Tag Archives: Diabetes

Is Diabetes A Sugar Problem? No.

Majid Ali, M.D.

Suite 3 C, 344 Prospect Avenue

Hackensack, New Jersey 07601

201-966-0027


 

Is diabetes mellitus (Type 2 Diabetes) a sugar problem? No. The abnormalities of blood sugar seen in diabetes are the consequences of the derangements of cellular energetics and toxicity that collectively create what is commonly called diabetes. Is diabetes an insulin problem? No. The abnormalities of insulin functions are the consequences of plasticized (chemicalized) and hardened cell membranes that immobilize the insulin receptors embedded in them. Is diabetes a problem of blood vessels that causes blindness, kidney failure, stroke, heart attacks, and neuropathy? No. The abnormalities of blood vessels are the consequences of oxidizing and deoxygenizing influences in diabetes.

In this column, I marshal evidence for my view that the state of insulin resistance should be regarded as a “hardened cell membrane state.” The so-called metabolic syndrome should be visualized as a “gummed-up matrix state.” Prediabetes should be seen as a “mitochondrial dysfunction state.” The strategies for the prevention and reversal of diabetes yield better long-term clinical results if diabetes is recognized as a “dysfunction oxygen signaling,” or dysox, state.

In type 1 diabetes, insulin itself becomes a potent autoantigen and initiates autoimmune injury to pancreatic islet cells.1-3 I will show how this recently documented role of insulin in the pathogenesis of diabetes fits in the dysox model of diabetes presented here. In type 2 diabetes, insulin cannot function – insulin resistance, in the common jargon – and hyperinsulinemia develops, which triggers and amplifies the inflammatory response.4-6 In all types of diabetes, the endothelial cells produce nitric oxide and other bioactive factors in abnormal quantities and proportions.7,8 Diabetes causes neuropathy, retinopathy, nephropathy, dementia, stroke, and heart attacks. I will describe how those complications of diabetes can be better understood when the problems are seen through the prism of oxygen signaling.


 

Clinical, Epidemiologic, and Experimental Evidence Links Obesity With Insulin Toxicity

The link is supported by known metabolic roles of nonesterified fatty acids (NEFAs) and altered paracrine and endocrine functions of fat cells (adipocytes) in the energy economy of the body. For example, in a healthy state, NEFAs serve as substrates for adenosine triphosphate (ATP) generation. In obesity, these fatty acids are retained in excess in biomembranes of all cell populations of the body and within adipocytes. NEFAs, along with trans fats and oxidized lipids, then “harden” the cell membranes to clamp down on insulin receptors – rusting and impacting the crank, so to speak – to cause insulin resistance.12 Those lipids also “gum up” the matrix, blocking molecular cross-talk there. Eventually, those elements, along with other toxins, uncouple respiration from oxidative phosphorylation and impede mitochondrial electron transfer events.


 

In obesity, output of fattening hormones in adipocytes (fat cells) is chaotic in the ways in which it further increases cellular fat build-up and sets the stage for the development of diabetes.13,14 However, the obesity/diabetes link does not prevail in all populations of the world. For instance, in India, there is also an epidemic of low body-weight (LBW) diabetes15 – a phenomenon that clearly points to the existence of environmental factors unrelated to obesity that are involved in the pathogenicity of diabetes, and supports the dysox model of diabetes.

