vitamins, and stay healthy. For the most part, that guidance holds up. But some nutrients have a more complicated story, and vitamin B12 is a fascinating example.

Also known as cobalamin, B12 is essential for life. It helps the body produce red blood cells, keeps the nervous system functioning, and plays a central role in how cells copy and repair DNA.

B12 is found naturally in animal products such as meat, fish, eggs, milk and cheese. Some cereals and breads are also fortified with it, helping people who do not eat meat get enough. Most people following a varied diet get the recommended amount, but vegans, people with certain gut conditions and older adults who absorb nutrients less efficiently may need supplements.

Without enough B12, things can go wrong, sometimes seriously, especially if deficiency is not recognised and treated. Yet in recent years, researchers have been asking whether high levels of B12 intake or high levels of B12 in the blood could be linked to cancer.

Staying balanced

The body is constantly making new cells. Every time a cell divides, it needs to copy its DNA accurately. Vitamin B12 is critical to that process. When levels are too low, DNA can be copied incorrectly, leading to mutations that, over many years, may increase the risk of certain cancers, particularly colon cancer. This is why B12 deficiency is taken seriously.

A 2025 case-control study from Vietnam found what researchers described as a U-shaped relationship between B12 intake and cancer risk, with both lower and higher intakes associated with increased risk. Because this kind of study can show an association but cannot prove cause and effect, the takeaway is not that B12 is dangerous. It is that balance matters.

It might seem logical that if B12 helps healthy cells thrive, taking extra doses should offer extra protection against cancer. But research does not fully support this. Vitamin B12 supports cell growth generally, not only the growth of healthy cells. One concern is that, if pre-cancerous cells are already present, very high availability of growth-supporting nutrients such as B12 could, in theory, support their growth too. But this remains difficult to prove in humans.

Overall, studies of high-dose B vitamin supplements taken over long periods have not shown clear protective effects against cancer incidence or cancer deaths. One analysis did report a reduced risk of melanoma, but this was a cancer-specific finding rather than evidence that high-dose B vitamins prevent cancer generally. Some observational research has also suggested a slight increase in lung cancer risk linked to long-term, high-dose B6 and B12 supplementation, particularly among men and smokers, although this kind of study cannot prove that the supplements caused the cancers.

Doctors have noticed that many cancer patients show unusually high levels of B12 in their blood. This raises an important question: does elevated B12 contribute to cancer, or can cancer itself cause B12 levels to rise?

Research in 2022 concluded that high B12 in cancer patients is often an “epiphenomenon”. In other words, the vitamin appears alongside the disease but does not necessarily trigger it. Further research from 2024 reached a similar conclusion.

This effect is thought to involve two main mechanisms. First, tumours can affect the liver, which stores large amounts of B12. When the liver is damaged or under strain, it may release more B12 into the bloodstream. Second, some tumours may increase proteins that bind to B12 in the blood. This can push blood test readings higher without necessarily meaning the body’s cells are receiving or using more B12.

Useful indication

Researchers are also recognising that elevated B12 may not be a cause of cancer, but it could be a useful marker of whether cancer is present or progressing. A large 2026 study found that colon cancer patients with very high B12 levels survived a median of around five years, compared with nearly eleven years for those with normal levels.

Similar patterns have been found in oral cancer and in patients receiving immunotherapy, where elevated B12 has been associated with poorer outcomes. This means that unexplained, persistent high B12, especially when it is not caused by supplements, should not be ignored. It may point to liver disease, blood disorders or an underlying cancer that has not yet been detected.

For most people, this is not something to worry about. B12 from a normal diet containing meat, fish, eggs, dairy or fortified foods is not usually the issue: it is very difficult to consume too much B12 from food alone. Deficiency remains a more common and better-established problem than excess.

The concern is prolonged high-dose supplementation without medical advice, or a blood test showing persistently high B12 when someone is not taking supplements.

