Tag Archives: Insulin Toxicity

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.
J. Clin. Invest. 2005;115:1111–1119.
8.Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance.
J. Clin. Invest. 2006;116:1793–1801.
9.World Health Organization Consultation on Obesity 1–253 (World Health Organization, Geneva, 2000).
10.Wild S, Roglic G, Green A, et al. Global prevalence of diabetes: Estimates for the year 2000 and projections for 2030.
Diabetes Care. 2004;27:1047–1053.
11.Hedley AA. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999–2002.
JAMA. 2004;291:2847–2850.
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.
13.Rosen ED, Spiegelman BM. Adipocytes as regulators of energy balance and glucose homeostasis.
Nature. 2006;444:847-853.
14.Nath D, Heemels M-T, Lesley Anson L Obesity and diabetes.
Nature. 2006;444, 839.
15.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.
16.Farmer SR. Transcriptional control of adipocyte formation.
Cell Metab. 2006;4:263–273.
17.Trayhurn P. Endocrine and signalling role of adipose tissue: New perspectives on fat.
Acta Physiol. Scand. 2005;184: 285–293.
18.Perreault M, Marette A. Targeted disruption of inducible nitric oxide synthase protects against obesity-linked insulin resistance in muscle.
Nature Med. 2001;7:1138–1143.
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.
Eur. J. Biochem. 2000;267:5952-5958.
21.Enerback S et al. Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese.
Nature. 1997;387:90–94.
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.
Nature. 2001:409;307-312.
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.
J. Clin. Invest. 2002;110:1093–1103.
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.
Nature. 2006;444:1027-1031.
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.

 

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

 

 

 

 

 

 

 

 

The Diabetes Question

Majid Ali, M.D.

Does Diabetes Begin As a Rising Blood Sugar Disease Or As a Rising blood Insulin Disease?

We Will Let Call It  

The Diabetes Question.


If the answer to the diabetes question is that it begins with rising blood insulin levels,  not with rising blood glucose levels, then the following new questions arise?

Question: Is excess insulin (hyperinsulinism) toxic to the body organs?

Answer, Yes, Excess insulin is fattening, fermentiing, and inflaming. It swells the liver and shrinks the brain. It is pro-cancer, pro-inflammation, and pro-degenerative diseases. In damages endo cells which lines the inside of the entire cardiovascular system and affects blood circulation everywhere in the body. Simply stated, excess insulin (insulin toxicity) is “pro-accelerated pro-aging.” 

Question: Can insulin toxicity be assessed with blood sugar tests?

Answer. No.

Question: In most people, how long does insulin toxicity go on undetected before blood sugar levels rise enough to make diabetes diagnosable with blood sugar tests?

Answer, for five, ten, or more years?

Question: Do doctors usually always test for blood insulin level before they test for blood sugar level?

Answer, No.


 

What Must Be Known About Crucial Diabetes and Its Complications

(In this article the terms diabetes and Type 2 dabetes are used interchangeably)

Diabetes (Type 2 Diabetes,T2D) Cannot Be Diagnosed In Time Without Insulin Tests, Diabetes Cannot Be Reversed Without Insulin Intelligence. Nor Can Diabetes Complications Be Prevented or Reversed Without Insulin Intelligence.


 

Summary

Diabetes Is Not a Sugar Problem,

It Is a Problem of Insulin Toxicity (Hyperinsulinism).

Insulin Toxicity Predates Diabetes by Five, Ten, or more Years, and Directly Leads to the Disease.


 

The Cost of Neglected Insulin Testing 

Hyperinsulinism (insulin toxicity) inflicts cellular injury in nearly all cellular populations in the body.  During the  years insulin toxicity remains ,undetected and untreated, simply because insulin testing is neglected by practitioners. Why?

Blood insulin testing is not considered a standard of care by those who control $1.3 trillion yearly spending for medical care in the United States. After considering the evidence I present in this and other articles in my “Diabetes Question Series,” the readers will decide for themselves as to the real reason for neglected insulin testing.  

I Leave the answer to readers.    


What Is Insulin Intelligence?

Simply stated, excess insulin (insulin toxicity and hyperinsulinism by other names)  is a fire which burns all parts of the body. It may start in different places and spread differently but the end result is always shortened life span with different diseases.