A growing number of free radicals, transcription factors, enzymes, and proteins has been – and continues to be – implicated in the pathogenesis of diabetes, including:
· nitric oxide16,17
· inducible nitric oxide synthase (iNOS)18
· mitochondrial uncoupling proteins (UCPs)19-21
· proinflammatory cytokines22-24
· resistin25,26
· leptin27,28
· adipokines29
· adiponectin30
· tumor necrosis factor-alpha (TNF-a)31
· peroxisome proliferator-activated receptor gamma (PPARgamma)32-34
· nuclear respiratory factor-1 (NRF-1)35
· suppression of cytokine signaling (SOCS) proteins36
· retinol-binding protein-4 (RBP4)37
· antibodies against glutamic acid decarboxylase38
· prothrombotic species, including fibrinogen, von Willebrand factor, and plasminogen activator inhibitor (PAI-1), adipsin (complement D), and acylation-stimulating protein (ASP) 39-42
· heat shock protein 60, voltage-dependent anion channel 1 (VDAC-1), and Grp7543
· hypercoagulable platelets44


Oxygen, Diabetes, Insulin References 


1.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.
2.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.
3.von Herrath M. Insulin trigger for diabetes.
Nature. 2005;435:151-152.
4.Eisenbarth GS, et al. Insulin autoimmunity: Prediction/precipitation/prevention type 1A diabetes.
Autoimmun. Rev. 2002;1:139-145.
5.Todd JA, Bell JI, McDevitt HO. HLA antigens and insulin-dependent diabetes.
Nature. 1988;333,710-712.
6.Ali M. Hypothesis: obesity is adipomyocytic dysoxygenosis.
J Integrative Medicine. 2004;9:19-38.
7.Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes.
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9.World Health Organization Consultation on Obesity 1–253 (World Health Organization, Geneva, 2000).
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Diabetes Care. 2004;27:1047–1053.
11.Hedley AA. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999–2002.
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12.Leung, et al. Prolonged increase of plasma non-esterified fatty acids fully abolishes the stimulatory effect of 24 hours of moderate hyperglycaemia on insulin sensitivity and pancreatic beta-cell function in obese men.
Diabetologia. 2004;247:204–213.
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Advances in Endocrinology, Metabolism, and Diabetes. Vol. 2. Delhi, India: Macmillian; 1994:42-53.
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18.Perreault M, Marette A. Targeted disruption of inducible nitric oxide synthase protects against obesity-linked insulin resistance in muscle.
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19.Suh YH, Kim SY, Lee H, et al. Overexpression of short heterodimer partner recovers impaired glucose-stimulated insulin secretion of pancreatic beta-cells overexpressing UCP2.
J Endocrinol. 2004;183:133-44.
20.Ceddia1 RB, William WN, FB, et al. Leptin stimulates uncoupling protein-2 mRNA expression and Krebs cycle activity and inhibits lipid synthesis in isolated rat white adipocytes.
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21.Enerback S et al. Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese.
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22.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.
23.Shoelson, SE, Lee J. Goldfine AB. Inflammation and insulin resistance.
J. Clin. Invest. 2006;116: 1793–1801.
24.Murphy KG, Bloom SR. Gut hormones and the regulation of energy homeostasis.
Nature. 2006;444:854-859.
25.Stepphan CM, Bailey ST, Bhat S, et al. The hormone resistin links obesity to diabetes.
