Category Archives: Dr. Ali Course on Insulin Toxicity

Majid Ali, M.D.

New York  212-873-2444

New Jersey . 201-996-0027


 

Unless specified otherwise,

the word at this web site is used for Type 2 diabetes.


 

BEWARE!

  1. If you think, diabetes is a sugar problem, tests done for blood sugar levels for screening for diabetes will be misleading most of the time.
  2. The diagnosis of diabetes will be delayed for five, ten, or more years.
  3. If you are overweight, it will be much more difficult to lose weight. 
  4. Unless you are at your optimal weight, undetected insulin toxicity will injure all your body organs to varying degrees until diabetes is diagnosed and treated for years, usually five to ten or more years.

 

References for Insulin Toxicity and Diabetes 

  1. Ali M. Fayemi AO, Ali O, Dasoju S, et al. Shifting Focus From Glycemic Status to Insulin Homeostasis for Stemming Global Tides of Hyperinsulinism and Type 2 Diabetes. Townsend Letter. 2017; 402:91-96.
  2. Ali M. Importance of Subtyping Type 2 Diabetes Into Subtype A and Subtype 2A and Subtype 2B.  Townsend Letter. 2014; 369:56-58.
  3. Ali M, Dasoju S, Karim N, et al. Study of responses to carbhydrate and non-carbohydratechallenges in insulin-based care of metabolic disorders. Townsend Letter. 2016; 391: 48-51.

 

What IS Insulin Toxicity

Blood insulin test should be done for the following conditions since there is high probability that the underlying fires of these conditions are fed by insulin toxicity.

 

·       Loss of Vigor

·       Weight gain

·       Course skin

·       Acne in teenager

        Skin pigmentation changes

·       Facial hour for young women

·       Tingling and numbness in toes and fingers

·       Brain fog

·       Cognitive difficulties

·       Memory loss

·       Any infections that do not heal

·       Any inflammation that does not heal

·       Colitis of immune-inflammatory disorders

·       Arthritis of immune-inflammatory disorders

·       Connective tissue diseases

·       Any skin conditions that do not heal

·       Neurodermatitis

·       Brain atrophy

·       Brain degenerative conditions

·       Rising blood creatinine level

·       Rising liver enzyme levels

·       Rising CRP test results

·       Liver ultrasound with fatty liver disease, steatosis, or steatonecrosis.


 

Blood Cells Tell The Insulin Toxicity Story

Healthy Blood Cells for Comparative Study. Figure 1

Early Stress on Red Blood Cells (lower picture) . Figure 2


Red Blood Cells in a Micro-clot In Uncontrolled Diabetes (upper Picture) Figure 3

Red Blood Cell Clot Breaking Up (lower Picture) Figure 4


Micro-plaque Formation In Uncontrolled Diabetes (both pictures) Figures 5-6


 

Figure 7 (top) illustrates severely damaged erythrocytes in a 52-year-old man with persistent atrial fibrillation. Close examination shows some zones of congealing surrounding many damaged red blood cells.

Figure 8 (bottom) illustrates a zone of plasma congealing unaccompanied by any cellular elements of the blood (seemingly a “spontaneous” phenomenon) in a diabetic with IHD. In our view, such congealing represents accelerated oxidative stress on plasma.


 

Figure 9 (top) shows some needle-like and amorphous granular microclots in a patient with unstable angina.

Figure 10 (bottom) shows a “dirty” blood smear of a man with severe peripheral vascular disease and extensive bilateral leg ulcerations, showing zones of plasma congealing and lumpiness, platelet clumping, and some other zones of plasma congealing unaccompanied by any blood corpuscular elements, representing diffuse changes of AA oxidopathy.


 

Figure 11 (top) shows a microclot formed by a large aggregate of platelets and congealed plasma in a patient five days after angioplasty.

Figure 12 (bottom) shows another field from the same smear and illustrates how microclots in oxidative coagulopathy grow in size when oxidative stress persists.


 

Figure 13 (top) and figure 14 (bottom) show two microplaques in a patient who had received three unsuccessful angioplasties for advanced IHD. Photomicrographs were taken the day after a major nosebleed. Note the compaction of necrotic debris and blood elements in microplaques as contrasted with loose structure of microclots in figure 11.

 


References for Oxygen, Inflammation, Insulin, and Diverse Diseases

 

1.    Ali M. Spontaneity of Oxidation in Nature and Aging, (monograph). Teaneck, NJ, 1983.

2.    Ali M. Leaky Cell Membrane Disorder (monograph). Teaneck, NJ, 1987.

3.    Ali M. The agony and death of a cell. In: Syllabus of the Instruction Course of the American Academy of Environmental Medicine. Denver, Colorado, 1985.

4.    Ali M. Molecular medicine. In: The Cortical Monkey and Healing. Institute of Preventive Medicine, Bloomfield, NJ, 1990.

5.    Ali M. Ascorbic acid reverses abnormal erythrocyte morphology in chronic fatigue syndrome, Am J Clin Pathol. I990;94:5I5.

6.    Ali M. Ascorbic acid prevents platelet aggregations by norepinephrinc, collagen, ADP and ristocetin. Am J Clin Pathol 1991;95:281.

7.    Ali M. The basic equation of life. In: The Butterfly and Life Span Nutrition. The Institute of Preventive Medicine Press, Denville, New Jersey. pp 225-236, 1992,

8.    Ali M. Oxidative theory of cell membrane and plasma damage. In Rats, Drugs and Assumptions. 1995. Life Span, Denville, New Jersey. pp 281-302, 1995.

9.    Ali M, Ali O. AA oxidopathy: the core pathogenetic mechanism of ischemic heart disease. J Integrative Medicine 1997;1:1-112.

10.  Ali M. Ali O. Oxidative coagulopathy in fibromyalgia and chronic fatigue syndrome. Am J Clin Pathol 1999; 112:566-7.

