AbGAD

[Guest guest]

Long, long ago in a galaxy far, far away¹, I was a diabetologist (internal

medicine physician subspecializing in endocrinology and sub-subspecializing

in diabetes mellitus). I kept up with the literature before I joined the

Air Force, but because there are no diabetics on flying status (at least

none I was aware of), my interest in the area gradually gave way to more

relevant concerns. Nevertheless, I remember reading in the early 1990s

about " anti-glutamic acid decarboxylase antibodies " , then a relatively new

discovery in the pathogenesis of insulin-deficient or insulinopenic (Type 1)

diabetes.

So imagine my surprise when I recently received a letter from the PSVAHCS

(local VAMC) telling me that the Diabetes group there was inviting me to

participate in a Phase III-IV clinical trial study on a particular

medication in those with " pre-diabetes " ! I guess they searched through

computerized records of relevant lab data and pulled up any of us who met

their criteria. They invited me to call them. I did, and at least on the

basis of my history and other facts, I qualify for the study. When I get

back from DC, I'm going to arrange to go in for the initial screening (blood

tests and stuff). Of note, I haven't had any fasting blood glucose tests in

two or three years. Since diseases left to themselves characteristically

get worse over time, it'll be interesting to learn the results of my

screening tests.

I don't have any known risk factors for diabetes. I'm slightly overweight

by some standards, but at the upper limits of normal by others. In all

other respects, I don't fit the profile for classic hyperinsulinemic

diabetes (Type 2).

This sent me back to the literature, and I found some truly amazing

information. It seems that interest in antibodies to glutamic acid

decarboxylase has really accelerated in recent years. First, a recent paper

from the same local Puget Sound VA Health Care System-University of

Washington Diabetes group published a detailed review (including many of

their own previously-published clinical studies) on a type of diabetes

associated with elevated levels of anti-glutamic acid decarboxylase

antibodies. (These are actually known as anti-glutamate decarboxylase

antibodies, but are colloquially termed " AbGAD " because it makes a word of

sorts.) They creatively named it " Type 1.5 " , since it doesn't fit either

the strict definition for Type 1 or Type 2.

But AbGAD doesn't stop with diabetes. As I read further, it seems AbGAD is

now implicated in epilepsy, acquired cerebellar ataxia, other endocrine

autoimmune diseases, and is being investigated in many more. Every

AbGAD-related syndrome somehow involves " excitable " cells such as neurons,

muscles, pancreatic beta cells, and others. In the central nervous system,

AbGAD disrupts cells that produce gamma-amino butyric acid (GABA), an

important inhibitory neurotransmitter. It stands to reason that when

inhibitory influences decrease, excitatory stimulation takes over, producing

many of the neurological syndromes reported in those of us who received the

anthrax immunization.

AbGAD isn't the last word, of course. We have to keep looking for other

antibodies and as many other indicators of the immunological toxicity of the

anthrax immunization (Biothrax, Bioport) as we can. Some of these (like

anti-squalene antibodies) may or may not be indicative of anthrax

immunization toxicity, and may simply be indicators of exposure. Of

significance, AbGAD is of the immunoglobulin-G (IgG) class of antibodies, so

it may cross the placenta. If so, it might underlie the known

teratogenicity of the anthrax immunization. Meanwhile, in my admittedly not

humble opinion, AbGAD is a promising line of inquiry, and could help link

syndromes that are not obviously autoimmune (like epilepsy and other CNS

syndromes) definitively to the anthrax immunization.

The truth is out there!²

We will win this!

____________________

¹ The Jedi Chronicles

² Fox Mulder