Do You Know Your Diabetes 2 Subtypes?

Majid Ali, M.D.

Diabetes Type 2A and Diabetes Type 2B Are Two Different Problems and Need to be Managed Differently. 


Importance of Subtyping Diabetes Type 2

Into Diabetes Type 2A and Diabetes Type 2 B

(First published in Townsend Letter in April 2014)


In a previous column, I presented The Oxygen Model of Diabetes and the Crank-Crankshaft Model of Insulin Dysfunction.1 In my book entitled “Dr. Ali’s Plan for Reversing Diabetes,”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.



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



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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



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Reasons for Subtyping Diabetes Type2

Diabetes Type 2A with insulin excess and diabetes Type 2B with insulin-depletion arequite 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 5, I present data that supports my position.

Normalizing Insulin Homeostasis By Freeing Up Insulin Receptor

In my book on reversing diabetes,2 I established that 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 publications 1-3, 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 greased and chemicalizedplasticized, so to speakand hardened, immobilizing the insulin receptors embedded in the membranes. I introduced the term cellular grease for accumulation of oxidized lipids, misfolded proteins, altered sugars, molecular debris, and cellular waste caused by toxicities of foods, environment, and thought. One of the consequences of grease buildup on cell membranes is that insulin receptor becomes turned and twisted, literally and figuratively. The crank/crank-shaft model of insulin receptor dysfunction is based on my Oxygen Model of Inflammation and is supported by a large number of studies linking inflammation with peripheral insulin resistance.5-9

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.

Case Study 1

A 55-year-old 5’5″ woman weighing 234 lbs. consulted me for fibromyalgia, hypothyroidism, allergy, and Pruritis. Her previous doctors had neither performed tests for glucose intolerance nor for hyperinsulinemia. Table 4 shows her insulin and glucose profiles at the time of initial evaluation.

I implemented my previously described1,3 integrative program for restoring insulin and glucose homeostasis (for more details, please consider my three-part video seminar entitled ” Reversing Diabetes” downloadable from The follow-up insulin and glucose profiles performed after 20 months of implementing the program showed a lowering of one-hour blood insulin level from 107 to 44 uIU and a fall in the one-hour glucose value from 198 mg/dL to 171 mg/dL. So, where a pretreatment insulin level of 107 uIU was needed to keep blood glucose level to 198, after the treatment only 44 uIU were required to drop the glucose level to 171 mg/dL, a clear evidence of much improved insulin efficiency.

Table 4. Normalizing Insulin Homeostasis By Freeing Up Insulin Receptor of 55-year-old 5’5″ Woman Weighing 234 lbs. (Case Study 1).



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Not done

Not done




Not done

Not done

Beta Cell Regeneration and Increased Insulin Production in Diabetes Type 2B

Type 1 diabetes results from destruction of the pancreatic ß cells by ß cell–specific autoimmune responses.5-10 In experimental models of diabetes Type 1, in-vivo expansion of the ß-cell mass and consequent restoration of normoglycemia has been reported. Betacellulin is one beta-specific growth factors which induces ß-cell growth and differentiation.11-13 Application of this knowledge to human diabetes Type 1 is problematic for three main reasons: (1) it is difficult to produce and sustain sufficient numbers of ß cells for sustained normoglycemia; (2) newly formed ß cells are vulnerable to autoimmune attack which cause the disease in the first place; and (3) compliance to the pancreas regeneration program is not as big an issues in mice as it is for men (and women) .

Case Study 2

A 51-yr-old 5’9″ man weighing 167 lbs. was treated with Metformin for one year before consulting me. He discontinued Metformin within six months of our program. His subsequent A1c values ranged between 5.5% and 5.8%, indicating healthful insulin and glucose homeostasis. Table 5 shows increased insulin production in his case. His subsequent A1c values ranged between 5.5% and 5.8%, indicating healthful insulin and glucose homeostasis.

Table 5. Increased Insulin Production Due to Beta Cell Regeneration In Diabetes Type 2B. The subject Is a 51-yr-old Man Who Received Metformin for About Two Years Before Implementing the De-diabetization Plan. After Discontinuing Metformin Within 6 Months, His A1c Values Ranged Between 5.5% and 5.8%.



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I anticipate the question: Doesn’t his April 7, 2012 glucose profile show that he is still diabetic? The issue of the differences in blood sugar responses to the sudden and large glucose load (glucola for testing) and “insulin-friendly” meals14,15 is important. His low A1c values (between 5.5% and 5.8% point to improved glucose tolerance. It can be reasonably expect that response to glucola-like load will also improve with time as insulin homeostasis improves further.


1. Ali M.The Dysox Model of Diabetes and De-Diabetization Potential. Townsend Letter-The examiner of Alternative Medicine. 2007; 286:137-145.

2. Ali M. Beyond insulin resistance and syndrome X: The oxidative-dysoxygenative insulin dysfunction (ODID) model. J Capital University of Integrative Medicine. 2001;1:101-141.

3. Ali M. Oxygen, Darwin’s Drones, and Diabetes. Volume 1—Dr. Ali’s Plan for Reversing Diabetes. 2011. New York, Canary 21 Press.

4Ali M. Oxygen governs the inflammatory response and adjudicates the man-microbe conflicts. Townsend Letter for Doctors and Patients. 2005;262:98-103.

5 1.Rabinovitch, A (2004). Roles of cell-mediated immunity and cytokines in the pathogenesis of type 1 diabetes mellitus. In:LeRoith, D, Olefsky, JM and Taylor, SI (eds.). Diabetes Mellitus: A Fundamental and Clinical Text,Lippincott Williams & Wilkins: Philadelphia, PA. pp. 519–538.

6. Nakayama M, Norio Abiru N, Moriyama H, et al. Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice. Nature. 2005; 435, 220-223.

7 Kent SC, Chen Y, Bregoli L, et al. Expanded T cells from pancreatic lymph nodes of type 1 diabetic subjects recognize an insulin epitope. Nature. 2005;435:224-228.

8. von Herrath M. Insulin trigger for diabetes. Nature. 2005;435:151-152.

9. Eisenbarth, G. S. et al. Insulin autoimmunity: prediction/precipitation/prevention type 1A diabetes. Autoimmun. Rev. 2002;1:139-145.

10. Eisenbarth, G. S. et al. Insulin autoimmunity: prediction/precipitation/prevention type 1A diabetes. Autoimmun. Rev. 2002;1:139-145.

11. Shin S, Na Li1, Kobayashi N, et al. Remission of Diabetes by ß-Cell Regeneration in Diabetic Mice Treated With a Recombinant Adenovirus Expressing Betacellulin. Jun1,3 Molecular Therapy (2008); 16 5 854–861.

12. Chen S, Ding, J, Yu, C, et al. Reversal of streptozotocin-induced diabetes in rats by gene therapy with betacellulin and pancreatic duodenal homeobox-1. Gene Therapy. 2007;14:1102–1110.

13. Liu M, Shin S, Li N, et al. Prolonged Remission of Diabetes by Regeneration of ß Cells in Diabetic Mice Treated with Recombinant Adenoviral Vector Expressing Glucagon-like Peptide-1 free. Molecular Therapy15, 86-93 .

14. Dr. Ali’s Insulin Diet.

15. Oxygen, Insulin Waste, and Insulin Depletion/,_insulin_waste,_and_insulin_depletion.htm


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