11.  Ali M, Ali O. Fibromyalgia: An oxidative-dysoxygenative disorder (ODD) J Integrative Medicine, 1999;1:1717.

12.  Ali M. Syllabus of capital University of Integrative Medicine, 1997 Washington, DC.

13.  Ali M. Oxidative regression to primordial cellular ecology (ORPEC): Evidence for the hypothesis and its clinical significance. J Integrative Medicine 1988;2:4-55.

14.  Ali M. Primacy of the erythrocyte in vascular ecology. J Integrative Medicine. 2000;3:5-18.

15.  Ali M. The Oxidative-dysoxygenative perspective of apoptosis. J Integ Medicine. 2000;4:5-45.

16.  Ali M, Ali 0, Fayemi A, et al: Improved myocardial perfusion in patients with advanced ischemic heart disease with an integrative management program including EDTA chelation therapy. J Integrative Medicine. 1997;1:113-145.

17.  Ali M: Hypothesis: Chronic fatigue is a state of accelerated oxidative molecular injury. J Advancement in Medicine, 1993;6:83-96.

18.  Efficacy of ecologic-integrative management protocols for reversal of fibromyalgia: an open prospective study of 150 patients. J Integrative Med 1999:3:48-64.

19.  Ali M. Oxidative coagulopathy In environmental illness. Environmental Management and Health. 2000;11:175-191.

20.  All Recent advances in integrative allergy care. Current Opinion in Otolaryngology & Head and Neck Surgery 2000:8:260-266.

21.  Ali M. The agony and death of a cell. Syllabus of the instructional course of the American Academy of Environmental Medicine Denver, Co. 1985.

22.  Ali M. Intravenous Nutrient protocols in Nutritional Medicine, (monograph). Institute of Preventive Medicine. Denville, New Jersey 1991.

23.  Ali M. Oxidative theory of cancer. In: Rats, Drugs and Assumptions. 1995. Life Span, Denville, New Jersey. pp 1995:281-302

24.  Ali M. Amenorrhea, oligomenorrhea, and polymenorrhea in CFS and fibromyalgia are caused by oxidative menstrual dysfunction. J Integrative Medicine 1998;3:101-124.

25.  Ali M, Ali 0, Fayemi A, et al: Efficacy of an integrative program including intravenous and intramuscular nutrient therapies for arrested growth. J Integrative Medicine 1998:2:56-69.

26.  Ali M. Oxidative theory of cell membrane and plasma damage. In: Rats, Drugs and Assumptions. Life Span, Denville, New Jersey, 1995:281-302.

27.  Ali M. Darwin, oxidosis, dysoxygenosis, and integration. J Integrative Medicine l999;1:11-16

28.  Ali M. Darwin, Oxidosis, Dysoxygenosis, and Integration. J Integrative Medicine. 1999;3:11-16.


 

Coronary Heart Disease Is Not a Plumbing Problem

Majid Ali, M.D.

New York  212-873-2444

New Jersey . 201-996-0027


 

Endo Health for Vascular Health

Oxygen-Insulin Signaling Matrix

Insulin-Endotoxicity and Cardiovascular Diseases


Two Enemies of the Heart: Conflict and Anger

Conflict cannot be cleared by letting the steam out.

Anger sometimes can be cleared by letting the steam out.


Clearer the Knowledge,

Better the Cardiovascular Health

Two Critical Links: the More the Coronary Plaques, Fewer the Heart Deaths 

The More-Coronary-Plaques-Fewer-Deaths Paradox

Conviction Concerning the Oxygen-Insulin Signaling Matrix


What Is Endothelium?

What Are Good Endo Spices?

What Are Good Endo Herbs


 

What Hurts Endos Most?

Perverted Oxygen-Insulin Signaling Matrix.


 

Crucial Endo Factors

Endothelium Maintains the Vasodilation and Vasoconstriction Balance

inhibition and promotion of the migration and proliferation of smooth muscle cells, fibrinolysis and thrombogenesis as well as prevention and stimulation of the adhesion and aggregation of platelets.


 

What Are Endos?

The vascular endothelium is a multifunctional organ and is critically involved in modulating vascular tone and structure. Endothelial cells produce a wide range of factors that also regulate cellular adhesion, thromboresistance, smooth muscle cell proliferation, and vessel wall inflammation. Thus, endothelial function is important for the homeostasis of the body and its dysfunction is associated with several pathophysiological conditions, including atherosclerosis, hypertension and diabetes. Patients with diabetes invariably show an impairment of endothelium-dependent vasodilation.


Endo Workers

  1.  Reactive Oxygen Species
  2.  Nitric Oxide
  3. Angiotensin II
  4.  EDHF      Endothelium-derived Hyperpolarization Factor
  5. .  Prostacyclin (PGI2
  6.    Antithrombotic (NO and PGI2 both inhibit platelet aggregation) 
  7.   Prothrombotic molecules [von Willebrand factor,
  8.   Plasminogen activator inhibitor-1 (PAI-1)

 

Nitric oxide

NO is a crucial player in vascular homeostasis. NO is synthesized within endothelial cells during conversion of l-arginine to l-citrulline by endothelial nitric oxide synthase (eNOS) [15]. It is released from endothelial cells mainly in response to shear stress elicited by the circulating blood or receptor-operated substances such as acetylcholine, bradykinin, or serotonin [16]. NO diffuses to vascular smooth muscle cells (VSMC) and activates soluble guanylate cyclase (sGC), yielding increased levels of cyclic guanosine-3,5-monophosphate (cGMP) and relaxation of VSMC [1,17]. Additionally, NO also prevents leukocyte adhesion and migration, smooth muscle cell proliferation, platelet adhesion and aggregation, and opposes apoptosis and inflammation having an overall antiatherogenic effect (Fig. 3) [18].