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26.Berti L, Kellerer M, Capp E, et al. Leptin stimulates glucose transport and glycogen synthesis is in C2C12 myotubes: Evidence for a P3-kinase mediated effect.
Diabetologia.1997;40:606-609.
27.Minokoshi Y et al. Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase.
Nature. 2002; 415: 339–343.
28.Farooqi IS, et al. Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency.
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29.Shimomura I, Hammer RE, Ikemoto S, et al. Leptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystrophy.
Nature. 1999;401:73–76.
30.Fain JN, Madan AK, Hiler ML, et al. Comparison of the release of adipokines by adipose tissue, adipose tissue matrix, and adipocytes from visceral and subcutaneous abdominal adipose tissues of obese humans.
Endocrinology. 2004;145:2273–2282.
31.Scherer PE. Adipose tissue: From lipid storage compartment to endocrine organ.
Diabetes. 2006;55:1537–1545.
32.Atherton HJ, Bailey NJ, Zhang W, et al. A combined 1H-NMR spectroscopy- and mass spectrometry-based metabolomic study of the PPAR-alpha null mutant mouse defines profound systemic changes in metabolism linked to the metabolic syndrome.
Physiol Genomics. 2006;27:178-186.
33.Kadowaki T et al. Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome.
J. Clin. Invest. 2006;116:1784–1792.
34.Farmer SR. Transcriptional control of adipocyte formation.
Cell Metab. 2006;4:263–273.
35.Yang Q, et al. Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes.
Nature. 2005;436:356–362.
36.Mooney RA, et al. Suppressors of cytokine signaling-1 and -6 associate with and inhibit the insulin receptor. A potential mechanism for cytokine-mediated insulin resistance.
J. Biol. Chem. 2001;276:25889–25893.
37.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.
38.von Boehmer H, Sarukhan A. DAG, a single autoantigen for diabetes.
Science. 1999;284:1135-1136.
39. Van Gaal LF, Mertens IL, De Block CE. Mechanisms linking obesity with cardiovascular disease.
Nature. 2006;444:875-880.
40.Matsuzawa Y. The metabolic syndrome and adipocytokines.
FEBS Lett. 2006;580:2917–2921.
41.Konstantinides S, Schafer K, Koschnick S, et al. Leptin-dependent platelet aggregation and arterial thrombosis suggests a mechanism for atherothrombotic disease in obesity.
J. Clin. Invest. 2001;108:1533–1540.
42.Bernal-Mizrachi E, Wen W, Stahlhut S, et al. Islet cell expression of constitutively active Akt1/PKB induces striking hypertrophy, hyperplasia, and hyperinsulinemia.
J. Clin. Invest. 2001;108:1631–1638.
43.Turko IV, Murad F. Quantitative protein profiling in heart mitochondria from diabetic rats.
J Biol Chem. 2003;278(37):35844-35849.
44.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.
45.Sakaue M, Fuke Y, Katsuyama T, et al. Austronesian-speaking people in Papua New Guinea have susceptibility to obesity and type 2 diabetes.
Diabetes Care. 2003 26: 955-956.
46.Katulanda P, Sheriff MH, Matthews DR. The diabetes epidemic in Sri Lanka – a growing problem.
Ceylon Med J. 2006;51:26-28.
47.Landau BR, Chandramouli V, Schumann WC, et al. Estimates of Krebs cycle activity and contributions of gluconeogenesis to hepatic glucose production in fasting healthy subjects and IDDM patients.
Diabetologia. 1995;38:831-838.
48.Tian J, Zekzer D, Lu Y, et. al. B cells are crucial for determinant spreading of T cell autoimmunity among b-cell antigens in diabetes-prone NOD mice.
Journal of Immunology. 2006; 176: 2654-2661.
49.Jaeckel E, Lipes MA, von Boehmer H. Antigen-specific foxp3-transduced t-cells can control established type 1 diabetes.
Nature Immunol. 2004;5:1028-1035.
50.Lieberman SM, Evans AM, Han B, et al. Identification of the beta cell antigen.
