Category Archives: Diabetes Reversal With Insulin Detox

Insulin Essentials

Majid Ali, M.D.

Very little of What I Learned About Diabetes In Medical School Has Been Validated by My Patients, My True Teachers.


Insulin Essentials

  1. Insulin is the master energy hormone of the body, for energy generation as well as energy expenditure.
  2. The energy demands of chronically-injured cells increase because repair of injured tissues needs more energy.
  3. Increased demands for cellular repair energy can be met only with increased supply of fuel (glucose) for producing more cellular energy.
  4. Higher demands for glucose require higher insulin activity.
  5. The validity of these statements can be tested only with direct blood insulin tests, not by doing blood tests for glucose (fasting blood glucose, A1c test, two-hour post-prandial blood sugar, or three-hour glucose tolerance test after a glucose load.
  6. other forms of sugar.
  7. Anyone can test the validity of the above statement with blood insulin tests.


What My Professors Did Not Tell Me About Insulin Essentials

  1. Newborn babies with birth weight larger than eight pounds are insulin toxic.
  2. Mothers of babies with birth weight larger than eight pounds are insulin toxic.
  3. Expecting moms with gestational diabetes are insulin-toxic and will remain so after delivering their babies for variable periods of time.
  4. Boys with widespread persistent acne are insulin-toxic.
  5.  Young girls with polycystic ovarian cystic syndrome are insulin-toxic.
  6. Nearly all obese children are insulin-toxic.
  7. Children and adults with fatty liver and steatosis are insulin-toxic.
  8. Most patients with pulmonary fibrosis, bronchiectasis, and active tuberculosis are insulin-toxic. 
  9. Most individuals with psoriasis and sarcoidosis are insulin-toxic.
  10. Most individuals with chronic autoimmune disorders (rheumatoid arthritis, lupus, scleroderma, and others) are insulin-toxic.
  11. Most patients with chronic renal failure are insulin-toxic.
  12. Most individuals with memory loss, dementia, Alzheimer’s disease, and diverse chronic diseases of the brain are insulin-toxic.
  13. Most individuals with cancer are insulin-toxic.
  14. Nearly all people become insulin-toxic after receiving chemotherapy.



  1. Individuals with psoriasis are insulin-toxic.
  2. babies with birth weight larger than eight pounds are insulin toxic.
  3. In


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


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.

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 Published Paper
Article: Hulsegge G, Spijkerman AMW, van der Schouw, et al. Trajectories of metabolic risk factors and biochemical markers prior to the onset of type 2 diabetes: the population-based longitudinal Doetinchem study.  Nutrition & Diabetes (2017) 7, e270; doi:10.1038/nutd.2017.23

Risk factors often develop at young age and are maintained over time, but it is not fully understood how risk factors develop over time preceding type 2 diabetes. We examined how levels and trajectories of metabolic risk factors and biochemical markers prior to diagnosis differ between persons with and without type 2 diabetes over 15–20 years.
A total of 355 incident type 2 diabetes cases (285 self-reported, 70 with random glucose 11.1mmoll−1) and 2130 controls were identified in a prospective cohort between 1987–2012. Risk factors were measured at 5-year intervals. Trajectories preceding case ascertainment were analysed using generalised estimating equations.
Among participants with a 21-year follow-up period, those with type 2 diabetes had higher levels of metabolic risk factors and biochemical markers 15–20 years before case ascertainment. Subsequent trajectories were more unfavourable in participants with type 2 diabetes for body mass index (BMI), HDL cholesterol and glucose (P<0.01), and to a lesser extent for waist circumference, diastolic and systolic blood pressure, triglycerides, alanine aminotransferase, gamma glutamyltransferase, C-reactive protein, uric acid and estimated glomerular filtration rate compared with participants without type 2 diabetes. Among persons with type 2 diabetes, BMI increased by 5–8% over 15 years, whereas the increase among persons without type 2 diabetes was 0–2% (P<0.01). The observed differences in trajectories of metabolic risk factors and biochemical markers were largely attenuated after inclusion of BMI in the models. Results were similar for men and women.
Participants with diabetes had more unfavourable levels of metabolic risk factors and biochemical markers already 15–20 years before diagnosis and worse subsequent trajectories than others. Our results highlight the need, in particular, for maintenance of a healthy weight from young adulthood onwards for diabetes prevention.