 Therefore, understanding and treating endothelial dysfunction is a major focus in the prevention of vascular complications associated with all forms of diabetes mellitus. The mechanisms of endothelial dysfunction in diabetes may point to new management strategies for the prevention of cardiovascular disease in diabetes. This review will focus on the mechanisms and therapeutics that specifically target endothelial dysfunction in the context of a diabetic setting. Mechanisms including altered glucose metabolism, impaired insulin signaling, low-grade inflammatory state, and increased reactive oxygen species generation will be discussed. The importance of developing new pharmacological approaches that upregulate endothelium-derived nitric oxide synthesis and target key vascular ROS-producing enzymes will be highlighted and new strategies that might prove clinically relevant in preventing the development and/or retarding the progression of diabetes associated vascular complications.


Decreased formation of NO

eNOS is a dimeric enzyme depending on multiple cofactors for its physiological activity and optimal function. eNOS resides in the caveolae and is bound to the caveolar protein, caveolin-1 that inhibits its activity. Elevations in cytoplasmic Ca2 + promote binding of calmodulin to eNOS that subsequently displaces caveolin and activates eNOS


 

Vascular Function and Endothelium

The endothelium is a monolayer of cells covering the vascular lumen. For many years this cell layer was thought to be relatively inert, a mere physical barrier between circulating blood and the underlying tissues. It is now recognized, however, that endothelial cells are metabolically active with important paracrine, endocrine and autocrine functions, indispensable for the maintenance of vascular homeostasis under physiological conditions [1,2]. The multiple functions of vascular endothelium are summarized in Fig. 1 and include regulation of vessel integrity, vascular growth and remodeling, tissue growth and metabolism, immune responses, cell adhesion, angiogenesis, hemostasis and vascular permeability. The endothelium plays a pivotal role in the regulation of vascular tone, controlling tissue blood flow and inflammatory responses and maintaining blood fluidity.


 

Crucial Endo Factors

Endothelium Maintains the Vasodilation and Vasoconstriction Balance

, inhibition and promotion of the migration and proliferation of smooth muscle cells, fibrinolysis and thrombogenesis as well as prevention and stimulation of the adhesion and aggregation of platelets.


  1.  Reactive Oxygen Species
  2. Nitric Oxide
  3. Angiotensin II
  4.  EDHF      Endothelium-derived Hyperpolarization Factor
  5. .  Prostacyclin (PGI2
  6.    Antithrombotic (NO and PGI2 both inhibit platelet aggregation) 
  7.   Prothrombotic molecules [von Willebrand factor,
  8.   Plasminogen activator inhibitor-1 (PAI-1)

Endothelium-derived factors with vasodilatory and antiproliferative effects include endothelium-derived hyperpolarization factor (EDHF) [], nitric oxide (NO) [8,9] and prostacyclin (PGI2) [10], while endothelin-1 (ET-1) [11], angiotensin II and reactive oxygen species (ROS) are among the mediators that exert vasoconstrictor effects [12,13]. Endothelial cells also produce antithrombotic (NO and PGI2 both inhibit platelet aggregation) and prothrombotic molecules [von Willebrand factor, which promotes platelet aggregation, and plasminogen activator inhibitor-1 (PAI-1), which inhibits fibrinolysis] [5].

As a major regulator of vascular homeostasis, the endothelium maintains the balance between vasodilation and vasoconstriction, inhibition and promotion of the migration and proliferation of smooth muscle cells, fibrinolysis and thrombogenesis as well as prevention and stimulation of the adhesion and aggregation of platelets (Fig. 2) [5]. Disturbing this tightly regulated equilibrium leads to endothelial dysfunction.


 

Many Faces of Endothelium

Fig. 1. Multiple functions of endothelium.


 

Spices and Herbs For Endo Health

 

 

 

 

 

 

 

 

Insulin Toxicity – Early Signs

Majid Ali, M.D.

Early Signs of Insulin Toxicity Are Diabetes Complications Not Diagnosed for Years Before They Actually Diagnosed.  


 

What Google Told Me About Complications of Diabetes

  
·       Cardiovascular disease. …
·       Nerve damage (neuropathy). …
·       Kidney damage (nephropathy). …
·       Eye damage (retinopathy). …
·       Foot damage. …
·       Skin conditions. …
·       Hearing impairment. …
·       Alzheimer’s disease

What My PatientsTaught me About Insulin Toxicity

Blood insulin test should be done for the following conditions since there is high probability that the underlying fires of these conditions are fed by insulin toxicity.
 
·       Loss of Vigor
·       Weight gain
·       Course skin
·       Acne in teenager
        Skin pigmentation changes
·       Facial hour for young women
·       Tingling and numbness in toes and fingers
·       Brain fog
·       Cognitive difficulties
·       Memory loss
·       Any infections that do not heal
·       Any inflammation that does not heal
·       Colitis of immune-inflammatory disorders
·       Arthritis of immune-inflammatory disorders
·       Connective tissue diseases
·       Any skin conditions that do not heal
·       Neurodermatitis
·       Brain atrophy
·       Brain degenerative conditions
·       Rising blood creatinine level
·       Rising liver enzyme levels
·       Rising CRP test results
·       Liver ultrasound with fatty liver disease, steatosis, or steatonecrosis.


 

DR. Ali’s Library of Diabetes

 

 


Top Seven for Diabetes Foot

Majid Ali, M.D.


What Is Diabetic Foot?

What Is Insulin Foot?

A diabetic foot is a generic term used for any chronic pathologic lesions (conditions) that results directly from diabetes (Type I, Type II, or other types or diabetes, or from chronic complications of diabetes of any type.
Since hyperinsulinism (insulin toxicity) predates Type 2 diabetes (T2D, the common form of diabetes mellitus)) by five, ten, or more years, and since diabetes foot often develops during these years, the term “insulin foot” is more appropriate than diabetes foot. The use of insulin foot draws sharp focus on insulin, both for the patient and the physician.