Proc Natl Acad Sci U S A. 2003; 100:8384-8388.
51.Arif S, Timothy I. Tree1 TI, , Thomas P. Astill TP, et al. Autoreactive T cell responses show proinflammatory polarization in diabetes but a regulatory phenotype in health.
J. Clin. Invest. 2004;113:451-463.
52.Kent SC, Chen Y, et al. Expanded T cells from pancreatic lymph nodes of type 1 diabetic subjects recognize an insulin epitope.
Nature. 2005;435:224-228.
53.Rotimi CN, Chen G, Adeyemo AA. A genome-wide search for type 2 diabetes susceptibility genes in West Africans: the Africa America Diabetes Mellitus (AADM) study.
Diabetes. 2004:53:1404.
54.Memon RA, Bessman SP, Mohan C. Impaired mitochondrial metabolism and reduced amphibolic Krebs cycle activity in diabetic rat hepatocytes.
Biochem Mol Biol Int. 1995;6:1079-1089.
55.Hotta K et al. Circulating concentrations of the adipocyte protein adiponectin are decreased in parallel with reduced insulin sensitivity during the progression to type 2 diabetes in rhesus monkeys.
Diabetes. 2001;50:1126–1133.
56.Giroix MH, Rasschaert J, Sener A, et al. Study of hexose transport, glycerol phosphate shuttle and Krebs cycle in islets of adult rats injected with streptozotocin during the neonatal period.
Mol Cell Endocrinol. 1992;83:95-104.
57.Rosen, E. D. et al. PPAR is required for the differentiation of adipose tissue in vivo and in vitro.
Mol. Cell. 1999;4:611–617.
58.La Selva M, Beltramo E, Pagnozzi F, et al. Thiamine corrects delayed replication and decreases production of lactate and advanced glycation end-products in bovine retinal and human umbilical vein endothelial cells cultured under high glucose conditions.
Diabetologia. 1997;40:741-742.
59.Sullivan KA, Feldman EL. New developments in diabetic neuropathy.
Curr Opin Neurol. 2005;18:586-590.
60.Xie XM, Yang ZW, Chen MF. Effects of advanced glycation endproducts on the activity of NF-kappaB and the expression of fibronectin mRNA in the endothelial cells in aged rats.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2006;31:883-887.
61.Després J-P, Lemieux I. Abdominal obesity and metabolic syndrome.
Nature. 2006;444: 881-887.
62.Ali M. Integrative Cardiology and Chelation Therapies: The Oxidative-Dysoxygenative Model and Chelation Therapies.
Principles and Practice of Integrative Medicine 6. 2nd ed. New York: Canary 21 Press; 2006.
63.Ali M. Oxygen governs the inflammatory response and adjudicates the man-microbe conflicts.
Townsend Letter for Doctors and Patients. 2005;262:98-103.
64.Ali M. Under Darwin’s Glow [editorial].
J Integrative Medicine. 1999. 3:1
65. Ali M. Darwin, fatigue, and fibromyalgia.
J Integrative Medicine. 1999;3:5-10.
66.Ali M. Darwin, oxidosis, dysoxygenosis, and integration.
J Integrative Medicine. 1999;3:11-16.
67.Ali M.
The Ghoraa and Limbic Exercise. Denville, New Jersey: Life Span Books; 1993.
68.Turnbaugh.PJ, Ley RU, Mahowald MA, et al. An obesity-related gut microbiome with increased capacity for energy harvest.
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69.Ley RE, Turnbaugh PJ, Klein S, et al. Human gut microbes associated with obesity.
Nature. 2006;444:1022.
70.Bajzer M, Seeley RJ. Obesity and gut flora.
Nature. 2006;444:1009-1010.
71.Ali M. Hurt human habitat and energy deficit – healing through the restoration of krebs cycle chemistry.
Townsend Letter. October 2006:112-116.
72.Ali M. Integrative Nutritional Medicine: Nutrition Seen Through the Prism of Oxygen Homeostasis.
Principles and Practice of Integrative Medicine 5. 2nd ed. New York: Canary 21 Press; 2005.
73.Ali M. Darwin, Dysox, and Disease.
The Principles and Practice of Integrative Medicine 11. New York: Canary 21 Press; 2002.