A practitioner who answers this questions with the “diabetes-hyperinsulinism” prevailing view does not, in my opinion, serve his patients well. Anyone who answers the question with one-liners recognizing insulin as the “life-span” hormone without does not deserve anyone’s time. As for me, I want to invite you to consider these questions by taking my free-of-cost course at this web site. A library of my selected article, published papers, and short videos is included in this post. Readers interested in my book on reversing diabetes and video seminar downloads can access these materials at http://www.aliacademy.org.


 

The Diabetes Question:

Can insulin regulation be assesses with sugar tests?

Specifically, can diabetes be detected in time with fasting blood sugar test, A1c blood tests, two-hour post prandial (after a meal) blood sugar level?

The answer: Categorically not.


 

What Is Optimal Insulin Homeostasis?

First, when the blood insulin levels after a glucose challenge are quite low;

Second, blood glucose after a glucose challenge are within low physiologic range.

Third, when there is no history of diabetes in parents and grandparents.

Fourth, when there is no insulin toxicity.

Fifth, when the immune system is robust and there is no chronic . immune-inflammatory disease.

Question: Can one optimize one’s insulin homeostasis? One can only answer this question for oneself.


 

One can tell oneself lies, but nature does not grant permission to believe one’s own lies. 


Can insulin homeostasis (insulin regulation as a whole) be assessed with blood sugar tolerance  test, A1c blood tests, two-hour post prandial (after a meal) blood glucose tests, as for instance the tolerance test done for gestational diabetes?

The answer: Categorically not.


To provide a broader context for due deliberation of the above questions, please consider sets of blood insulin and glucose profiles below which were prepared with fasting and timed post-glucose challenge.
       Table  1  Control Profiles
       Table 2,3 Blood glicose tests are inappropriate for assessing insulin homestasis
       Table 4.  Hyperinsulinism in Autism Spectrum Disorder 

Table 1. Two Sets of Control Insulin and Glucose Profiles

1.Healthy control subject:. Case 1.

                 INSULIN :    <2 uIU/mL, 18, uIU/mL, 4,       and <2;    

                 GLUCOSE:    77, 168, 109, 74, 52.

2. Healthy Control Subject: Case 2  

               INSULIN :    3 uIU/mL, 11, uIU/mL, 7,   and <2;    

               GLUCOSE:    81  157, 98, 63, 52.


The Challenge in Reversing Diabetes

is not to know what any doctor thinks about diabetes and drugs used to treat diabetes but how to learn to think for yourself about insulin, health, and healing.

I suggest you spend time at http://www.alidiabetes.org 


The Most Important Question in the Prevention and Reversal of Diabetes (Type 2)

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


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. For more info, go to http://www.Ali Diabetes.Org for the author’s free-access course at
http://www.Ali Diabetes.Org.

https://wordpress.com/post/alidiabetes.org/2966


Table 2. 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)
(less than time and a half higher) 
231.0
(nearly 17 times higher)
#   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, a subgroup of optimal 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 insulin homeostasis, peak insulin  between <40 and 80 uU/mL;  accompanied by unimpaired glucose tolerance; ; (3) moderate insulin homeostasis, peak insulin  between <80 uU/mL and 160 uIU/mL accompanied by unimpaired glucose tolerance;  and (4) severe insulin homeostasis, peak insulin  > 160 uU/mL accompanied by unimpaired glucose tolerance.

Why Do Diabetics Need Insulin Shots?

Because Their Pancreas Has Exhausted Its Lifetime Capacity of Produce Sufficient Insulin

Note the extremely high blood insulin level (298 uIU/mL) still cannot keep the blood glucose level in the normal non-diabetic level.
Table 3. 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, Moderate    N =  42
24.0%
242.1   (13.45)
112.4
Diabetic Hyperinsulinism, Severe          N =  24
13.9%
224.6   (12.47)
298.0
Diabetic  Insulin Deficit                             N =  59
33.1%
294.0    (16.33)
22.9

What Is Optimal Insulin Homeostasis?