Signs and Symptoms of Insulin Foot

1. Pain
2. Low skin temperature with or without cold sensitivity
3. Numbness, tingling, pins and needles
4. Skin color change (redness, pigmentation change)
5. Loss of sensation (leading to cigarette burn for instance)
6. Slow healing wounds
7. Slow healing infections

Common terms used  for diabetic foot include:
 
1.   Diabetic nerve pain
2.   Diabetic neuropathy
3.   Diabetic foot pain
4.   Diabetic peripheral nerve dysfunction
5.   Diabetic peripheral vascular dysfunction

Top Seven for Diabetic Foot 

1.     Optimal Diabetes Control With Insulin Detox
2.     Attention to Early Negative Changes
            2. a  Poor circulation
            2.b  Pigmentation changes
            2.c   Nail fungus
            2.d  Poorly healing small wounds
            2.e  Poorly healing minor infections
            2.f  Foot and ankle puffiness
            2.g  Local pressure changes
3.        Vigorous treatment of early infections         
4.       Castor oil topical for early inflammatory lesions
5.       Hydrogen Peroxide foot soaks
6.       Nutrient Supplementation for Improved Circulation


 


Dr. Ali’s VideoLibrary

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This is a pragmatic view of an integrative physician, not a delusional plausibility of an ideologue. I hope you will consider the Program. It should serve you well for life. Kindest regards, Majid Ali, M.D.. Majid Ali, M.D. Updated June 20, 2010. COURSE 1: PHILOSOPHY OF BEING ONE’S OWN PRIMARY PHYSICIAN.

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This is a pragmatic view of an integrative physician, not a delusional plausibility of an ideologue. I hope you will consider the Program. It should serve you well for life. Kindest regards, Majid Ali, M.D.. Majid Ali, M.D. Updated June 20, 2010. COURSE 1: PHILOSOPHY OF BEING ONE’S OWN PRIMARY PHYSICIAN.
Jun 11, 2014 – The matters of doubt and uncertainty are of central importance to Being One’s Own Primary Physician. The uncertainty principle offers us an antidote to the risk of habitual thinking, blind trust, and static belief that impedes learning and threatens success. The subject of uncertainty brings to mind some of the …
May 11, 2014 – If your symptoms recurred after sinus surgery, please think of mold allergy, mold infections, and mold toxins. For the … Being One’s Own Personal Physician. I define … For example, a forty-year-old man who develops acute sinusitis and fever cannot be his primary physician for that acute illness. However …
Aug 20, 2014 – Majid Ali, M.D.. My patients with coronary heart disease have taught me this: Heart disease is a state of separation from one’s nature. This separation is caused by: 1. Deep disappointments of ….. For reversing coronary artery disease one must become one’s own primary physician. This, however, takes time.
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Jul 8, 2014 – What Is Allergy? A Great Masquerader That Must Be Banished to Enjoy Health Majid Ali, M.D. Allergy is a great masquerader of the immune system. Sneezing, stuffy nose, itchy eyes, skin rashes, and sinusitis are only the surface problems in allergy. There are many deeper and more serious problems …
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Get appointment information and hours of operation for Majid Ali, practicing Public Health & General Preventive Medicine doctor in New York, NY.
Missing: being ‎own
Being One’s Own Primary PhysicianMajid Ali, M.D.. I define disease in two ways: * First, disease is a state of separation from one’s nature. * Second, disease is a state of evolution in reverse. Since no one else can know one’s nature —nor the degrees of separation from it—one can have only one authenticphysician: …
Sep 3, 2014 – Posts about Majid Ali MD written by Majid Ali MD. … far beyond the classical and wholly inadequate notion of it being a process characterized by edema, erythema, tenderness, pain, and infiltrate of inflammatory cells. ….. For reversing coronary artery disease one must become one’s own primary physician.

store.payloadz.com › Movies and Videos › Educational
Buy and Download > Description. In this 35-minute video seminar, Professor Majid AliM.D. explains why he rejects the diagnostic criteria for prediabetes established by the American Diabetes Association (ADA) and the World Health Organization (WHO). He asserts diabetes can neither be prevented nor reversed as long …

Jun 11, 2014 – The matters of doubt and uncertainty are of central importance to Being One’s Own Primary Physician. The uncertainty principle offers us an antidote to the risk of habitual thinking, blind trust, and static belief that impedes learning and threatens success. The subject of uncertainty brings to mind some of the …
May 11, 2014 – If your symptoms recurred after sinus surgery, please think of mold allergy, mold infections, and mold toxins. For the … Being One’s Own Personal Physician. I define … For example, a forty-year-old man who develops acute sinusitis and fever cannot be his primary physician for that acute illness. However …
Aug 20, 2014 – Majid Ali, M.D.. My patients with coronary heart disease have taught me this: Heart disease is a state of separation from one’s nature. This separation is caused by: 1. Deep disappointments of ….. For reversing coronary artery disease one must become one’s own primary physician. This, however, takes time.
Dec 25, 2014 – In the United States today, blocker drugs, stents, and bypass procedures are promoted as the primarytherapies for coronary artery disease. … This is what I call being one’s own doctor—cardiologist in the current context. … A Chick Comes Out of an Egg and Drops Dead of a Heart AttackMajid Ali MD …
Jul 8, 2014 – What Is Allergy? A Great Masquerader That Must Be Banished to Enjoy Health Majid Ali, M.D. Allergy is a great masquerader of the immune system. Sneezing, stuffy nose, itchy eyes, skin rashes, and sinusitis are only the surface problems in allergy. There are many deeper and more serious problems …
Rating: 5 – ‎5 reviews
Get appointment information and hours of operation for Majid Ali, practicing Public Health & General Preventive Medicine doctor in New York, NY.
Missing: being ‎own
Being One’s Own Primary PhysicianMajid Ali, M.D.. I define disease in two ways: * First, disease is a state of separation from one’s nature. * Second, disease is a state of evolution in reverse. Since no one else can know one’s nature —nor the degrees of separation from it—one can have only one authenticphysician: …
Sep 3, 2014 – Posts about Majid Ali MD written by Majid Ali MD. … far beyond the classical and wholly inadequate notion of it being a process characterized by edema, erythema, tenderness, pain, and infiltrate of inflammatory cells. ….. For reversing coronary artery disease one must become one’s own primary physician.

store.payloadz.com › Movies and Videos › Educational
Buy and Download > Description. In this 35-minute video seminar, Professor Majid AliM.D. explains why he rejects the diagnostic criteria for prediabetes established by the American Diabetes Association (ADA) and the World Health Organization (WHO). He asserts diabetes can neither be prevented nor reversed as long …

 


Dr. Ali’s Insulin Library

Majid Ali, M.D.