 

Reversing Diabetes With Insulin Detox

Majid Ali, M.D.

Free Access Comprehensive Internet Library for Insulin Detox for Reversing Diabetes


Important Questions

Q: Can your diabetes be reversed?

Ans: Only you can answer this question.

Q: How Do I Go About Answering This Question?

Ans: By Being Honest With Yourself and Becoming Insulin-Literate?

Q: How Does Diabetes (T2D), the Common Type) Begin?

Ans: With Insulin Toxicity.

Q: So the Way to Reversing Diabetes Is Insulin Detox?

Ans: Exactly right.

Q: What if only succeed only 30% to 40% percent in reversing diabetes with insulin detox?

Ans: This is crucial question. There are three important things to remember here:

  1. If 30% to 40% is behind you the next 20% to 30% is going to be a lot simpler;
  2. You don’t undue the insulin detox done by simply going off the program for three to six months;   , and this also holds for the remaining path;
  3. Most people who reverse diabetes with insulin detox do not get it done in just one attempt.; and
  4. Reversing diabetes is a way of life, diet-wise, physically, and spiritually.  

 

Majid Ali MD, Insulin Health and Free Insulin Course on Vimeo

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Please consider my FREE course on Insulin if you want to prevent or reverse diabetes. Learn aboutInsulin-Monitored Diabetes Reversal Plan. .


Shifting Focus From Glycemic Status to Insulin Homeostasis


Dr. Ali’s Breakfast for Losing Weight, Reversing … – Majid Ali MD Life

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 conviction on the subjects of the need and the optimal type of breakfast that I seldom complete a visit with one of my patients without addressing it. Indeed, next to the …

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

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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. 1,615 more words · 4 months, 1 week ago. Blavatar. Ali Diabetes …


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. * Keep insulin low without drugs and live longer, or. * keep blood sugar low with drugs and die young. The pandemic of diabetes can be neither understood nor …


 Seven Stages of Insulin Toxicity | The Ali Academy Community

Download Youtube mp3 – Majid Ali, M.D. What Is Insulin Resistance?

Insulin is a hormone produced by the pancreas gland located in the abdomen behind the stomach. I regulates blood sugar level when it rises after a mea…

Insulin Toxicity | Ali Academy

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

Majid Ali, M.D. – Insulin Detox for Wight Loss and Diabetes Reversal

In sulin toxicity (hyperinsulinism) is the root cause of unwanted weight gain, obesity, and diabetes Type 2. I outline my plan to clear insulin toxicity with insulin detox.

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

You have all read about how Platelet-Rich Plasma or PRP Therapy reduces chronic joint pain and helps patients get back their quality of life without drugs or surgery. Now you can hear it directly from one of our satisfied patients who got her life back thanks to PRP.

Insulin Test For Meneiers Disease And Genital Herpes Majid Ali, Md

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Insulin Test For Meneiers Disease And Genital Herpes Majid Ali, Md. Related videos. Truth About Genital Herpes · Majid Ali, M.d. Why Do I Consider Blood Insulin Test To Be The Single Most Important Test · Genital Herpes Stages. Ex B Lipid Testing And Cardiovascular Disease · Genital Herpes Symptoms Healthexpress …

Diabetes Reversal With Insulin Profiling : Dr Majid Ali : Free Download …

May 5, 2014 – Professor Majid Ali shares information about Diabetes Reversal With Insulin ProfilingFor more information on the subject , please consider Prof.Ali`s Video…


Diabetes Reversal With Insulin Profiling : Dr Majid Ali : Free Download …

May 5, 2014 – Professor Majid Ali shares information about Diabetes Reversal With Insulin ProfilingFor more information on the subject , please consider Prof.Ali`s Video…

Majid Ali MD at drali2 – WordPress.com

Jun 18, 2015 – Majid Ali, M.D.. Here is a onderful insulin-smart recipe for a delicious breakfast or dessert. Test it and pass it on if you like. Recipe. 1. Nut Flour One and half cups. 2. Eggs 4-5 Eggs. 3. Baking Soda One-third teaspoon. 4. Vanilla liquid One teaspoon (or more to taste). 5. Cinnamon One-fifth teasppon (or to …

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

Shifting Focus From Glycemic Status to Insulin Homeostasis for Stemming Global Tides of Hyperinsulinism and Type 2 Diabetes by Majid Ali, MD, FRCS (Eng), FACP; Alfred O. Fayemi, MD, MSc (Path), FCAP; Omar Ali, MD, FACC; Sabitha Dasoju, MB, BS; Daawar Chaudhary; Sophia Hameedi; Jai Amin; Kadin Ali; Benjamin …

