I'm not sure from what group I snipped the original information of what
Dr. Atkins stated in NY but I did ask for further information and
this is what I received privately this morning, shown with the
authors standing permission to share his insights and comments:

<[log in to unmask]> wrote:

> "At a nutritional conference in New York City on Tues. 10/14/97,
> Dr. Atkins stated that he had success treating juvenile diabetes
> using the nutrient Calcium EAP along with a carbohydrate restricted
> diet."
>
> I know that a lowcarb diet goes a long way in helping to manage
> BG levels, reduce the risk of diabetic complications and/or if
> starting such a diet after complications have presented, a person
> can reasonably expect a degree of stabilization.
>
> But what is Calcium EAP and what might it do?
>

good question.
for the sake of argument assume EAP = AEP...and let us briefly visit the
land of mineral transporters.

calcium 2-AEP = calcium 2-aminoethylphosphoric acid.
2-AEP is a neurotransmitter that also functions as a mineral transporter
(as do aspartates, orotates, arginates); which means that the metal ion
chemically tied to to the transporter is liberated at a specific place
within a cell.

metalx 2-AEP is transported to the outer layer of the outer membrane of
a cell where the metalx is liberated and the 2-AEP is metabolized
within the cell membrane structure.

calcium 2-AEP is, (i believe), used in the treatment of MS in Germany.
its mode of action is protective of the myelin sheath that covers
nerve fibers against auto-immune aggression; that it functions in a similar
protective fashion for other cells is not too suprising given simply its
mode of action and, if you like, the long history of the use of certain
calcium-based mineral transporters in fighting autoimmune agression
(see Nieper, 1969).

there is considerable research into the use of the amino acid L-arginine
in niddm (see study abstract below) that may lead to more extensive use
of mineral transporters in the treatment of diabetes.
for treatment of vasodilation/insulin sensitivity problems in niddm it is
the mineral transporter form of L-arginine that will win the popularity
polls over the raw amino acid.   the rationale being that a very high
percentage
of people harbor the herpes virus and its dormancy/eruption is a function of
the ratio of L-arginine and another amino acid L-lysine, both of which are
commonly found in food.   excess L-arginine leads to a herpes outbreak and
that excess does not have to be very large at all.  the whole point of this
viral excursion is that whereas the naked, amino acid L-arginine may cause
a viral outbreak, the use of an arginate will not, all the while preserving
the desired beneficial effects.



Effects of low-dose L-arginine on insulin-mediated vasodilatation and
insulin sensitivity.
Wascher TC, Graier WF, Dittrich P, Hussain MA, Bahadori B, Wallner S, Toplak H
Department of Internal Medicine, Karl-Franzens University of Graz, Austria.
Eur J Clin Invest 1997 Aug; 27(8):690-695.2

abstract:
The present study was carried out to evaluate the effect of a low-dose
intravenous supplementation of L-arginine on insulin-mediated vasodilatation
and insulin sensitivity. The study was performed in healthy subjects (n = 7)
and patients with obesity (n = 9) and non-insulin-dependent diabetes
mellitus (NIDDM) (n = 9). Insulin-mediated vasodilatation was measured by
venous occlusion plethysmography during the insulin suppression test,
evaluating insulin sensitivity. Experiments were performed twice in each
subject in the presence or absence of a concomitant infusion of L-arginine
(0.52 mg kg-1 min-1). L-Arginine restored the imparied insulin-mediated
vasodilatation observed in obesity (22.4 +/- 4.1%, P < 0.01 vs. without
L-arginine) and NIDDM (20.3 +/- 3.2%, P < 0.01 vs. without L-arginine). In
healthy subjects, no effect on insulin mediated-vasodilatation was observed
(24.8 +/- 3.1% vs. 21.4 +/- 3.1%). Insulin sensitivity was improved
significantly (P < 0.001) in all three groups by infusion of L-arginine. No
effect of L-arginine was observed on insulin, insulin-like growth factor I
(IGF-I), free fatty acids (FFAs) or C-peptide levels during the insulin
suppression test. Our data indicate that defective insulin-mediated
vasodilatation in obesity and NIDDM can be normalized by intravenous
L-arginine. Furthermore, L-arginine improves insulin sensitivity in obese
patients and NIDDM patients as well as in healthy subjects, indicating a
possible mechanism that is different from the restoration of
insulin-mediated vasodilatation.


The anti-inflammatory and immune-inhibiting effects of calcium orotate on
bradythropic tissues;
Nieper, H.A;
Agressologie, (1969), 10(4): 349-54.