1. Why anyone is looking for this at all
The premise is sound and it is the reason this field exists. Glaucoma can progress even when the pressure is well controlled. Lowering pressure is the only treatment there is, it demonstrably slows the disease, and it does not stop it in everyone. So the search is for something that protects the optic nerve itself — neuroprotection — rather than acting on pressure.
The nicotinamide hypothesis has a real mechanism behind it. Retinal ganglion cells have extraordinary energy demands. NAD+, the coenzyme those cells run on, declines with age. Nicotinamide is a precursor to NAD+. Give more of it, the argument runs, and you make the cells harder to kill.
2. What has actually been shown, in order of strength
| Study | What it was | What it found |
|---|---|---|
| Williams 2017, Science | Mice bred to develop glaucoma | Oral nicotinamide dramatically reduced the development of glaucoma. The finding that started the field — and it is a mouse finding |
| Hui 2020, Australia | Crossover randomised trial, 57 participants, 12 weeks, 3 g/day | Improved inner retinal function on electroretinography — the photopic negative response |
| De Moraes 2022, JAMA Ophthalmol | Phase 2 randomised trial, 32 participants, 9 weeks, nicotinamide 3 g/day plus calcium pyruvate | Median improvement of 8 visual field test locations against placebo |
| Phase 3, Columbia and Stanford | ~200 patients, 21 months | Still running. Results expected late 2027 |
| NAMinG (UK) | 1.5 g then 3 g/day, up to 27 months | Not reported |
| TGNT (Sweden and Australia) | Visual field progression over two years | Not reported; registered completion end-2026 |
Fifty-seven people and thirty-two people. Those are the two human trials this entire subject rests on, and both are short. That is not a criticism of the investigators — it is what phase 2 is for. It is a reason to be careful about what is being claimed on the strength of it.
3. What the specialty societies say, which is the most useful sentence available
In 2025 the American Glaucoma Society and the American Academy of Ophthalmology issued a joint position statement on nicotinamide, precisely because patients and doctors were asking. On the trial results above, it says that the endpoints are functional findings detectable in a research setting that do not consistently translate to visual recovery that is impactful to the patient.
That is two specialty bodies, writing about a treatment their own members are being asked for, saying the measurements moved and the patients did not notice. It is the single most informative statement on this page.
Graded Emerging. The mechanism is plausible, the animal work is striking, the human trials are small and positive on research endpoints, the definitive trial reports in late 2027, and nothing here is approved for treating glaucoma.
4. The dose is the part that needs saying plainly
The trials used 1.5 g/day escalating to 3.0 g/day. A typical multivitamin contains something like 16 mg. This is a pharmacological dose that happens to be sold as a supplement, roughly two hundred times a nutritional one, and the fact that you can buy it without asking anyone does not make it a nutritional decision.
- Nicotinamide, not niacin. Nicotinamide — niacinamide — is the form studied. Flushing niacin (nicotinic acid) at gram doses causes intense flushing and carries a recognised risk of hepatotoxicity. The two are not interchangeable and they sit next to each other on the shelf.
- The trials themselves treat it as a drug. NAMinG excludes anyone unwilling to stop taking over-the-counter B3 for the duration — which is a clearer statement about what gram doses are than anything on a supplement label.
- Liver monitoring is not optional at these doses. The trials monitored liver enzymes. Anyone taking grams of nicotinamide outside a trial should be doing so with a doctor who knows about it and is checking.
- It complements pressure-lowering treatment and does not replace it. Stopping drops in favour of a supplement would be the single worst thing a reader could take from this page.
Where this site's own view lands. This is the same shape as several arguments elsewhere here: a real mechanism, a genuine unmet need, small positive trials on surrogate endpoints, and a definitive trial not yet reported. The brain supplements chapter has just watched a very large trial move every biomarker and change nothing clinically. That is not a prediction about nicotinamide — it may well work. It is a reason to notice that we are at the stage of the argument where enthusiasm usually runs ahead, and that 2027 will answer this properly.
5. Breathing exercises and eye pressure
The other thing currently being promoted for glaucoma is slow-paced breathing, usually the “365” protocol: three sessions a day, six breaths per minute, five minutes each, sustained over about six weeks.
The trial behind it is real, and small. A single-centre randomised controlled trial in patients with early-to-moderate open-angle glaucoma, added to standard treatment, reported roughly an 11% reduction in intraocular pressure — about 2 mmHg — at six weeks, with lower serum cortisol and a measurable shift in heart rate variability toward parasympathetic dominance.
And three things about it need saying together.
- You cannot blind a breathing exercise. Participants knew which group they were in, and so did the people around them. Intraocular pressure is not immune to that.
- Pressure is a surrogate here too. This site treats surrogate endpoints the same way whether it likes the intervention or not — and a breathing exercise gets the same treatment as a drug. What matters is visual field preserved over years. That has not been measured.
- 2 mmHg is real but modest. It is a fraction of what a prostaglandin drop or SLT achieves, and it is an addition to those rather than an alternative.
Graded Emerging for a small adjunctive pressure reduction, and ungraded for preserving sight, because nobody has looked.
That said, the risk-benefit here is unusually favourable. Five minutes of slow breathing three times a day costs nothing, has no side effects, and has independent evidence behind it for stress and blood pressure — see the blood pressure chapter. If someone with glaucoma wants to do it alongside their treatment, there is no reason to talk them out of it. The objection is only to it being sold as a way to lower eye pressure naturally in place of something that works.