Text continued
Although it has been well established that adverse levels of risk factors often develop early in life and are maintained over time,123456 it is not fully understood how they progress to type 2 diabetes (T2D). For example, T2D might be preceded by a gradual accumulation of the adverse effects of risk factors starting at a young age, or by a relatively sudden deterioration in risk factors before disease onset, or by a combination of both. The comparison of long-term trajectories of risk factors between those who do and those who do not develop T2D may help to identify at which time point these trajectories start to deviate before the development of overt disease. Such insight into the timing and the extent of pathophysiological changes before symptoms occur may provide indications for the optimal timing of preventive actions. Trajectories of BMI and waist circumference are of particular importance since these are strong modifiable risk factors of T2D.78 Other relevant factors associated with T2D include glucose levels,9 β-cell function,10 insulin resistance,10 blood pressure,8lipids,8 liver fat markers,1112 markers of chronic inflammation13 and kidney function.14
Several studies have described gradual changes in β-cell function, insulin resistance, fasting glucose and 2-h post-load glucose many years before diagnosis of T2D with steeper unfavourable changes 3–5 years before diagnosis.1516171819 Only a few studies, mainly among men, have examined progressive changes of other risk factors, such as BMI, but so far findings have been inconsistent. The Whitehall II study showed that adults who developed T2D had similar trajectories of BMI and C-reactive protein (CRP) but more unfavourable trajectories of systolic blood pressure and high-density lipoprotein (HDL) cholesterol compared with adults without T2D, over a period of ~14 years.2021 In contrast, a small study of 177 men observed larger changes in BMI, but no differences in blood pressure, HDL cholesterol and liver fat markers in men who developed impaired fasting glucose compared with men who did not, over a 9-year period.22 A short-term study (that is, over 1.5 years) observed differences in changes of alanine aminotransferase (ALT) and triglycerides but not in blood pressure, total cholesterol and HDL cholesterol between high-risk men with incident T2D and controls.17
A longer follow-up period in a population-based study and inclusion of other metabolic risk factors and biochemical markers is needed for more insight in the physiological changes preceding the onset of T2D. There is also a need to investigate differences between men and women since previous studies reported several sex-related differences in the associations of risk factors such as systolic blood pressure, HDL cholesterol and uric acid with T2D.2324 Therefore, we examined whether trajectories of metabolic risk factors and biochemical markers among initially healthy men and women differed for those who developed T2D and those who did not over a period of up to 15–20 years.

More Information at Dr. Ali’s Diabetes Library linked below:

Majid ali Insulin Neuropathy diabetes hyperinsulinemia nerve damage …

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

Aug 4, 2012 – in my book “Dr. Ali’s Plan for Reversing Diabetes,” I presented the following 3-M schema of the development of insulin toxicity. In this schema …

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Shifting Focus From Glycemic Status to Insulin Homeostasis for Stemming Global Tides ofHyperinsulinism and Type 2 Diabetes by Majid Ali, MD, FRCS (Eng), …

Shifting Focus From Glycemic Status to Insulin Homeostasis (Jan 2017 …

Shifting Focus From Glycemic Status to Insulin Homeostasis for Stemming Global Tides ofHyperinsulinism and Type 2 Diabetes by Majid Ali, MD, FRCS (Eng), …

Dr. Ali’s Insulin Reduction Protocol

Dr. Ali’s Insulin Reduction Protocol. For Improving Insulin Efficiency. Majid Ali, M.D.. To reverse pre-diabetes and diabetes (completely or partially), my primary …

Dr. Ali’s Diabetes Reversal program – Dr. Ali’s Virtual Medical Library’s_diabetes_reversal_guidelines.htm

Dr. Ali’s Diabetes Reversal Guidelines. Majid Ali, M.D.. The science and philosophy of reversing diabetesType 2 associated with excess insulin is simple to …

Reversing Diabetes – Majid Ali –

In this 40-minute seminar, Professor Majid Ali, M.D. Presents his reasons for why … Simply stated,diabetes Type 2A is a state of insulin toxicity created by insulin …

Dr. Ali’s Breakfast for Losing Weight, Reversing Diabetes, and Staying …

Aug 28, 2014 – Majid Ali, M.D.A Breakfast for Insulin-Smart Eating and Healthful Aging There is never a valid reason for missing breakfast. So strong is my …

