Glaucoma is associated with lower plasmatic nicotinamide levels

[pattismith]

Nicotinamide Deficiency in Primary Open-Angle Glaucoma
2019

Judith Kouassi Nzoughet; Juan Manuel Chao de la Barca; Khadidja Guehlouz; Stéphanie Leruez; Laurent Coulbault; Stéphane Allouche; Cinzia Bocca; Jeanne Muller; Patrizia Amati-Bonneau; Philippe Gohier; Dominique Bonneau; Gilles Simard; Dan Milea; Guy Lenaers; Vincent Procaccio; Pascal Reynier

Abstract

Purpose: To investigate the plasma concentration of nicotinamide in primary open-angle glaucoma (POAG).

Methods: Plasma of 34 POAG individuals was compared to that of 30 age- and sex-matched controls using a semiquantitative method based on liquid chromatography coupled to high-resolution mass spectrometry. Subsequently, an independent quantitative method, based on liquid chromatography coupled to mass spectrometry, was used to assess nicotinamide concentration in the plasma from the same initial cohort and from a replicative cohort of 20 POAG individuals and 15 controls.

Results: Using the semiquantitative method, the plasma nicotinamide concentration was significantly lower in the initial cohort of POAG individuals compared to controls and further confirmed in the same cohort, using the targeted quantitative method, with mean concentrations of 0.14 μM (median: 0.12 μM; range, 0.06–0.28 μM) in the POAG group (−30%; P = 0.022) and 0.19 μM (median: 0.18 μM; range, 0.08–0.47 μM) in the control group. The quantitative dosage also disclosed a significantly lower plasma nicotinamide concentration (−33%; P = 0.011) in the replicative cohort with mean concentrations of 0.14 μM (median: 0.14 μM; range, 0.09–0.25 μM) in the POAG group, and 0.19 μM (median: 0.21 μM; range, 0.09–0.26 μM) in the control


Conclusions: Glaucoma is associated with lower plasmatic nicotinamide levels, compared to controls, suggesting that nicotinamide supplementation might become a future therapeutic strategy. Further studies are needed, in larger cohorts, to confirm these preliminary findings.

 

[Mary]

Very interesting @pattismith - my dad had glaucoma and had to take drops for years and years, and a couple of my siblings have it. I get tested every year but am fine so far. I also take a lot of niacin at night for sleep - perhaps that's helping?

 

[pattismith]

Very interesting @pattismith - my dad had glaucoma and had to take drops for years and years, and a couple of my siblings have it. I get tested every year but am fine so far. I also take a lot of niacin at night for sleep - perhaps that's helping?

intraocular hypertension/high Intraocular pressure/High IOP runs in my mother's family and I am affected as well.
I also suspect I do have elevated intracranial pressure/High ICP/IIH when I stay supine, for at less one year. I have morning headache and dry eyes, but soon after I wake up, tears are coming and it lasts less than 1h00.
It happens now that I take high dose nacinamide riboside, I no longer have these morning symptoms for two days which is unusual.
So I did some investigations and found this interesting study above and also an interesting theory on IOP/ICP relationship :

CSF Theory of Glaucoma

Fleishman and Berdahl have postulated the CSF theory of glaucoma that defines that the balance between the two pressures (ICP and IOP) determines the TLPG. If the ICP is reduced or the IOP is increased, the TLPG will increase and the damage to the LC will appear, with an increase in ASLC depth and cupping of optic disk. The reverse effect of the CSF theory can be seen in clinical conditions like idiopathic intracranial hypertension (IIH) and ocular hypotony. All of these conditions cause an unbalanced anteriorly directed force either due to an elevated ICP and normal IOP (IIH) or a normal ICP and low IOP (ocular hypotony).
The net result is a negative cupping effect or swelling optic disk.
Patients with IIH may tend to have ocular hypertension to counterbalance the increased ICP, maintaining a homeostatic gradient.
It has been proposed that a clinically increased IOP may be a treatment option for patients with IIH.[18] (Fig.1) Health of the optic nerve head is maintained by a homeostatic pressure difference between the posteriorly directed IOP and an anteriorly directed ICP.

Another hypothesis trying to explain the correlation of low ICP with glaucoma progression is that CSF flow to the optic nerve is reduced or cutoff when ICP is low or IOP is high. Several studies in animal and human subjects did demonstrate reduction of CSF flow to the optic nerve in glaucoma and NTG subjects. [19][20][21]