Majid Ali, M.D. Dr. Ali’s Insulin Course – Basics – Vidmoon

Majid Ali, M.D. Dr. Ali’s Insulin Course – Basics. Majid Ali 2016-01-11 20:57:15. 1. Views. 0. 0 …

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Ferritin Level – What Does Low Value Mean · How Much Carnitine for Heart Healing – Majid Ali, MD · Insulin

Upload Stars – Facila Hair With Insulin Toxicity

Professor Majid Ali shares information about “Facila Hair With Insulin Toxicity” For more information on the …

Reporting a comment for the article : The road to restoring neural …

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Nov 10, 2016 – Majid Ali said: Integration of Empirical Therapies for Brain Rejuvenation. Majid Ali, M.D.. Writing about the restoration of neural circuits for the treatment of … will eventually be established as primarily rooted in disruptions of oxygen signaling, insulin homeostasis, an


 

Shifting Focus From Glycemic Status to Insulin Homeostasis.


 

Neuropathy – Majid Ali

aliacademy.org/neuropathy1.htm

The commonest cause of neuropathy (pain, tingling, electric senses) in toes, legs, and hands is insulintoxicity. This develops in most cases long before diabetes is diagnosed. I offer guidelines to prevent and reverse it. Insulin Neuropathy Reversed With Natural Remedies Majid Ali, M.D.. In my clinical experience, the most …


 

Prediabetes, Insulin Toxicity, and saying NO to Diabetes Seminar by …

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Buy and Download > Description. In this 35-minute video seminar, Professor Majid Ali, M.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 …


What Comes First Rising Blood Sugar Level, Or Rising Blood Insulin Level?

 

Majid Ali, M.D.

No question is more important for stemming the global tides of insulin toxicity and diabetes than the question in the title.

(Part of the Diabetes Question Series)


 

The Answer:

Insulin levels rise first, usually by five, ten, or more years before blood sugars level rise.

Why is this important?

Because insulin toxicity continues to cause cellular damage in the liver, kidneys, heart, brain, eyes and other organs unknown to the patient and the doctor if insulin tests are not done.


 

Not Moving Away From Diabetes Is Moving Towards It

 

Majid Ali, M.D.

Insulin toxicity and diabetes have eclipsed All Chronic Diseases Worldwide. I am grateful to my Patients (My Truest Teachers) Who Helped Me Recognize This Disturbing Reality. 


 

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.

 

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 …

Should Fasting Glucose Be Used for Screening for Diabetes? No.

Majid Ali, M.D.

Insulin and Glucose Profiles of An Reversing Diabetes D3 Series


 

I have seen far too many cases in which the results of fasting blood glucose test were misleading for diagnosing diabetes or ruling it out.


 

Blood Glucose Level In Normal Range Hides Serious Insulin Toxicity

The glucose and insulin profiles in Table 1 and 2 belong to a healthy man and a healthy woman respectively.  These profiles represent ideal insulin and carbohydrate fitness. Note the  low levels of blood insulin concentrations accompanied by blood glucose levels in the normal range. Then recognize how much higher the insulin levels are of the patients whose values are  shown in Table 3. The blood glucose levels here do not reach the levels seen in prediabetes, let alone diabetes.