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May 24, 2017 – Shifting Focus From Glycemic Status to Insulin Homeostasis for Stemming Global Tides of Hyperinsulinism and Type 2 Diabetes by Majid Ali, …

Majid Ali MD | Ali Academy | Page 4

Sep 16, 2014 – Diabetes Reversal Case Study 2 – Diabetes Reversal With Control of Hyperinsulinism Majid Ali, M.D. This article describes a case of reversal …

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Jun 9, 2016 – Majid Ali said: … The plans for hyperinsulinism modification and Type 2 diabetestreatment in this model are based on the simplicity of …

Majid Ali MD, Dr. Ali’s Book on Reversing Diabetes – Dr. Ali’s Plan for … › Majid Ali › Videos
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I outline the contents of this book on reversing diabetes Type 2. I explain how it begins with 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 … Majid Ali, M.D. * Insulin Toxicity ……betes-reversal …

Apr 2, 2015 – Majid Ali, M.D. (Published in Town send Letter April 2014) In a previous column, I presented The Oxygen Model of Diabetes and the …

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Oct 6, 2014 – 10 posts – ‎6 authors

There’s a doctor (Majid Ali, MD), who tests or has tested insulin levels of many patients with or withoutdiabetes. He has found, over years of …

[PDF]Oxygen, Insulin Toxicity, Inflammation, and the … – ENCOGNITIVE.COM

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Beyond insulin resistance and syndrome X:

Majid Ali, M.D.

Oxidative – Dysoxygenative Model

of Insulin Toxicity and DiabetesHomeostasis (2001)


Beyond insulin resistance and syndrome X: tThe oxidative-dysoxygenative insulin dysfunction (ODID) modelof Insulin Toxicity--Part II. 

Nitric Oxide Dynamics and ODID

Reactive oxygen species (ROS) induce production of reactive nitrogen species (RNS). RNS, in turn, stimulate the generation of reactive oxygen species. The feedback loops provided by ROS-RNS dynamics feed the oxidative fires and inflict oxidative cellular injury. Under physiologic conditions, superoxide dismutase, catalase, glutathione peroxidase, and a host of enzymes support the reduction arm of redox equilibrium. In hyperinsulinemic and hyperglycemic states, the ROS/RNS loops significantly add to cumulative oxidosis. (158-160)

Endothelium-derived nitric oxide exerts several homeostatic effects in the vascular ecology, including regulation of vasomotor tone, inhibition of platelet aggregation, and prevention of adhesion of leukocytes to the endothelial surface (Vane 1990). In animal models as well as in both type 1 and type 2 diabetes, nitric oxide-dependent vasodilation is impaired. (158) Ascorbic acid improved the vasodilatory response in both types of diabetes. (29,30) Endothelium-dependent vasodilation is impaired in healthy subjects after six hours of hyperglycemic clamp. (159) Studies with incremental brachial artery administration of methacholine chloride during euglycemia and hyperglycemia support one of the core tenets of oxidative insulin dysfunction in that hyperglycemia contributes to abnormal endothelial function through production of superoxide anion. (37)

Higher concentrations of insulin in the blood increase blood flow to the skeletal muscle. (164-170) Some of the increase in the cellular glucose uptake has been attributed to that effect of insulin on the blood flow. The precise mechanism of action of insulin in blood vessel musculature has not been elucidated, but the role of nitric oxide in it has been postulated. (167) Other data suggest that the vasodilatory effect in the skeletal muscle is dependent on hyperinsulinemia and not consequent upon changes in carbohydrate metabolism. There is also evidence there is a reduction in insulin-induced vasodilation in insulin resistance associated with obesity. (165,169,170) in other words, insulin facilitates its own delivery to the cell membrane and degradation.

Activation of endothelial NO-synthase in higher concentration is deemed necessary for initiation of the oxidative cascade in endothelial cells that leads to production of excess reactive oxygen species and induction of NF-[kappa]B.

Tumor Necrosis Factor (TNF-[alpha]) and ODID

The secretion of TNT-[alpha] by adipocytes is of special interest to me in the context of the proposed oxidative insulin dysfunction model

of insulin resistance and type 2 diabetes. This cytokine plays many well-established and crucial roles in the inflammatory and immune responses. (94,171-176) It is expressed in excess in adipocytes of obese patients and is known to cause insulin resistance through its effects on insulin-mediated cellular signaling pathways.

