Is Diabetes Really A Sugar Problem? No.

 

Majid Ali, M.D.

New York  212-873-2444

New Jersey . 201-996-0027


 

No, Diabetes Is Not a Sugar Problem.

It is an insulin Problem.


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.

 

Large Scientific Claims Require Large Scientific Evidence

The Common Diabetes Is Not a Sugar Problem, But An Insulin Toxicity Problem.


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
14.3
Optimal Homeostasis,N=  126
24.9 %
121.2
26.7
Hyperinsulinism, Mild,       N =  197
38.9 %
136.5
58.5
Hyperinsulinism, Moderate,  N =  134
26.5 %
147.0 
109.1
Hyperinsulinism, 
Severe,  N =  49

9.7 %

150.0

1.3 – Fold Increase

231.0

17-Fold Increase

#   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

Large Scientific Claims Require Large Scientific Evidence

The Common Diabetes Is Not a Sugar Problem, But An Insulin Toxicity Problem. 

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


How Absurd Can the Lab Normal Ranges Become?

Insulin Reference Ranges  in uIU/mL of Six Laboratories in New York Metropolitan Area*
Laboratory
 
 
Fasting
 
 
1 Hr
 
 
2 Hr
 
 
3 Hr
 
 
Laboratory 1
 
1.9 – 23
 
8  –  112
 
5 – 35
 
Not Reported
 
Laboratory 2
 
2.6 – 24.9
 
0.0  – 121.9
 
0.0 – 163.5
 
Not Reported
 
Laboratory 3 
 
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.**
*Upper and lower limits of laboratory reference ranges for blood insulin concentration determined following a Standard 75-gram glucose challenge.
**Personal communications with clinicians revealed that they do not find this laboratory note to be satisfactory in their clinical decision-making.

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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

.


 

Microplaques in Circulating Blood

When Blood Glucose Level Rises Above 200 mg/dL 

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.


 

 

 


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.

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

 

 

 

 

 

 

 

 

Fatty Liver Or Fatty Liver Disease or Insulin-Toxic Liver

 

Majid Ali, M.D.

Insulin -Toxic Liver Disease – A Global Pandemic


.

A free course on Liver Health NOW | Majid Ali MD | The Ali Academy …

Nov 28, 2014 – Liver HEALTH NOW It is one of the profound ironies of prevailing drug medicine that there is no concept of liver detox among liver specialists. Treatment of most liver diseases in the hands of gastroenterologists and hepatologists is confined to the use of immune-suppressive therapies, such as steroids, …

A course on Liver Detox with Natural Therapies | The Ali … – Majid Ali MD

Dec 18, 2014 – This is an Update March 17, 2015 Dietary sugar consumption, in particular sugar-sweetened beverages and the monosaccharide fructose, has been linked to the incidence and severity of non-alcoholic fatty liver disease (NAFLD). Intervention studies in both animals and humans have shown large doses of …

Liver Disorders | The Ali Academy Community – Majid Ali MD

Mar 30, 2015 – Liver HEALTH NOW It is one of the profound ironies of prevailing drug medicine that there is no concept of liver detox among liver specialists. Treatment of most liver diseases in the hands of gastroenterologists and hepatologists is confined to the use of immune-suppressive therapies, such as steroids, …

Liver videos part 3 | The Ali Academy Community – Majid Ali MD

Liver Detox for Fibromyalgia from Majid Ali on Vimeo. Liver Hemagioma and Vascular Malformation of the Brain from Majid Ali on Vimeo. Hemagioma of the Liver – Insignificant Malformation from Majid Alion Vimeo. PLEASE HELP OUR STAFF! The goal of this website is to provide thousands of free videos and articles …

Dr. Ali’s Bowel Detox and Colon Cleanse | The Ali Academy Community

Nov 17, 2012 – Majid Ali, M.D.. Here are the crucial lessons which my patients, my microscopes, and my friends on my autopsy tables taught me in the last fifty-four years: * As roots are to roses, so the bowels to the brain. * As roots are to roses, so the bowels to the heart. * As roots are to roses, so the bowels to the liver.

