B-complex vitamins, particularly B6, B9, B12, and choline when taken as supplements, could help slow the progression of glaucoma. These findings come from an experimental study published in Cell Reports Medicine and conducted by Karolinska Institutet in Stockholm, Sweden, which also indicates that elevated homocysteine may be a consequence rather than a cause of the disease, challenging previous theories.
If confirmed by further investigations, these results could position these nutrients as a potential therapeutic avenue for glaucoma—a condition characterized by the loss of retinal ganglion cells (RGCs), a leading cause of blindness for which there are currently no neuroprotective therapies. To evaluate whether this approach might work in humans, researchers launched a clinical trial enrolling patients with several glaucoma forms: primary open-angle glaucoma (the most common chronic form and typical in older adults); slow-progressing glaucoma; and pseudoexfoliation glaucoma with more rapid progression. Globally, glaucoma affects around 64 million people, including about a million in Italy, with roughly half of those affected unaware of their condition.
The Role of Homocysteine in Animal Models
Earlier literature appears to be in agreement about a role for homocysteine, an amino acid, in glaucoma development, with a potential synergistic effect from B vitamins—especially B12, B6, and folic acid. This cluster of nutrients would not only help break down homocysteine into other compounds essential for the body, but also convert homocysteine into two other amino acids: methionine and cysteine.
To test this idea, Swedish researchers conducted experiments in glaucoma-affected animal models given supplementation with vitamins B6, B9, B12 and choline, observing neuroprotective effects. Specifically, slowed progression of glaucoma in some animals and a halt to optic nerve damage in others.
In short, to explore and confirm the impact and/or role of elevated homocysteine levels in glaucoma, the researchers increased the amount of vitreous homocysteine, a factor raising retinal ganglion cell death by about 6% following ocular hypertension, thereby allowing them to observe that a genetic association with higher homocysteine does not influence glaucoma-related outcomes drawn from the UK Biobank, nor does it drive the progression of the glaucomatous visual field.
These results would therefore support the hypothesis that elevated homocysteine is a pathogenic feature, not a causal factor, of glaucoma. Additionally, they would show that homocysteine metabolism contributes to early dysregulation guided by the genes involved in carbon metabolism, interacting with essential cofactors and precursors (B6, B9, B12 and choline) throughout the retina, at the optic nerve head (optic disc) and at the retinal ganglion cells. In conclusion, the supplementation of these substances in animal models would promote neuroprotection in acute forms, preventing neurodegeneration by supporting visual function in chronic glaucoma models.
The Human Study
Exploration of these possible findings and the role of homocysteine in glaucoma patients yielded similar results in humans. Specifically, elevated levels of the molecule did not appear to influence disease progression, supporting a downstream role in glaucomatous pathology rather than acting as a trigger for the disease itself. Finally, identifying particular abnormalities in metabolic pathways—also in humans—including slowed retinal metabolism due to changes in vitamin intake, would support the involvement of metabolism in the onset of glaucoma.
Source
Tribble JR, Wong VHY, Stuart KW et al. Dysfunctional one-carbon metabolism identifies vitamins B6, B9, B12 and choline as neuroprotective in glaucoma. Cell Reports Medicine, 2025, Vol. 6, Issue 5, 102127. Doi: 10.1016/j.xcrm.2025.102127
Abbonati a Karla Miller