It is the lowest blood insulin levels that can keep the blood glucose levels in the normal range.
In other words, It is ideal state of insulin utilization, in which insulin toxicity does not exist, nor is insulin wasted because there is too much of it in the blood.
is not wasted .
In 2017, in a large survey of insulin and glucose profiles in the general New York metropolitan population, my colleagues and I reported a hyperinsulinism prevalence of 75.1%. Below is the link to get free access to the full text of this report:

http://www.townsendletter.com/Jan2017/insulin0117.html

Or, you may get the report on this website by entering , please use the the following words on the search box of the site:  “Shifting Focus from Glycemic Status.”

Examples of Insulin and Glucose Profiles of Individuals With Perfect Insulin Regulation

Table 1. Post-Glucose Load Insulin and Glucose Profiles of Seven Individuals With Optimal Insulin Homeostasis as Defined Above.
Fasting
½-Hr
1-Hr
2-Hr
3-hr
Insulin Profile 1. Insulin And Glucose Profiles of a 47-yr-old 5′ 5″ Male Runner Weighing 130 lbs. Who Presented With Inhalant Allergy and Hemorrhoids.
Insulin uIU/mL
1.5
9.7
9.0
4.6
<1.0
Glucose mg/dL
72
148
134
108
54
Insulin Profile 2. Insulin and Glucose Profiles of a  45-Yr-Old  5’9″Man Weighing 125 lbs. Presenting With Allergy and Dry Skin.
Insulin uIU/mL
1.0
2.7
9.8
2.7
<1.0
Glucose mg/dL
85
110
75
70
52
Insulin Profile 3. Insulin and Glucose Profiles of a 51-year-old 5’6″ Man Weighing 120 lbs. He Consulted Me for Cardiac Rhythm Disorder, Hypothyroidism and  Allergy.
Insulin uIU/mL
2.9
6.0
11.5
2.5
Glucose mg/dL
89
103
134
110
59
Insulin Profile 4. Insulin and Glucose Profiles of a 52-Yr-Old 5’1″ Woman Weighing 120 lbs. Presenting With Constipation and  Allergy.
Insulin uIU/mL
<2
17
15
6
Glucose mg/dL
78
61
72
71
Insulin Profile 5. Insulin and Glucose Profiles of a  52-Yr-Old 5’ 7″ Man Weighing 155 lbs. Presenting With Anxiety, Depression, and Diarrhea. A1c. 5.3%
Insulin uIU/mL
2.0
8.1
19.6
17.7
4
Glucose mg/dL
94
140
158
91
73
Insulin Profile 6. Insulin and Glucose Profiles of a  62-Yr-Old  5’3″ Woman Weighing 114 lbs. Presenting With Allergy and Hand Arthralgia.
Insulin uIU/mL
1.8
17.8
11.0
10.0
Glucose mg/dL
80
159
76
75
68
Insulin Profile 7. Insulin and Glucose Profiles of a 51-year-old 5’2″ Woman Weighing 120 lbs. She Consulted Me for Hypothyroidism and  Allergy
Insulin uIU/mL
3.2
11.8
2.4
1.9
Glucose mg/dL
86
110
75
70
52
Insulin Lab Reference Ranges Not  Fit for Use
In a previous report the author and his colleagues have highlighted the serious problem of inappropriate prevailing reference ranges for blood insulin concentrations.13 The data in Table 2 reproduced from that publication dramatically illustrates the dimension of this problem with findings of a survey of major laboratories in the New York City metropolitan area. The study data also calls into question the clinical value of single and random blood insulin test results. Photographs of illustrative lab reports are posted online.14

Absurd Laboratory Reference Ranges

Table 2. Upper and Lower Limits of Laboratory Insulin Reference  Ranges Expressed In uIU/mL Following a Standard Glucose Load From Six Major Clinical Laboratories in the New York Metropolitan Area.2
Laboratory
Fasting
1 Hr
2 Hr
3 Hr
Laboratory 1
1.9 – 23
8  –  112
5 – 35
Laboratory  2
2.6 – 24.9
0.0  – 121.9
0.0 – 163.5
Laboratory  3
2.6 – 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. Personal communications with clinicians revealed that they do not find this laboratory note to be helpful.
 