Liver Detox – Majid Ali MD

Dec 2, 2017 – Majid Ali, M.D. This Article Is a Part of Dr. A. Liver Course Series The Liver Is the MainDetoxification Organ of the Body. Dr. Ali’s Top Seven Suggestions for liver detox are: 1. Love Without Notions of control 2. Restoring oxygen signaling 3. Prayer 4. Insulin Optimization 5. Dr. Ali’s Breakfast (with lecithin and …

Dr. Ali’s Liver Detox Course – Majid Ali MD

Dec 2, 2017 – Majid Ali, M.D. This Article Is a Part of Dr. A. Liver Course Series The Liver Is the MainDetoxification Organ of the Body. Dr. Ali’s Top Seven Suggestions for liver detox are: 1. Love Without Notions of control 2. Restoring oxygen signaling 3. Prayer 4. Insulin Optimization 5. Dr. Ali’s Breakfast (with lecithin and …

Liver Detox for Fibromyalgia -Majid Ali, MD on Vimeo

https://vimeo.com › Majid Ali › Videos
Apr 16, 2014 – Uploaded by Majid Ali

Professor Majid Ali shares information about “Liver Detox for Fibromyalgia”

Dr. Ali’s Liver Detox – Dr. Ali’s Virtual Medical Library

drali1.org/dr__ali’s_liver_detox.htm

Dr. Ali’s Liver Detox. Majid Ali, M.D.. In this DVD video seminar, Prof. Ali describes his guidelines for gentle daily liver detox. He explains the advantages of this approach over intense one-week to 3-week programs which, notwithstanding their temporary benefits, often create adverse effects. LIST OF VIDEOS. * Master DVD …

Insulin Toxicity – Early Signs

Majid Ali, M.D.

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


 

What Google Told Me About Complications of Diabetes

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

What My PatientsTaught me About Insulin Toxicity

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


 

DR. Ali’s Library of Diabetes

 

 


Top Seven for Diabetes Foot

Majid Ali, M.D.


What Is Diabetic Foot?

What Is Insulin Foot?

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

Signs and Symptoms of Insulin Foot

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

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

Top Seven for Diabetic Foot 

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


 


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

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

Dr. Ali’s VideoLibrary
drali1.org/healer_course.htm
This is a pragmatic view of an integrative physician, not a delusional plausibility of an ideologue. I hope you will consider the Program. It should serve you well for life. Kindest regards, Majid Ali, M.D.. Majid Ali, M.D. Updated June 20, 2010. COURSE 1: PHILOSOPHY OF BEING ONE’S OWN PRIMARY PHYSICIAN.
Jun 11, 2014 – The matters of doubt and uncertainty are of central importance to Being One’s Own Primary Physician. The uncertainty principle offers us an antidote to the risk of habitual thinking, blind trust, and static belief that impedes learning and threatens success. The subject of uncertainty brings to mind some of the …
May 11, 2014 – If your symptoms recurred after sinus surgery, please think of mold allergy, mold infections, and mold toxins. For the … Being One’s Own Personal Physician. I define … For example, a forty-year-old man who develops acute sinusitis and fever cannot be his primary physician for that acute illness. However …
Aug 20, 2014 – Majid Ali, M.D.. My patients with coronary heart disease have taught me this: Heart disease is a state of separation from one’s nature. This separation is caused by: 1. Deep disappointments of ….. For reversing coronary artery disease one must become one’s own primary physician. This, however, takes time.
Dec 25, 2014 – In the United States today, blocker drugs, stents, and bypass procedures are promoted as the primarytherapies for coronary artery disease. … This is what I call being one’s own doctor—cardiologist in the current context. … A Chick Comes Out of an Egg and Drops Dead of a Heart AttackMajid Ali MD …
Jul 8, 2014 – What Is Allergy? A Great Masquerader That Must Be Banished to Enjoy Health Majid Ali, M.D. Allergy is a great masquerader of the immune system. Sneezing, stuffy nose, itchy eyes, skin rashes, and sinusitis are only the surface problems in allergy. There are many deeper and more serious problems …
Rating: 5 – ‎5 reviews
Get appointment information and hours of operation for Majid Ali, practicing Public Health & General Preventive Medicine doctor in New York, NY.
Missing: being ‎own
Being One’s Own Primary PhysicianMajid Ali, M.D.. I define disease in two ways: * First, disease is a state of separation from one’s nature. * Second, disease is a state of evolution in reverse. Since no one else can know one’s nature —nor the degrees of separation from it—one can have only one authenticphysician: …
Sep 3, 2014 – Posts about Majid Ali MD written by Majid Ali MD. … far beyond the classical and wholly inadequate notion of it being a process characterized by edema, erythema, tenderness, pain, and infiltrate of inflammatory cells. ….. For reversing coronary artery disease one must become one’s own primary physician.

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

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

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

 


Top Seven for Diabetic Foot

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Top seven diabetes
Mon, Mar 5, 2018 5:27 pm
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