Two Examples of Healthy Insulin Profiles

Table 1. Ideal Insulin Profile (Peak Value, 18 uIU/mL) of a 60-yr-old 5′ 7″ Male Film-maker weighing 147 lbs. Without Health Problems and Interested in Healthfl Aging. His Three “Secrets to Health” Are: Beautiful Thoughts, Diet, and Exercise.”
6.8.2013 Fasting 1/2 Hr 1 Hr 2 Hr 3 Hr
Insulin <2 18 14 4 <2
Glucose 77 168 109 74 52
Table 2. Ideal Insulin Profile of a 51-year-old 5’2″ Woman Weighing 120 lbs. She Consulted Me for Hypothyroidism and Allergy.
Fasting ½ Hr 1 Hr 2 Hr 3 Hr
Insulin 3.2 11.8 2.4 1.9
Glucose 85 110 75 70 52

 

 

Table 3. Insulin and Glucose Profiles of a 41-Yr-Old  6’ Man Weighing 260 Lbs. Who Presented With Allegry, IBS, And, Numbness on Face And Limbs.

September 15, 2016 Fasting ½ Hr 1 Hr 2 Hr 3 Hr
Insulin / uIU

10.9

148.8 183.5 25.5

9.0

Glucose / mg/

 

83

141 159 91

60

November 17, 2016

Insulin / uIU

5.9

38.8 57.4 28.7

6.5

Glucose / mg/

 

76

124 178 136

82


 

More Post-Glucose Load Insulin and Glucose Profiles

For seeing more pairs of insulin and glucose profiles obtained after  a 75-gram glucose challenge, please consider the article entitled “Shifting Focus From Glycemic Status to Insulin Homeostasis” on this site.

 

 

Screening for Prediabetes

Majid Ali, M.D.

Here are four essentials issues in screening for prediabetes:

1. Prediabetes and diabetes are not sugar problems and cannot be screened for with sugar testing, whether with fasting or two-hour post-prandial.

2. Prediabetes and diabetes are not sugar problems and cannot be screened for with tests for sugar stuck to proteins, such as hemoglobin (re:A1c test).

3. Predia betes and diabetes are not kidney problems and cannot be screened for with tests for protein in the urine.

4. Prediabetes and diabetes are not insulin problems and can only be screened for with insulin tests.

Anyone who disagrees with the above statements has not tested even ten patients with three-hour insulin profiles. If anyone consider my words dogmatic, she or he should consider my free course entitled “Dr. Ali’s Diabetes Course” and then decide if I am being so.


My Diabetes Course  is spread over the following two websites:

http://www.AliDiabetes.Org

http://www.AliHealing.Org


Image result for corn fructose  Image result for corn fructose

Forxiga Treats Diabetes Type 2 By Spilling Glucose in the Urine – and Wasting Energy

Majid Ali, M.D.

A reader asked, “How does Forxiga, the new drug for diabetes, work? Here is mt answer:  Forxiga lowers blood glucose level by spilling glucose from the kidneys. What does that really mean? It means wasting large amounts of energy in the body.


We Need Good Drugs

Good drugs are needed for people with diabetes Type 2 for individuals not willing or able to learn, understand, and know how to reverse the disease.

 which lower blood glucose level by removing glucose from the kidneys. What does that really mean? It means wasting large amounts of energy in the body.

Forxiga, a new heavily marketed drug doe treating diabetes Type 2 belongs to a new class of drugs called Gliflozins, which lower blood glucose level by removing glucose from the kidneys. What does that really mean? It means wasting large amounts of energy in the body.

What individuals need is to make excess glucose in their blood be driven into the cells for efficient extraction of extract ATP energy from it. Simply spilling glucose in the urine is wasting sorely needed energy. Please read my article entitled “The Crank and Crank-shaft Model of Diabetes” for detailed information.

Forxiga belongs to the Gliflozins family of drugs and may prove very helpful for people who must have some drugs for diabetes. Drugs in this family are specific and potent inhibitors of the sodium-glucose linked transporter2 (SGLT2) protein, Development of gliflozins has focused on their inhibition of SGLT2 protein function in the kidney while their mode of action in other metabolic tissues has not been characterized.

Early in 2015, 4AstraZeneca announced that its Forxiga (diabetes drug) sales ripped higher by 139% in 2014, fueled by the strong launch of the drug. This, of course, says nothing aboiut the real value of Forxiga.

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