Tumor necrosis factor [alpha] (TNF-[alpha]) is a potent inhibitor of insulin signaling in myocytes and adipocytes. (174) Since serum concentrations of TNF-[alpha] are very low in lean as well as obese subjects, this cytokine produced in the muscle and fat cells appears to function in a paracrine fashion. TNT-[alpha] expression is high in the muscle and fat cells of obese and diabetic subjects. Furthermore, the administration of antibodies that neutralize TNF-[alpha] to genetically obese Zucker (fa/fa) rats reverses insulin resistance. (171) That creates another mechanism of insulin resistance in mice. Interestingly, administration of the same antibodies to diabetic patients did not reverse insulin resistance. (175)

All known inflammatory and immunologic responses are initially triggered as well as regulated by oxidative and oxygenative phenomena. (173-175) Blockade of TNF-[alpha] can ameliorate, albeit for limited periods of time, both experimental and clinical forms of antoimmune disorders, such as Crohn's colitis and rheumateid arthritis. (177-180) Hypersecretory TNF-[alpha] responses induced by oxidative stresses are likely to play a role in insulin homeostasis in states of oxidosis associated with hyperinsulinism.

NF-[kappa]B, Endothelial Cells, and ODID

NT-[kappa]B is a potent proinflammatory molecule. (181-133) Blockade of NF-[kappa]B decreases inflammatory responses in experimental and such as Crohn's colitis and rheumatoid arthritis. (184-186) All inflammatory responses create regional oxidosis and most also lead to systemic oxidosis. Such theoretical considerations strongly suggest that NF[kappa]B might play some roles in the pathogenesis of oxidative-dysoxygenative insulin dysfunction.

Thus, it comes as no surprise that high concentrations of glucose (10-30 mM) result in excess generation of reactive oxygen species which, in turn, activate NF-[kappa]B and induce endothelial cell apoptosis. (187) Studies with 3O-methyl-D-glucose (a glucose derivative which is taken up but not metabolized by cells) and L-glucose have shown that endothelial reactivity is mediated by glucose-specific pathways. This finding is of direct relevance to the pathogenesis of oxidative coagulopathy in uncontrolled diabetics. Endothelial apoptosis results in denudation of the nonthrombogenic inner lining of the vessel wall, resulting in the exposition of highly thrombogenic subendothelial matrix.

IGF-1, IGF-2, and ODID

Both insulin-like growth factor 1 (IGF-1) and insulin-like growth factor 2 (IGF-2) have insulin-like effects on glucose transport in the myocyte and adipocyte. (188-190) That is not unexpected in light of close sequence homologies between insulin and both IGF-1 and IGF-2. In addition, there is also a high degree of sequence homology between the insulin receptor and the IGF-1 receptor. Again, not surprisingly, intracellular signaling pathways activated by both receptors are similar. Like insulin, IGF-1 affects translocation of GLUT-4 to the myocyte surface in vitro (188) and exerts a potent hypoglycemic effect. (191)

In health, the glucoregulatory roles of IGF-1 and IGF-2 have been thought not to be significant since these factors arc sequestered by specific binding proteins and their serum concentrations in a free state are low. IGF-1 bypasses the insulin receptor and, under those conditions, exerts a significant glucoregulatory role by facilitating glucose uptake in the myocyte and adipocyte. (192) This has been shown in persons with type 1 and type 2 diabetes as well as in instances of mutations in the insulin receptor.

In the oxidative insulin dysfunction states, however, oxidatively induced alterations in the structure and function of those binding proteins are likely to occur. Indeed, there is some evidence that is so in patients with severe insulin resistance, hyperinsulinemia, and poorly controlled diabetes.

