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Two Subtypes of Diabetes Type 2 - 

Subtype 2A and Diabetes Subtype 2 B

Majid Ali, M.D.

In previous columns, I presented The Oxygen Model of Diabetes and the Crank-Crankshaft Model of Insulin Dysfunction.1-4 In my book entitled "Dr. Ali’s Plan for Reversing Diabetes," 5 I presented several insulin profiles and illustrated two subtypes of diabetes Type 2: diabetes Type 2A and diabetes Type 2B. Simply stated, diabetes Type 2A is a state of insulin toxicity created by insulin resistance and hyperinsulinism whereas diabetes Type 2B is an insulin-depletion state. In this article, I focus on the importance of subtyping diabetes type 2 and offer seven reasons for doing so, underscoring the profound clinical significance of the differences between the two subtypes.

In Tables 1-3, I present insulin and glucose profiles of three patients: (1) an individual in physiological insulin-glucose homeostasis; (2) a patient with diabetes Type 2A; and (3) a patient with diabetes Type 2B. Comparison of insulin profiles in Tables 2 and 3 illustrate the essential difference between the two subtypes. Later in this article, I present additional insulin and glucose profiles (Tables 4 and 5) to illustrate how diabetes Type 2A and Type 2B can be expected to respond to effective integrative de-diabetization management plans (outlined in a previous column and described at length in my book cited above).

 

Table 1. Insulin and Glucose Profiles of a 77-Yr-Old Metabolically Fit 5' 5" Man Weighing 133 Lbs. He Was Seen for Allergy Treatment.

6.23.2010

Fasting

1 Hr

2 Hr

3 Hr

Insulin

<2

24

29

30

Glucose

78

96

75

71

Table 2. Diabetes Type 2A. Insulin and Glucose Profiles of a 50-Yr-Old Man With Neuropathy and Prehypertension.

11.26.2012

Fasting

1 Hr

2 Hr

3 Hr

Insulin

13.2

73.0

178.7

56.4

Glucose

137

246

275

191

 

Table 3. Diabetes Type 2B. Insulin and Glucose Profiles of a 60-year-old 5' 10" Man Weighing 146 lbs With Hypertension, GERD, Recurrent Sinusitis

3.29.2010

Fasting

1 Hr

2 Hr

3 Hr

4 Hr

Insulin

<2

4

10

3

2

Glucose

104

300

166

62

69

 

Reasons for Subtyping Diabetes Type2

Diabetes Type 2A with insulin excess and diabetes Type 2B with insulin-depletion are quite different in their:

1. Basic natures of the disorder

2. Treatment goals of the disorder

3. Explanations of the disorder for the patient

4. Laboratory Tests for assessing treatment effectiveness

5, Expected duration of treatment for de-diabetization

6. Consequences of making exceptions in the dietary plans

7. Re-thinking insulin-dependent diabetes

1. Basic Nature of the Disorder

All clinical and pathological features in diabetes Type 2A are caused by the two primary lesions of insulin resistance and hyperinsulinemia. By contrast, metabolic derangements in diabetes Type 2B are caused by insulin deficit.

2. Treatment Goals for Diabetes Subtypes A and B

The primary treatment goal in diabetes Subtypes A and B is fundamentally different. The goal in subtype A is to restore insulin’s metabolic and energetic roles, and consequently lower its blood level. The primary treatment goal in diabetes Subtype B is exactly opposite of that: create islet cell conditions so insulin production can be resumed, as has been documented in experimental animal studies.

3. Explanations of the Disorder for the Patient

A core requirement for success in integrative medicine is to recruit the patient in her/his treatment plan for assuring strong compliance. This, of course, mandates that the patient not only be very well-informed but clear-eyed about the management plan. In my clinical work, I take time to explain that diabetes cannot be reversed, nor its complications prevented by focusing on blood sugar levels. These goals are only possible by focusing on insulin dynamics and precise insulin measurements.

4. Laboratory Tests for Assessing Treatment Effectiveness

I assess the effectiveness of my integrative plan with the following "Three-Step-Insulin-Testing" approach:

A. A 3-hour insulin and glucose profile following a standard glucose load before beginning the program

B. Fasting and one-hour post protein and fat food load insulin and glucose profile (a protein powder, lecithin, ground flaxseed, and organic vegetable juice are used for this purpose). Please Google "Dr. Ali’s Breakfast for details.

C. A 3-hour insulin and glucose profile following a standard glucose load one year after beginning the program.

The profiles obtained in step provides the patient the best indication of how her/his insulin response changes with an all protein and fat food load . The comparative study of the profiles in A and C categories provides a clear indication of the degree of "insulin optimizing" over a period of one year.

5. Expected Duration of Treatment for De-diabetization

Creating microecologic conditions for pancreatic regeneration in diabetes 2B requires a strong commitment both for the patient and the physician. A high level of patient compliance is needed long periods of time (several months or longer) for the reasons given above. The required program for addressing toxicities of foods, environment, and thoughts is much more demanding in diabetes 2B than in diabetes 2A. Lowering blood insulin levels by improving insulin receptor function (by "de-greasing the cell membrane") using dietary and detox measures can be achieved in most patients with diabetes 2A within some months.

6. Consequences of Making Exceptions in the Dietary Plans

Individuals on integrative de-debiatizing plans cannot always avoid making exceptions in their dietary and detox program. It follows from points made in item 5 that such exceptions (wrong food choices, missed supplements, neglected detox measures, and others) will exact a larger toll from patients with in diabetes 2B than on those with diabetes 2A. So this crucial aspect of recovery must be clearly understood by them.

