Disorders of Blood Sugar

Roberto Victor Illa, M.D.

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The below is the Forward from the newly published book The Illa Protocol (see full reference at end).

TH E   I L L A








For many years I have been aware that the guidelines for the treatment of diabetes mellitus taught to doctors have been scanty and largely in error. For that reason I began a re-evaluation of the medical literature on the topic about five years ago. What I found was astonishing.1,2 In this volume I will share my discoveries with you. What evolved was a multi-pronged approach to the metabolic abnormalities found in the diabetic patient rather than a linear trial and error approach centered around the lowering of the Hemoglobin A1c as promulgated by the American Diabetes Association and others.3

Each group of pharmacologic agents used in the treatment of diabetes has a unique mode of action, weaknesses and strengths. As you will see, when employed in a logical fashion, each can benefi t the patient to which they are matched. It is obvious to all professionals managing diabetes mellitus that not all medications are appropriate for all diabetics.

I will introduce you to a method of classifying your diabetic patients based on their quantitative responses to probe doses of medications appropriate for them. Selection of the proper medications is, in part, done through analysis of the line graph report derived from their home glucose meter. This inexpensive technique reduces the cost of laboratory tests and gives a more current view of the patient’s condition; as opposed to the HgbA1c, which “looks back” in time three months to indicate the average blood sugar in that time span. Because it is inherently retrospective it cannot be used a guide to the current state of the patient’s pancreatic beta cell mass.

However, frequent testing and graphing of the blood glucose provides a better guide to changes in medications which might need to be made. This day-by-day monitoring and adjustment of treatment will result in the desired reduction in both the excursions of blood glucose and the average blood glucose. Post-prandial hyperglycemia will be dampened or eliminated. Remarkably, this is achieved without inducing hypoglycemia.

There are a number of critical theoretical concepts that must be enunciated before we proceed.

  1. Even if a small amount of insulin is used to initiate therapy, the patient will not develop ketoacidosis. By “small” amount I mean a dose of insulin which is a fraction of what they will eventually need. However, this is true only if the patient is free from three things: (a) infection, (b) infl ammation (e.g. pancreatitis) and (c) dehydration. This understanding is liberating for the clinician, who can then proceed in a stepwise fashion from low dose to higher dose as dictated by the patient’s blood sugar response to treatment. (Tables are provided later in this book to guide your selection of dose.)

  2. Make changes slowly. Rapid, large changes upset the patient’s already fragile homeostatic process, and are likely to induce hypoglycemia at some point.

  3. Ketoacidosis will very likely be prevented by a number of agents directed toward the alpha cell, inhibiting its release of glucagon. Inappropriate postprandial release of glucagon is a cardinal fi nding in all diabetics.4 Thus, if a small amount of insulin is present and glucagon release is suppressed to some degree, release of ketoacids by the liver will be suppressed. In fact, it is useful to view diabetes as being initiated by an “alpha-cell disease process” with the complication of later exhaustion of the beta cells.

  4. Hypoglycemia is a double-edged sword. On the one hand it is dangerous to brain and pancreatic tissue5,6 and is to be studiously avoided. On the other hand, by anticipating hypoglycemia and being more sensitive to the variety of its symptomatic presentations, we use it as the primary indicator that a change in medication is needed. Thus, in this technique when any blood sugar reading falls to 90 mg% or below, the next day’s therapy is reduced; whether this be insulin or oral agents.

  5. The very last pharmacologic agent reduced in dose or stopped is the thiazolidinedione (TZD).

  6. TZD’s stimulate regeneration of pancreatic beta cells primarily.7 This has been shown in both animals and humans. They do not, for practical purposes, reduce “insulin resistance.” You may prove this to yourself by measuring a C-Peptide level on your patient before and after treating them with the Illa Protocol.

  7. Recurrent hypoglycemia reduces the response of counter-regulatory hormones, as a result of damage to alpha cells and other tissues.8 For example, catecholamine release may be impaired.

  8. Hypoglycemia unawareness as a result of previous episodes of hypoglycemia is commonplace. It is seen in both insulin overtreatment and patients overtreated with oral agents.

I have used Power Point slides in this volume to focus attention on key issues. By the time this volume is published software should be available to assist you in implementing the Illa Protocol. See my website at www.DiabetesControlTower.com.

Roberto Victor Illa, M.D.

1 September 2007


1. The DCCT Group. Epidemiology of severe hypoglycemia in the diabetes control and complications trial. The DCCT Research Group. 1991 Apr 90; 450-9.

2. Holman RR, Thorne KI, Farmer AJ, Davies MJ, Keenan JF, Paul S, Levy J.; the 4-T Study Group. Addition of Biphasic, Prandial or Basal Insulin to Oral Therapy in Type 2 Diabetes. NEJM 2007 Sep 21 (in print Oct. 25).

3. Grant RW, Wexler DJ, Watson AJ, Lester WT, Cagliero E, Campbell EG, Nathan DM. How Doctors Choose Medication to Treat Type II Diabetes: A National Survey of Specialists and Academic Generalists. Diabetes Care. 2007 Jun; 30(6):1440-1553.

4. Unger RH, et.al. Glucogone Physiology and Pathophysiology. NEJM. 1971 Aug 19; 285(8):443-449.

5. Cryer PE. Insulin Therapy and Hypoglycemia in Type 2 Diabetes Mellitus. Insulin. 2007 July 2(3):127-133.

6. Perros P, Deary IJ, Sellar, RJ, Best, JJ, Frier BM. Brain abnormalities demonstrated by magnetic resonance imaging in adult IDDM patients with and without a history of recurrent severe hypoglycemia. Diabetes Care. 1997 Jun; 20(6):1013-8.

7. Bell DS. Beta-cell rejuvenation with thiazolidinediones. Am J Med. 2003 Dec 8; 115 Suppl 8a:20s-23s.

8. Cryer PE. Mechanisms of hypoglycemia-associated autonomic failure and its component syndromes in diabetes. Diabetes. 2005 Dec; 54(12):3592-3601 (review).

The above is the Forward from the newly published book:

The Illa Protocol

Copyright © 2007 by Roberto Victor Illa, M.D. and Stanley Eric Lieberson, Ph.D.

Library of Congress Control Number: 2007907530

ISBN: Softcover 978-1-4257-8483-6

Hardcover 978-1-4257-8484-3

All rights reserved.

To order copies of this book, contact:

Xlibris Corporation