PPAR[gamma] and ODID

Adipocytes are rich in nuclear factor called peroxisome proliferation activator receptor-[gamma] (PPAR[gamma]). This receptor is an important determinant of adipogenesis and stimulates adipogenesis in fibroblasts. (193) Persons heterozygous for a dominant-negative PPAR[gamma] allele suffer from severe insulin resistance. (194) Mice heterozygous for a null PPAR[gamma] allele on a high-fat diet have increased insulin sensitivity and develop adipocyte hypertrophy. (195)

Ligands for PPAR[gamma] include thiazolidinediones (TZDs), a class of drugs for diabetes (discussed later). PPAR[gamma] binding in vitro correlates well with in vivo lowering of blood glucose levels. Non-TZD PPAR[gamma] ligands also increase insulin sensitivity. Furthermore, activators of the PPAR[gamma] heterodimer partner, retinoid X receptor, also increase insulin sensitivity and exert antidiabetic effects. (196)

The antidiabetic effects of some drugs, such as those in the thiazotidinedione class, are due to their ability to decrease insulin resistance. This effect is mediated by a nuclear receptor protein called peroxisome proliferator activated receptor-[gamma] (PPAR[gamma]). This protein is involved in the differentiation of adipocytes and is found in large quantities in those cells. PPAR[gamma] also affects insulin sensitivity by mechanisms that are presumed to involve altered gene dynamics in adipocytes. Specifically, it was thought that some factor like PPAR[gamma] might switch on and off some adipocyte-specific gene involved in insulin-mediated signaling pathways. …

Library of Articles On Insulin Homeostasis


Majid Ali, M.D.

What Is Insulin Homeostasis? | Ali Diabetes

Apr 23, 2017 – Majid Ali, M.D. Insulin is the minister of energy and metabolism to Oxygen King of the human body. So I define insulin homeostasis as body …

Insulin Homeostasis | Ali Diabetes

Apr 18, 2017 – Majid Ali, M.D. Dr. Ali’s Insulin Homeostasis Course Insulin | The Ali Academy Community Nov 30, 2014 …

What Is Insulin Homeostasis? | Ali Diabetes

Jan 13, 2017 – So insulin homeostasis means optimal functionalities of the energy … Majid Ali MD, Voices From the Pre-East Course Part 1 – Introduction.

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Dr. Ali’s Insulin Reduction Protocol

Majid Ali, M.D. … Concurrent Reduction of Blood Insulin and Blood Sugar Levels With Dr. Ali’s InsulinReduction Protocol in …. Insulin Homeostasis and Diabetes.

Insulin Homeostasis and Diabetes

Insulin Homeostasis and Diabetes. Majid Ali, M.D.. Related Artilces. * Oxygen Homeostasis and Oxygen Models of Diseases. * Insulin Homeostasis and …

I Have Diabetes, I have to Lose it – Part One: Insulin Toxicity | The Ali …

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Nov 16, 2016 – Majid Ali, M.D. I coined the term oxygen signaling to refer to all … homeostasis (overall balance) and Insulin-based Diabetes Reversal Plan©.

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Nov 7, 2014 – Majid Ali, M.D. The Principles and Practice of Integrative Medicine (14 Volumes) … Medicine: Nutrition Seen Through the Prism of Oxygen Homeostasis. … Medicine Volume XIII: Insulin-Monitored Diabetes Reversal Plan.


Majid Ali, M.D.

Ideas, Not Products

A Line of Low-Cost, Time-efficient, Insulin-Smart Recipes
for Preserving Health, Reversing Hyperinsulinism, and Making Effort to Reverse Type 2 Diabetes


I offer my line of omelettes which are delicious, low-cost, and time-efficient. But these are the primary advantages of my omelettes. My primary purpose is to help people achieve optimal metabolic and immune health, lose weight (when desired), prevent insulin toxicity and diabetes, and through these effects, improve resistance to infections and cardiovascular health.

Why Don’t You Give Cooking Times for Your Omelette Recipes?

Dr. Ali’s Chopped Onion Omelette

Dr. Ali’s Coconut-Raisin Omelette

My Spice Omelettes for Memory Concerns and Alzheimer’s Diseasze from Majid Ali on Vimeo.

My Preferred Spice Remedies Are Omelettes from Majid Ali on Vimeo.

Dr. Ali’s Ginger Omelette Part Two

Dr. Ali’s Spicy Garlic Omelette

Dr. Ali’s Turmeric Omelette

Dr. Ali’s Turmeric Insulin-friendly Omelette

Dr. Ali’s Turmeric-Raisin Insulin-friendly Omelette

Dr Ali’s Top Three Weight Loss and Anti-diabetes Omelettes

Dr Ali’s Best Omelette Recipes for Weight loss and Preventing and Reversing Diabetes


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