The broader message is simple: more is not always better. Cancer cannot be prevented by loading up on any single vitamin. Long-term habits matter more: eating a balanced diet, exercising regularly, avoiding smoking, protecting your skin and attending routine health screenings.

So what about vitamin B12? Get enough through food or supplementation if you need it, especially if you are vegan, older or have a condition that affects absorption. But leave the megadoses on the shelf unless a doctor advises them. With B12, as with many nutrients, the goal is not as much as possible. It is the right amount.

The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.

In 1950, two researchers noticed something that didn’t quite add up. Hector Chevigny, a writer who had lost his sight in adulthood, and psychologist Sydell Braverman were studying the psychological lives of blind people when they stumbled upon an intriguing pattern: schizophrenia, a serious mental illness affecting people across virtually every known society, appeared to be entirely absent in people who had been blind from birth.

The observation sat largely ignored for decades, held back by limited understanding of the disease and a lack of patient data. Then, in the early 2000s, large national health databases allowed researchers to follow entire populations from birth into adulthood, and the pattern held up.

The most rigorous evidence comes from a 2018 whole-population study tracking nearly half a million children born in Western Australia between 1980 and 2001. Of those, 1,870 developed schizophrenia, but not one of the 66 children with cortical blindness did.

That sample of blind children is small, but the pattern holds across more than 70 years of evidence: not a single congenitally blind person with schizophrenia has ever been reported. The protection seems to be specific to cortical blindness, which is caused by damage to the brain’s visual cortex.

People who lose their sight later in life, or whose blindness is caused by damage to the eyes rather than the brain, can still develop the condition. This makes it clear that blindness itself isn’t the deciding factor. Something specific about the visual brain is.

This might seem odd. Schizophrenia is most commonly associated with hearing voices or holding unusual beliefs, not with vision. But the explanation lies not in what people see, but in how the brain uses vision to make sense of the world.

Scientists now understand schizophrenia as, at least in part, a disorder of prediction. The brain is constantly generating expectations about its surroundings and checking them against signals from the senses. In schizophrenia, this process appears to go wrong. Weak or random signals are given too much weight. Coincidences feel significant. Thoughts can seem to come from somewhere outside oneself. The boundary between imagination and reality begins to blur.

A question of prediction

Vision plays a powerful role in shaping this system, particularly in early life. The visual cortex is one of the brain’s largest and most richly connected regions, involved not just in sight but in learning, attention and emotion. When it receives no input from birth, the brain develops differently. Brain imaging studies show that in people with congenital cortical blindness, this area is often repurposed for tasks such as language, memory and reasoning.

Some researchers believe this early reorganisation may offer a kind of protection. Without visual input generating a constant stream of ambiguous or unpredictable signals, the brain may settle into more stable ways of interpreting the world, reducing the risk of the misfiring predictions that characterise schizophrenia.

Timing matters enormously. Losing vision later in life, even in childhood, does not appear to offer the same protection. By then, the brain has already been shaped by years of visual experience.

None of this suggests that blindness could ever be a practical safeguard against schizophrenia. But it does open up new ways of thinking about the condition and potentially new ways of treating it.

Most current treatments target brain chemistry, particularly the dopamine system. These drugs help many people, but they don’t work for everyone and can carry significant side-effects. If schizophrenia is partly about how the brain learns to predict and interpret reality, then future treatments might also address perception, learning, and how the brain weighs up uncertain information.

Research is now looking at drugs that act on glutamate, a brain chemical involved in learning and communication between nerve cells. Glutamate systems are particularly active in the visual cortex and in circuits that help the brain filter out what’s important from what can be ignored. These aren’t treatments based on blindness itself, but on what congenital blindness reveals about how a stable, well-organised brain develops.

The field is still at an early stage. But the hope is that by better understanding brain development from the very beginning, scientists might one day find ways to reduce the risk of schizophrenia or prevent its most severe forms from taking hold.

Nearly a century later, the curious observation that Chevigny and Braverman had accidentally made continues to shape how scientists think about one of the most complex and least understood medical conditions.

The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.