My Oxygen Thinking Has Given Me Insights About the Roles of Insulin in Health and Disease which Robustly Challenge the Prevailing Notions of Insulin, Insulin Resistance, and Hyperinsulinism. 


 

Large Claims Require Large Bodies of Information

I offer my free-access library of insulin and hyperinsulinism (links included below) in an attempt to meet my obligation when I choose to challenge the prevailing dogmas of hyperinsulinism and Type 2 diabetes (T2D).

I would be most grateful to visitors to this website who find errors in my materials or disagree with me in other ways to send their disagreements to me at aliacademy7@yahoo.com.  


Dr. Ali’s Insulin Library


Community Texts : Free Books : Free Texts : Download & Streaming …

Majid Ali, M.D. Why I Don’t Recommend Skim Milk Products. – -. by Majid Ali, M.D.. texts … 20 20. 4. IJGMP Metabolic Syndrome. Aug 20, 2016 08/16. by IASET …

Seven Stages of Insulin Toxicity | The Ali Academy Community

Apr 30, 2011 – Majid Ali, M.D. In matters of life span, I summarize the lessons learned from my patients with the following simple words: Keep insulin low …

Insulin Toxicity and Dysfunction videos part 1 | The Ali Academy …

Insulin Literacy Understanding Insulin Dysfunction A1c and Insulin Toxicity from Majid Ali on Vimeo. Cheese Is Good For Reversing Insulin Toxicity Part Two …

The Oxygen Model of Insulin Toxicity – Majid Ali, M.D. | The Ali …

Aug 4, 2012 – I proposed my Oxygen Model of Insulin Toxicity as a unifying model that recognizes disturbances of oxygen functions as the fundamental …

INSULIN TOXICITY – Insulin Club

Insulin Toxicity. Majid Ali, M.D.. Related … Insulin Thinking Videos on YouTube Encyclopedia … Hypoglycemia) Is Nearly Always Caused by Insulin Toxicity.

Seven Stages of Insulin Toxicity – Dr. Ali’s Virtual Medical Library

drali1.org/insulin_seven_stages.htm

Seven Stages of Insulin Toxicity. Majid Ali, M.D. In matters of the life span, I summarize the lessons learned from my patients with the following simple word.

Insulin Toxicity – Dr. Ali’s Virtual Medical Library

drali1.org/insulin-toxicity.htm

Dr. Ali’s nsulin Toxicity Course Majid Ali, M.D.. I divide my Insulin Toxicity Course in the following two parts: Insulin Toxicity Course Part One. Insulin Toxicity …

Majid Ali, M.D. * Insulin Toxicity De-mystifies the Metabolic Syndrome …

Jun 28, 2012 – Uploaded by majid ali

The true mature of the metabolic syndrome is insulin toxicity. The term metabolic syndrome creates creates …

Seven Stages of Insulin Toxicity Seminar Majid Ali MD on Vimeo

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May 12, 2014

Professor Majid Ali shares information about “Seven Stages of Insulin ToxicitySeminar”

Insulin Toxicity De-mystifies the Metabolic Syndrome Majid Ali MD on …

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Apr 6, 2014

Professor Majid Ali MD. shares information about Insulin Toxicity De-mystifies the Metabolic Syndrome.

Dr. Ali’s Course on Insulin Toxicity | – Ali Healing Community

Jan 11, 2017 – Majid Ali, M.D. Workable Simplicity to Understand Maddening Complexity of Three Scourges of Our Time Dr. Ali’s Insulin-Diabetes Video and …

Ali Diabetes | Preventing and Reversing Diabetes With Insulin Literacy

5 days ago – Preventing and Reversing Diabetes With Insulin Literacy. … Majid Ali, M.D. ….. Majid Ali, M.D. * Insulin Toxicity De-mystifies the Metabolic …

Insulin Toxicity | Ali Academy

Feb 9, 2015 – Posts about Insulin Toxicity written by Majid Ali MD.

Dr. Ali’s Autism Course | Childrens Health Corps

Sep 20, 2015 – Majid Ali, M.D. Evidence for My Proposed Insulin-Autism Connection … studies of the energetic-molecular of autism, as well as insulin toxicity.

Dr. Ali Course On Insulin Toxicity — Blogs, Pictures, and more on …

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Diabetes Is Rooted In Insulin Toxicity – Part Two. Majid Ali, M.D.. Diabetes Begins 15–20 years before it is diagnosed. Text Reproduced From An Important …

Insulin Neuropathy Reversed With Natural Remedies Majid Ali, MD

aliacademy.org/neuropathy1.htm

Majid Ali, M.D.. In my clinical experience, the most common cause of neuropathy is insulin toxicity. Some years ago, I introduced the term “insulin neuropathy” for …

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DIABETES – Insulin Toxicity and Reversal of Diabetes Seminar by …

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In this 55-minute video seminar, Professor Majid Ali, M.D. discusses the causes, clinical features, and consequences of insulin toxicity, including pre-diabetes …

Majid Ali MD, Gestational Diabetes Is Insulin Toxicity of the Unborn …

Jan 22, 2017 – It is regrettable that doctor order glucose tolerance for expecting mothers but do not include insulin tests with the same blood tests. Excess …

Dr. Majid Ali, MD discusses the serious impact of insulin toxicity …

http://www.ihealthtube.com Dr. Cal Streeter talks about the dangers of a couple of traditional cancer treatments. He also talks about the body’s own ability to kill …

Two Dimensions of Insulin Dysregulation

Majid Ali, M.D., FRCS (Eng), FCAP (Path)

Type 2 Diabetes (TD2) Is Rooted In the First Dimension of Insulin Dysregulation. Type 2 diabetes does not occur when the first dimension of insulin dysregulation is detected and reversed.