7. Re-thinking Insulin-dependent Diabetes

The prevailing opinion among diabetologists and endocrinologists worldwide is that individuals with so-called insulin-dependent diabetes require insulin treatment for rest of their lives. This is unfortunate. In many such cases the use of insulin can be safely discontinued. In Table 6, I present data that supports my position.

Correcting Hyperinsulinemia By Freeing Up Insulin Receptor

Hyperinsulinemia is the result of insulin receptor dysfunction. The insulin receptor is a protein that criss-crosses the cell membrane like a cord, with one end protruding to the exterior and the other to the interior of the cell. In a previous paper, I offered the analogy of a crank and a crank-shaft to explain insulin resistance and hyperinsulinemia. In this analogy, insulin is visualized as a cranka device that transmits rotary motionand the insulin receptor protein as a crank-shaft embedded in the cell membrane. The cell membranes become resistant to insulin action when they become chemicalizedplasticized, so to speakand hardened, immobilizing the insulin receptors embedded in the membranes. One of the consequences of grease buildup on cell membranes is that insulin receptor becomes turned and twisted, literally and figuratively. In a previous paper, I offered the analogy of a crank and a crank-shaft to explain insulin resistance. I visualize insulin as a cranka device that transmits rotary motionand the insulin receptor protein as a crank-shaft embedded in the cell membrane.

The goal in my de-diabetization plan is to de-grease the cell membranes, free up the insulin receptors, restore insulin function, and so correct hyperinsulinemia. Data in Table 4 show how this goal is met in one case. Note the increased insulin efficiencyimproved insulin receptor function being the underlying change—as shown by lowering of one-hour blood insulin level from 107 to 44 concurrent with lowering of blood sugar levels.

Table 4. Diabetes Type 2B. Insulin and Glucose Profiles of a 55-year-old 5'5" Woman Eeighing 1234 lbs. With Headache, Fibromyalgia, Hypothyroidism, and Pruritis,

3.11.2010

Fasting

1 Hr

2 Hr

3 Hr

4 Hr

Insulin

13

107

85

17

 

Glucose

110

198

137

56

 

12.21.2011

 

10

44

     
 

109

171

     

 

Beta cell Regeneration for Diabetes Type 2B

 

Note the increased insulin production as shown by rising of two-hour blood insulin level from two to 22 while concurrently lowering of blood sugar level from 364 to 162.

The issue of insulin responses to sudden glucose (glucola for testing) and insulin-fiiendly meals is important. This patient is clearly not diabetic as shown by repeated A1c values below 5.8%. One can reasonable expect that response to glucola-like load will also improve with time as insulin homeostasis improves further.

 

Table 5. Diabetes Type 2B. Insulin and Glucose Profiles of a 51-yr-old yrs. 167 lb; 5'9" Man Weighing 167 lbs. Who was Treated With Metformin. For One Year Before Implementing the Plan. He discontinued Metformin Within Six Months of the Program. Subsequent A1c Values Stayed below 5.8%.

9.17..2011

Fasting

1 Hr

2 Hr

3 Hr

A1c

Insulin uIU

3

13

23

8

7.9

Glucose

130

246

229

125

 

4.7.2012

Insulin

8.8

24.2

38.2

 

6.5%

Glucose

137

241

182

   

9.26.2012

Insulin

10.9

29.6

42.6

19.4

5.6

Glucose

         

 

 

Table 6. Diabetes Type 2B. Insulin and Glucose Profiles of a 60-year-old 5' 10" Man Weighing 146 lbs With Hypertension, GERD, Recurrent Sinusitis Bertrum, Carlton 69-year-old 5' 9" man weighing 200. Lbs. Diabetes 10 yrs. hypertension, memory loss. A1c 8.0 to 6.2.

3.22..2010

Fasting

30 min

1 Hr

2 Hr

3 Hr

4 Hr

Insulin

9

19

2

3

15

12

Glucose

122

 

364

362

271

214

6.21.2011 (A1c dropped from 8.0% to 6.2%)

     

22

     
     

162

     

 

List of Tutorials

* Diabetes Pandemic

The Oxyegn Model of Diabetes

* DIabetes Reversal Case One

* Diabetes Reversal Case Two

Diabetes Reversal Case Three

*  Diabetes Reversal case Four - Beta cell Regeneration

 The Oxygen Model of Obesity

*    Insulin Evolutionary

* Seven Stages of Insulin Toxicity

* Prediabetes

* Subtypes of Diabetes Type 2

* Less Insulin, More Life

* Evidence for Insulin Toxicity

* If Mice Can Reverse Diabetes, Why Can't People?

* Dysox Explains the Exercise-Weight-Loss Disconnect

* Hypoglycemia: Diagnosis and Treatment


Insulin Toxicity
Weight and Obesity
Diabetes
Tutorial GG.16 The Dysox Model of Diabetes and De-Diabetization Potential. Townsend Letter-The examiner of Alternative Medicine. 2007; 286:137-145.

* Oxygen, Insulin Toxicity, Inflammation, And the Clinical Benefits of Chelation. Part I. Townsend Letter-The examiner of Alternative Medicine. 2009;315:105-109. October, 2009.

* Insulin Reduction and EDTA Chelation: Two Potent and Complementary Approaches For Preventing and Reversing Coronary Disease. Oxygen, Insulin Toxicity, Inflammation, and the Clinical Benefits of Chelation - Part II. Townsend Letter-The examiner

 

 

 

 

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