 

Spectrum of Insulin Dysfunction and Hyperinsulinism in Autism

Table 4 presents insulin and glucose profiles of 10 patients with dysautonomia. Note that all patients suffered from allergic disorders.
Table 4. Insulin and Glucose Profiles of Individuals With Autism.
The Blood Insulin and Glucose Levels Are Expressed in uIU/mL and mg/dL respectively.
Fasting
½ Hr
1 Hr
2 Hr
3 Hr
Autism Case 1. Insulin and Glucose Profiles of 14-Yr-Old 5’ 9” Boy Weighing 115 lbs.Who Presented Without Expressive Speech Since Birth.
Insulin uIU/mL
24
300
235
211
83
Glucose mg/dL
83
129
98
95
61
Autism Case 2. Insulin Profile and Glucose Profiles of 15-Yr-Old Boy With  Autism, Allergy, and Fatigue.
Insulin uIU/mL
10.4
43.7
37.6
33.7
7.8
Glucose mg/dL
79
104
86
82
53
Autism Case 3. Insulin and Glucose Profiles of 17-Yr-Old-Boy With Autism, Eczema, And Anxiety.
Insulin uIU/mL
24.4
N/A
73.8
71.6
28.0
Glucose mg/dL
95
N/A
79
79
69
Autism Case 4.  Insulin and Glucose Profiles of 8-Yr-Old Boy Presenting With Autism, Sudden Mood Shifts, and Inhalant Allergy.
Insulin uIU/mL
6.2
40.36
41.5
24.8
3.9
Glucose mg/dL
96
192
131
109
57
Autism Case 5. Insulin and Glucose Profiles of A Three-Year-Old  Boy With Asperger’s Syndrome, Temper Tantrums, Eczema, And Inhalant Allergy.
Insulin uIU/mL
1.28
14.3
0.33
Glucose mg/dL
71
126
88
Autism Case  6. Insulin and Glucose Profiles Of A Four-Year-Old Boy Weighing 35 lbs. Limited expressive speech, Often in non-communicative trance. Mother’s Words: “Very Intelligent In Things That Interest Him.”
Insulin uIU/mL
2.3
24.2
20.2
17.8
0.8
Glucose mg/dL
89
151
102
98
79
Autism Case 7 .  Insulin and Glucose Profiles of A 5-yr-old Boy With Autism Focus Disorder. No Expressive Speech Until Age 30 Months, Single Words 10-15 Words. No Voluntary Sentences. Eczema, Recurrent Ear Infections.
Insulin uIU/mL
1.31
47.16
43.99
Glucose mg/dL
64
127
150
Autism Case 8 . Insulin And Glucose Profiles  of  A 7-Yr-Old Boy Presenting With Diagnoses of Autism, Inhalant Eczema, Food Allergy, and History of Multiple Courses of Antibiotics for Sore Throats.
Insulin uIU/mL
11.0
Glucose mg/dL
73
Autism Case 9. Insulin And Glucose Profiles  of A Six-Yr-Old Boy Presented With Autism, Hypothyroidism, Food and Inhalant Allergy.
Insulin uIU/mL
13.0
Glucose mg/dL
85
The staff of a university hospital mishandled the blood samples on two different occasions.
Autism Case 10. Insulin and Glucose Profile of A 28-yr-old Man Who Was Diagnosed With Autism with complete Absence of Expressive Speech Until Age 4 And Then Transitioned to Asperger’s Syndrome. At Age 21, He Was An Excellent Athlete But Could Speak Only To His Mother.
Insulin uIU/mL
7
174
365
71.9
7.9
Glucose mg/dL
81
178
160
85
56
Follow-Up Testing One Year Later
Insulin uIU/mL
8.2
139.9
152.0
40.82
2.82
Glucose mg/dL
88
128
125
100
47

Free-Access Library for Reversing Diabetes.

First things first: Only you can reverse your diabetes, not anyone else.

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.


 

Insulin Toxicity, Silent Stroke, Brain Lacuna, and Coming Years

Majid Ali, M.D.

A brain lacuna is a localized area of loss of brain cells which does not cause any signs and symptoms of brain damage. It is considered as a small silent stroke. It must also be considered an important wake-up call for gardener thinking.


A Bit of Gardener Thinking for Brain Health

 

As roots are to roses, so the liver to the brain.