SPECIAL NOTES

Treatment plans for reversing prediabetes (hyperinsulinism) and diabetes are presented at this site under the titles of

Reversing Prediabetes and Diabetes With 3D Plan 

 Links to important related articles are included at the end of this article.


Two Dimensions of Insulin Dysregulation

The author recognizes two primary dimensions of insulin dysregulation: (1) the first dimension is of excess insulin accompanied by a multitude of adverse effects of hyperinsulinism without associated glycemic disruptions characteristic of Type 2 diabetes; and (2) the second dimension of excess insulin accompanied by glycemic disruptions that meet the numerical criteria of Type 2 diabetes (T2D). The first dimension is rooted in the toxicities of food, environment and thought, while the second dimension is rooted in the first dimension. The first dimension is optimally detected by measuring timed blood insulin concentrations following an oral glucose load as shown in Tables used for case studies. The core message of this short article is this: If the first dimension of insulin dysregulation can be reversed, the problem of the second dimension (T2D) simply does not arise.


The Oxygen-Insulin View of Insulin Dysfunction, Diabetes Type 2, and Reversing Diabetes 3D

Oxygen is the organizing principal of biology and governs the aging process. The author began his book Oxygen and Aging (2000) with those words. This simple statement was the essence of his interest and study of molecular biology of oxygen for twenty years.1-4 His interest in molecular biology of insulin5-8 arose from his work in oxygen. The “oxygen-insulin perspective” of the two dimensions of insulin dysfunction and its scientific underpinnings was comprehensively discussed in his book entitled Dr. Ali’s Plan for Reversing Diabetes (2011)9 as well as in a series of follow-up publications.10-18

Life is an injury-repair-injury cycle. Cellular injury is intertwined with cellular repair by diverse mechanisms. Patterns of repair change with varying types of injury and the prevailing tissue condition. The constant in all this is expanded energy requirement of cells in the repair processes. Whether cellular repair is in acne or psoriasis, in polycystic ovarian syndrome in young women or recurrent prostatitis in young men, in chronic GERD-gastritis complex or Crohn’s colitis, inflammatory arthritis or pulmonary interstitial fibrosis, steatosis of the liver or chronic renal failure, systemic lupus erythematosus (see illustrative case study in Table 4) or scleroderma, the core requisite of cellular repair is the same: increased energy demands. Hyperinsulinism, in this context, is pancreatic response to increased energy needs for repair of injured tissues. The author has documented the presence of the first dimension of insulin dysregulation in all of the above-mentioned pathologic entities.


 

Three Crucial Aspects of Two Dimensions of Insuloin Dysregulation

From a clinical standpoint, three other aspects of the two dimensions of insulin dysfunction are:

  1. Epigenetics play greater roles than genetics in both dimensions;
  2. Understanding the pathophysiology, clinical courses, and optimal management of both dimensions of insulin dysregulation calls for a shift of focus from glycemic status to insulin homeostasis;
  3. Since first dimension is not accompanied by glycemic disruptions, the lab tests for glycemic status (fasting and 2-hour postprandial blood sugar levels, and A1c test) are not suitable in the detection and reversal of the first dimension.

 

Neglect of the First Dimension Deepens the Suffering of the Second Dimension

The data in Tables 1 and 2 summarizes the core statistical relationships between the two dimensions of insulin dysfunction. The two columns presenting mean peaks of blood glucose and post-glucose-load insulin concentrations in Table 1 dramatically document how far the prevailing practices of neglecting the first dimension go to deepening the problems caused by the second dimension.

Table 1. Insulin Homeostasis Categories in 506 Study Subjects Without Type 2 Diabetes

Insulin Category* Percentage of Subgroup Mean Peak Glucose mg/dL(mmol/mL) Mean Peak Insulin (uIU/mL)
Exceptional Insulin Homeostasis   N =   12**
1.7% 110.2     (6.12) 14.3
Optimal Insulin Homeostasis         N =   126
24.9 % 121.2     (6.73) 26.7
Hyperinsulinism, Mild                       N = 197
38.9 % 136.5   (7.58) 58.5
Hyperinsulinism, Moderate           N = 134
26.5 % 147.0   (8.16) 109.1
Hyperinsulinism, Severe                 N = 49
9.7 % 150.0   (8.33) 231.0
Correlation coefficient, r value, for means of peak glucose and insulin levels in the five insulin categories is 0.84.

*Criteria for classification: (1) Exceptional insulin homeostasis, with fasting insulin concentration of <2 uIU/mL and mean peak insulin concentration of <20; (2) optimal insulin homeostasis, peak insulin <40 accompanied by unimpaired glucose tolerance; (3) mild hyperinsulinism, peak insulin <80 accompanied by unimpaired glucose tolerance; (4) moderate hyperinsulinism, peak insulin <160 accompanied by unimpaired glucose tolerance; (5) severe hyperinsulinism, peak insulin <160 accompanied by unimpaired glucose tolerance.

** Exceptional insulin homeostasis, a subgroup of optimal insulin homeostasis.


 

Table 2 Insulin Homeostasis Categories in 178 Study Subjects With Type 2 Diabetes
Insulin Category Percentage of Subgroup Mean Peak Glucose, mg/dL

(mmol/mL)
Mean Peak Insulin (uIU/mL)
Diabetic Hyperinsulinism, Mild       N =   53
29.0% 252.0   (14.00) 55.4
Diabetic Hyperinsulinism, Moderat N = 42
24.0% 242.1   (13.45) 112.4
Diabetic Hyperinsulinism, Seve       N =   24
13.9% 224.6   (12.47) 298.0
Diabetic Insulin Deficit                     N = 59
33.1% 294.0   (16.33) 22.9

 

Neglect of the First Dimension By Laboratory Professionals

 The neglect of first dimension by the laboratory professionals is one of the most disturbing aspects of the sordid story of the two dimensions of insulin dysregulation. For instance, the reference range for the 2-hr post challenge blood insulin concentration of laboratory 2 (Table 3) is an astonishingly and utterly clinically unusable 0.0 to 163.5.

