One of the interesting things here (in the material referenced above) is the glutamate toxicity - excitotoxin toxicity. What do most diabetics consume lots of and encouraged by their healthcare providers? Aspartame. Aspartame is a HUGE inducer of glutamate toxicity. My client drinks a punch daily that is sweetened with aspartame. I told her I would try to find her something similar but sweetened with Stevia. I don't love it because of the dyes and maltodextrin, BUT a huge improvement over what she has been using (there are several other flavors, too):

Early in the conversation with my client, I asked her what her usual fasting blood sugar readings are. I nearly fell off my chair when she said "between 350 and 400." WHAT? Just to put that into perspective, here is what is considered normal for people over 20.

My client related that two years ago she was feeling very strange and went to an urgent care facility. Her blood sugar was over 500!! She was taken to the hospital by ambulance and placed on insulin and antibiotics. She was there for five days, while they tried to bring her blood sugar down. She was kept on an ice-chip-only diet. The blood sugar issue was not resolved, BUT she noticed that while she was on insulin in the hospital her vision was perfectly clear.

As far as my part in things, now that I look more closely into the study material referenced above, to the supplements I have already recommended, I will add magnesium-l-threonate, a form of magnesium that supports the brain beautifully, should help repair damage from glutamate toxicity and act as a protector from further damage.

In addition, serrapeptase, a proteolytic enzyme that clears scar tissue and cellular debris, including the beta-amyloid plaque found in Alzheimer's disease and here, in the information above, the eyes of people with glaucoma.

Adding to that, medium-chain triglyceride oil (MCT/think coconut) to provide ketone energy to the brain due to the insulin issues.

B Xuan 1, D A McClellan, R Moore, G C Y Chiou

Affiliations expand

Background: Various insulin delivery systems have been considered for systemic absorption other than injections. Although the ocular route has been suggested, its use is limited by the amount of insulin absorbed systemically via eyes. In order to improve the absorption rate of insulin into systemic circulations, the effects of pH and absorption enhancers were studied with rabbit eyes.

Methods: Insulin eye drops were instilled into eyes of rabbits, and their blood glucose levels were measured with a Glucoscan 200 Meter (Lifescan, Mountain View, CA).

Results: Systemic absorption of insulin via the ocular route was much more prominent at higher pH (8.0) than at lower pH (3.5). When absorption enhancers such as glycocholate and fusidic acid were added, the insulin absorption increased further markedly.

Conclusion: It is feasible to administer insulin through the eyes at pH 8.0 with low concentrations of glycocholate or fusidic acid to achieve the therapeutic efficacy of insulin to lower blood glucose to normal levels.

Jessica Agostinone, Luis Alarcon-Martinez, Clare Gamlin, Wan-Qing Yu, Rachel O L Wong, Adriana Di Polo

Brain, Volume 141, Issue 7, July 2018, Pages 1963–1980, https://doi.org/10.1093/brain/awy142

Published: 21 June 2018 Article history

Dendrite pathology and synapse disassembly are critical features of chronic neurodegenerative diseases. In spite of this, the capacity of injured neurons to regenerate dendrites has been largely ignored. Here, we show that, upon axonal injury, retinal ganglion cells undergo rapid dendritic retraction and massive synapse loss that preceded neuronal death. Human recombinant insulin, administered as eye drops or systemically after dendritic arbour shrinkage and prior to cell loss, promoted robust regeneration of dendrites and successful reconnection with presynaptic targets. Insulin-mediated regeneration of excitatory postsynaptic sites on retinal ganglion cell dendritic processes increased neuronal survival and rescued light-triggered retinal responses. Further, we show that axotomy-induced dendrite retraction triggered substantial loss of the mammalian target of rapamycin (mTOR) activity exclusively in retinal ganglion cells, and that insulin fully reversed this response. Targeted loss-of-function experiments revealed that insulin-dependent activation of mTOR complex 1 (mTORC1) is required for new dendritic branching to restore arbour complexity, while complex 2 (mTORC2) drives dendritic process extension thus re-establishing field area. Our findings demonstrate that neurons in the mammalian central nervous system have the intrinsic capacity to regenerate dendrites and synapses after injury, and provide a strong rationale for the use of insulin and/or its analogues as pro-regenerative therapeutics for intractable neurodegenerative diseases including glaucoma.

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