Elizabeth Thiele Would Know

Not only am I not a physiatrist, I’m not – contrary to what my diploma suggests – much of a scientist, either. I know just enough bio-chem and human physiology these days to be dangerous. Keep that in mind when I tell you:
 
I just came across (great?) news that researchers from Harvard Medical School and the Dana-Farber Cancer Institute have learned how a protein called BAD teams up, in certain instances, with potassium ion cell-channels in the brain to effectively SHUT DOWN THE ELECTRICAL STORM ASSOCIATED WITH EPILEPTIC SEIZURES. Their findings stem from what was known previously of the ketogenic diet (used for years to protect against seizures) and recent experiments tied to the ways in which glucose and fat byproducts are metabolized in the body.

This could represent a BIG, BAD BREAKTHROUGH in that it:

1. Appears to explain the molecular mechanics behind how and why the ketogenic diet works.
2. May lead to the development of new anti-seizure treatments.

The news was to have been published in the May 24 issue of the journal Neuron. I’m anxious to learn how it's been received, one month in.

I have an interest in both the ketogenic diet and something called the low glycemic index treatment (LGIT) -- the latter of which I believe could be a more palatable alternative, literally and figuratively, for my daughter. Elizabeth Thiele, professor of neurology at HMS and director of the Pediatric Epilepsy Program at MassGeneral Hospital for Children, was one of the developers of LGIT. She's also the wife of one of the BAD /potassium pathways researchers. I found this: Researchers Identify BAD as Key Seizure-Suppressing Protein while searching her name.

LGIT is similar to the ketogenic diet in that glucose plays a key role. With the ketogenic diet, you try to minimize the amount of glucose available for metabolism by eating a high-fat and low-carb diet. (using fat byproducts, a.k.a., ketone bodies, to fuel the brain) LGIT, on the other hand, is thought to work primarily via maintaining stable blood glucose levels.

If I’ve got those facts right, I'm wondering now: 

What, if anything, does this new research do specifically for LGIT? Does it validate it? Invalidate it? Offer additional hope? Open up new avenues for improving (the) treatment? 

I’d welcome your input!