Table 3. Insulin Reference Ranges in uIU/mL of Six Laboratories in New York Metropolitan Area*

 

Laboratory Fasting 1 Hr 2 Hr 3 Hr
Laboratory 1 1.9 – 23 8 – 112 5 – 35 Not Reported
Laboratory 2 2.6 – 24.9 0.0 – 121.9 0.0 – 163.5 Not Reported
Laboratory 3 6 – 24.9 8 – 112 5 – 55 3 – 20
Laboratory 4 6 – 27 20 – 120 18 – 56 8 – 22
Laboratory 5 00 – 30 30 – 200 40 – 300 50 – 150
 

Laboratory 6

Does not include insulin ranges in the report. Instead it includes the following note: Insulin analogues may demonstrate non-linear cross-reactivity in this essay. Interpret results accordingly.**

*Upper and lower limits of laboratory reference ranges for blood insulin concentration determined following a Standard 75-gram glucose challenge.

**Personal communications with clinicians revealed that they do not find this laboratory note to be satisfactory in their clinical decision-making.


 

Mechanisms of Insulin Regulation and Two Dimensions of Insulin Dysregulation

 The following is text on the subject from the author’s comments e-published in June, 2017 by the journal Nature. “The work of Zhang and colleagues is important for physicians who treat diabetes because class B G- protein-coupled receptors (GPCRs) are important therapeutic targets. Beyond that, this work invites all physicians to a deeper study of the inner mechanisms of insulin homeostasis, a subject that is seldom duly considered in clinical medicine. Specifically, insulin dysregulation has two distinct dimensions: (1) the first dimension of pathophysiology of hyperinsulinism which predates Type 2 diabetes (T2D) and is not accompanied by glycemic abnormalities detectable by the laboratory tests in current use; and (2) the dimension of T2D accompanied by hyperglycemia and its biochemical consequences. This author has long recognized the need for a shift of clinical focus from glycemic status to insulin homeostasis for detecting and optimally managing adverse metabolic, proinflammatory, endothelial, developmental, and neurologic effects of hyperinsulinism (ref. 2-6).”

Table 4. Severe Hyperinsulinism In A 13-Yr-Old With SLE, ITP, Recurrent Pneumonia, and Optic Neuritis With Right Eye Blindness.

The Peak Insulin Fell from 718 to 238.5 In Four Months of Robust Integrative Treatment.

Fasting ½ Hr 1Hr 2Hr 3Hr
Insulin uIU/mL
27.9 362.5 424.0 718.2 571.7
Glucose mg/mL
      70 140 157 150 111
Insulin and Glucose Profiles Obtained After Four Months of Robust Integrative Therapies
Insulin uIU/mL
7.2 125.1 238.5 208.0 132.0
Glucose mg/mL
81 154 181 130 97
 

Table 5. Control of Hyperinsulinism With Reversal of Type 2 Diabetes In A 75-Yr-Old 5’ 2” Female Weighing 162 Lbs. With Hypertension and Chronic Sinusitis.

4.30.2013 Fasting ½ hr 1 hr 2 Hr 3 Hr
Insulin uIU/mL
16 37 59 113 152
Glucose mg/mL (mmol/L)
112 158 214 241 155
10.17.2014*
Insulin uIU/mL
23.8 19.3 36.9 114.7 75.2
Glucose mg/mL (mmol/L)
116 167 253 297 172
4.14.2015**
Insulin uIU/mL
6.2 22.1 42.9 51.2 39.7
Glucose mg/mL /L)
96 130 193 112 105

* A1c, 6.3%; ** A1c, 5.9%

 

Reversing Prediabetes (Hyperinsulinism) and Diabetes With 3D Plan

The insulin homeostasis protocol (the “Protocol”) evolved as a three-prong approach comprising: (1) diet; (2) detox; and (3) dysoxic comorbidities (oxygen-related coexisting pathologic entities) including disrupted hypothalamic and related neural pathways which regulate the energy economy of the body. The three “diabetes 3D” subjects are vast and clearly beyond the scope of this brief outline. A comprehensive discussion of all above subjects is presented at free access www.alidiabetes.org. Google search words are: majid ali, shifting focus from glycemic status to insulin homeostasis.


 

References

1.   Ali. M. Respiratory-to-Fermentative (RTF) Shift in ATP Production in Chronic Energy Deficit Disorders. Townsend Letter for Doctors and Patients. 2004.

2.   Ali M. Darwin, oxidosis, dysoxygenosis, and integration. J Integrative Medicine. 1999;3:11-16.

3.   Darwin, Dysox, and Disease. Volume 11. The Principles and Practice of Integrative Medicine 11. New York: Canary 21 Press; 2002.

4.   Ali M. The Principles and Practice of Integrative Medicine Volume I: Nature’s Preoccupation With Complementarity and Contrariety. New York. Canary 21 Press. 1998. 2nd edition 2005.

5.   Ali M. Epidemic of Dysoxygenosis and the Metabolic Syndrome. In: The Principles and Practice of Integrative Medicine. Volume 5. Pp 246-256. Canary 21 Press. New York. 2005.

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

7.   Ali M. Hypothesis: obesity is adipomyocytic dysoxygenosis. J Integrative Medicine. 2004;9:19-38.

8.   Kahn SE, 1, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature 2006;444, 840-846.

9.   Shoelson, SE, Lee J. Goldfine AB. Inflammation and insulin resistance. J. Clin. Invest. 2006;116: 1793–1801.
2

10.                  Murphy KG, Bloom SR. Gut hormones and the regulation of energy homeostasis. Nature. 2006;444:854-859.

11.                 .Kamada N, Seo S-U, Zhiming C, et al. Role of the gut microbiota in immunity and inflammatory disease. Nature Reviews Immunology. 2013;12:321-335.

