B12 And Blindness (But It's Not What You Think)

With a harrowing revelation at the end!

My vision has deteriorated for unknown reasons. It’s still not even bad enough to register on tests, but the subjective symptoms are nearly pathognomic for optic nerve damage. I’ll give a full update on that soon, but suffice to say I am still not having a good time. I’ve chalked it up to everything from the Lumina Probiotic to plain hysteria, but there’s one possibility that I find particularly interesting: Leber's Hereditary Optic Neuropathy. LHON is a mitochondrial disorder that essentially causes the retinal ganglion cells in your optic nerve to self-destruct around your mid-20s or so. It usually causes subacute central vision loss in one eye followed shortly by the other. The base rate on this is very low, especially when you’ve excluded two of the big three mutations that causes it, but it’s not a stretch to think that the mitochondria in my retinal ganglion cells might just be a little bit bad for other reasons and I’ve been stressing them hard enough that they’ve started showing subclinical signs of malaise. Maybe this happens to a lot of people but they just don’t notice the decline in color vision. Logically, the next step is to check risk factors for symptomatic conversion. It’s basically anything that puts additional stress on mitochondria: smoke in all forms most importantly, excessive drinking, a bunch of antibiotics (most likely it’s all of them, mitochondria are essentially just bacteria.) Anything that contains any cyanide.

But among that last category one substance stood out as particularly intriguing. I noticed that the Wikipedia articles on both LHON and Cyanocobalamin (The most commonly supplemented form of Vitamin B12) made careful note of the supposed harm it presents in early cases of LHON. Apparently taking the stuff can cause rapid optic nerve atrophy and instant blindness, presumably due to mitochondrial poisoning from the cyanide group. It sounds plausible, let’s check out the sources and become gravely concerned about our daily Red Bull habit…

First: Statpearls: Cyanocobalamin. This cites one particular study where one LHON patient was treated with cyanocobalamin… AFTER they developed rapid vision loss, proving ineffective.

[…] On examination the visual acuity of the right eye was 2/60 and that of the left 6/12, with a dense central scotoma in the right field of vision and a smaller cecocentral scotoma, more striking to a red target, in the left. The right optic disc was pale and the left edematous. […]

During the next 4 weeks the vision of the left eye deteriorated to 1/60 with an increase in the size of the central scotoma. There was striking bilateral optic atrophy. Leber’s hereditary optic atrophy was diagnosed when it was discovered that his maternal uncle had been diagnosed as a case of Leber’s hereditary optic atrophy in 1937, at the age of 36. The patient was registered as blind. The serum-vitamin-B12 level was 150 pg. per ml. (Euglena gracilis method) but other laboratory investigations were not significant.

He was treated first with cyanocobalamin 1 mg. intra-muscularly on alternate days for 2 weeks and then with prednisolone commencing with 40 mg. daily reducing to 5 mg. daily over 2 months, and thereafter at this dosage for 8 months longer, but the visual acuity remained unchanged.

They were then able to regain some vision after treatment with hydroxycobalamin, which can be used to detoxify cyanide already present in the body by binding it into cyanocobalamin which is much less toxic. This is speculated to be the reason treatment was effective, since the patient was a 40-cigarette-per-day smoker just like everyone in 1968. Hydroxocobalamin isn’t really known to be an effective treatment for LHON in general, I presume this patient probably had a mild case with low penetrance, a number of his RGCs were alive but disabled by the constant inhibition of cellular respiration from the cyanide in his cigarettes.

All the other sources on both Wikipedia articles either cite nothing or the same study. This is the only case in which cyanocobalamin treatment has been attempted for LHON, and it literally does not even back up the claim because nobody ever read the whole thing. This dire caution has even made it into the info pamphlets of various cyanocobalamin preparations.

The plausibility is there of course. LHON carriers are advised to avoid any and all potential sources of mitochondrial stress, even cooking fumes. An abundance of caution is reasonable when vision is at stake and cyanocobalamin does contain a cyanide group, but making the claim that individuals treated with cyanocobalamin are known to have suffered severe and rapid optic atrophy is seemingly just based on one paper that showed no such thing.

UNLESS

In one final twist… there actually is evidence that nobody anywhere has ever bothered to cite. It’s buried in a paper exploring the correlation of B12 deficiency and LHON conversion.

OOOOPS! Self-reported previous B12 supplementation is correlated to symptoms with p=0.009! Most commercially available B12 preparations are in cyanocobalamin form so it’s reasonable to assume that’s what’s happening here. I literally just realized this line was in this paper at the moment of writing, the conclusions just handwave it completely when it seems to me like the most important finding in the entire thing. I was leafing through it looking for evidence of no correlation to back up my prior conclusion, since that’s what I remembered from the last time I looked at it.

I think maybe people should be citing this instead, and more studies need to be done here. In reality I quit the energy drinks about a month ago out of an abundance of caution. The craving beat me for the first time today and I could swear colors are just a little bit even worse now. No reassurance to be found in the data today. Damn… my life sucks… can’t even have my Red Bull anymore.