As roots are to roses, so the the bowel to the liver.


 

Gardener Thinking

Gardeners are usually clear-headed. They don’t count wilting leaves and classify diseases by the number, form, and location of wilting leaves. They think of the health of the soil and sunlight for their flowering plants.


 

For bowel health, please consider my videos and articles under the Seed-Feed-Weed category.

Selected Articles and Videos

Hyperinsulinism (insulin toxicity) and stroke | The Ali Academy Community

Dr. Ali’s Diabetes Course – Part II

Majid Ali, M.D

Shifting Focus From Sugar to Insulin For Preventing and Reversing Type 2 Diabetes


Question: What is the commonest reason for delay in diabetes diagnosis?

Answer: Failure to do 3-hour blood insulin test.


Question: What is the commonest reason for failing to reverse diabetes?

 Answer:        Failure to do 3-hour blood insulin test.


Question: Is Fasting Blood Sugar (Glucose) Test Reliable for Screening for Diabetes?

Answer: No. It is common for me to  diagnosis diabetes with a full 3-hour glucose test when the fasing blood sugar level is in the normal range.


Question: Is Blood  A1c Test Reliable for Screening for Diabetes?

Answer: No. It is common for me to  diagnosis diabetes with a full 3-hour glucose test when the A1c is in the normal range

The Basics of Diabetes — My 1958 View of the Disease

Reversing diabetes was not a part of medical consciousness then.


Types of Diabetes

  1. Prediabetes
  2. Type 2 diabetes
  3. Type 1 diabetes
  4. Gestational diabetes
  5. Latent autoimmune diabetes of adults (LADA)
  6. Mitochondrial DNA Mutations diabetes

All of the above are forms of insulin toxicity


Diabetes was  a “sugar disease” then in which blood sugar levels were high due to deficiency of the hormone insulin produced by the pancreas, a gland found in the upper abdomen behind the stomach. I was taught diabetes causes loss of weight, weakness, increased hunger, increased thirst, and frequent urination.

If left untreated, diabetes causes many complications, including brain fog, confusion, tremors (ketoacidoss), muscle twitching, coma, and death. Less acute complications include foot ulcers, nerve injury (neuropathy), eye damage (retnopathy) kidney failure, stroke, and heart disease.


Two Core Aspects of the 2016 Diabetes Story

  1. One of two Chinese Have Diabetes or Prediabetes (JAMA 2013 report).
  2. Type 2 diabetes (the main type of diabetes) can be reversed by everyone willing and able to make the right effort to reverse diabetes.

Types of Diabetes

  1. Prediabetes
  2. Type 2 diabetes
  3. Type 1 diabetes
  4. Gestational diabetes
  5. Latent autoimmune diabetes of adults (LADA)
  6. Mitochondrial DNA Mutations diabetes

Essentials of Modern History of Diabetes

https://alidiabetes.org/2016/06/27/history-of-diabetes/


Pancreatic Diabetes

  1. Acute pancreatitis
  2. Chronic diabetes
  3. Pancreatic tumors
  4. Pancreatectomy

Diabetes of Endocinopathies

  1. Acromegaly
  2. Cushing syndrome
  3. Hyperthyroidism
  4. Glucagonoma
  5. Pheochromocytoma
  6. Hemochromotosis
  7. Cystic fibrosis

Genetic Forms of Diabetes

  1. Insulin gene mutations
  2. Insulin receptor mutations
  3. Genetic forms of diabetes

Three Parts of Dr. Ali’s Diabetes Course

Part 1:

The Basics of Diabetes — causes, symptom-complexes, clinical course, treatment options

Part 2:

Shift from glycemic status to insulin homeostasis (Getting away from the “sugar talk.” Knowing the truth.)

Part 3:

Clearing insulin toxicity, preventing diabetes, reversing Type 2 Diabetes, preventing and/or controlling complication, preparing to teach the course to otheres.


Limits on Students Taking the Course

  1. There are no limits who should take this FREE course..
  2. No medical background is necessary.
  3. The Course can be completed in six weeks or six months, or on an individual’s own pace.

One of two Chinese Have Diabetes or Prediabetes (JAMA 2013 report)

 

 

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