12.                 International Diabetes Federation. Diabetes Atlas. 2016. Seventh edition. www.diabetesatlas.org.

13.                 Shulman G. Ectopic Fat in Insulin Resistance, Dyslipidemia, and Cardiometabolic Disease. N Engl J Med. 2014; 371:1131‑1141.

14.                 Bahi-Buisson N, Roze E, Dionisi C, et al. Neurological aspects of hyperinsulinism-hyperammonaemia syndrome. Dev Med Child Neurol. 2008;50:945-9.

15.                Lillioja S, Mott DM, Spraul M, et al. Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependant diabetes mellitus: Prospective studies of Pima Indians. N Engl J Med. 1993;329:1988-1992.

16.                Ali M. Oxygen and Aging. (Ist ed.) New York, Canary 21 Press. Aging Healthfully Book 2000.

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

18.                Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J. Clin. Invest. 2005;115:1111–1119.

19.                 Ali M. Fayemy AO, Ali O. Dasoju S, et al. Shifting Focus From Glycemic Status to Insulin Homeostasis. .  Townsend Letter-The Examiner of Alternative Medicine. 2017;402:91-96.

20.                 Ali M. The Principles and Practice of Integrative Medicine Volume X: Darwin, Oxygen Homeostasis, and Oxystatic Therapies. 3 rd. Edi. (2009) New York. Institute of Integrative Medicine Press.

21.                 Ali M. The Principles and Practice of Integrative Medicine Volume XI: Darwin, Dysox, and Disease. 2000. 3rd. Edi. 2008. New York. (2009) Institute of Integrative Medicine Press.

22.                 Ali M. The Principles and Practice of Integrative Medicine Volume XII: Darwin, Dysox, and Integrative Protocols. New York (2009). Institute of Integrative Medicine Press.

23. Ali M. The Philosophy and Science of Healing. APPNA Journal. 2015;25:18-19.

24.                Nath D, Heemels M-T, Lesley Anson L Obesity and diabetes. Nature. 2006;444, 839.

25.                Das S. Identity of Lean-NIDDM: Clinical, metabolic and hormonal status. In: Kochupillai N, ed. Advances in Endocrinology, Metabolism, and Diabetes. Vol. 2. Delhi, India: Macmillian; 1994:42-53.

26.                 Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J. Clin. Invest. 2005;115:1111–1119.

27.                Patti ME, Butte AJ, Crunkhorn S, et al. Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: Potential role of PGC1 and NRF1. Proc Natl Acad Sci U S A. 2003;100:8466-8471.

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

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

30.                Xu H. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J. Clin. Invest. 2003;112:1821–1830.

31.                 Stanley SA, Kelly L, Kaasmashri N, et al. Bidirectional electromagnetic control of the hypothalamus regulates feeding and metabolism. Nature. 2016  531:647–650.

32.                Ali M. Autism. Nature

33.                Ali M. Ali M. Molecular basis of autism and dysautonomia. Townsend Letter-The examiner of Alternative Medicine. 2017 (in press).

34.                Ali M. Lab ranges www.alidiabetes.org

35.                 Kaveeshwar SA, Cornwell J. The current state of diabetes mellitus in India. Australas Med J. 2014;7:45-48.

36.                 Lesley J, Manning LA, Ogle GD. A survey of diabetes services in hospitals in Ali Papua New Guinea. P N G Med J. 2001: 44:88-95.))

37.                 Xu Y, Wang L, He J, et al. Prevalence and control of diabetes in Chinese adults. JAMA. 2013; 310: 948-59.

38.                 Ali M.  Oxygen model of hyperinsulinism.  xxxx

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

40.                 Ali M. Plan for Reversing Diabetes. New York, Canary 21 Press. Aging Healthfully Book 2011.

41.                 Ali M. Importance of Subtyping Diabetes Type 2 Into Diabetes Type 2A and Diabetes Type 2B. Townsend Letter-The Examiner of Alternative Medicine. 2014; 369:56-58.

42.                 Chouchani ET, Victoria R. Pell VR, Edoardo Gaude E, et. al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature 515, 431–435.

43.                 Ali M. Succinate Retention. In: Chouchani ET. Pel VR,  Gaude E, et al.Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature;2014;515:431. (commentary after references).

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Dementia Is Rooted in Insulin Brain Toxicity

Majid Ali, M.D.

All Known risk factors of dementia are first known risk factors of hyperinsulinism (insulin toxicity and then of Dementia.


Dementia Is rooted in insulin toxicity. I support my view by showing here that all known risk factors of dementia are rooted in insulin toxicity excess – hyperinsulinism, by another name.


 

Insulin Toxicity Can Be Reliably Detected Only by Blood Insulin Tests

The only direct and reliable method of detecting insulin toxicity is timed measurements of blood insulin concentrations after a glucose challenge. Employing this insulin test, in 2017, my colleagues and I documented a prevalence rate of hyperinsulinism of 75.1% in the general population in New York metropolitan area.1 This was not surprising since four years earlier the Chinese, employing blood glucose tests had reported a combined prevalence rate of prediabetes and diabetes of 50.1%.2

The core message of this short article, I state at the beginning, is: find out if you are insulin-toxic with blood insulin tests, and if this be the case, and you and on the path to dementia, clear insulin toxicity. For this purpose, I suggest my 3D Insulin Protocol comprising diet, detox, and dysox plans, and are presented in detail at www.alidiabetes.org.

 

Dementia Is rooted in insulin excess – hyperinsulinism, in the medical jargon is the term for it – which precedes Type 2 diabetes (T2D) by five, ten, or more years. This, succinctly stated, is the basic relationship between dementia, diabetes, insulin resistance and hyperinsulinism.

 

As for the cause of dementia, my assertion that insulin toxicity is the root cause of dementia was one of the prediction of both oxygen model of hyperinsulinism and the oxygen model of dementia. I put forth these models in 19951 as extensions of my oxygen model of aging proposed in 19802. These models were based on my studies of mitochondrial dysfunction and respiratory-to-fermentative shift in chronic immune-inflammatory and other disorders proposed on 1980.

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