Restoring Oxygen and Insulin Signaling for Neurodevelopmental and Neurodegenerative Disorders

 

Majid Ali, M.D.

Insulin – The Life Span Hormone

Series of Free Oxygen Course Series


 

Insulin –  The Premium Life Span Hormone

 Human life span is put in jeopardy by disruptions of molecular biology of oxygen and insulin homeostasis; life expectancy of an individual is shortened by diminished signaling of the former1-8 as well as by excessive signaling of the latter.9-15 Oxygen is the organizing principle of human biology and orchestrates all aging processes. In service of oxygen, insulin governs the energy economy of the body. Injured cells need more energy for repairing themselves. Glucose is the primary readily useable fuel for ATP energy generation. Insulin activates glucose transporters, drives glucose into the cells, initiates pathways of ATP energy generation, as well as energy utilization for life functions, and regulates energy transformations, producing proteins for cellular structural needs and fats for energy storage.16-21  So it can be rightfully designated as the “master energy hormone” for the life span.

The Oxygen-Insulin View of Insulin Homeostasis
The author introduced the term “oxygen-insulin view” of insulin homeostasis and the spectrum of insulin dysregulation – hyperinsulinism, metabolic syndromes, gestational diabetes, Type 2 diabetes spectrum (T2D), and diabetic complications – to present a synthesis of his clinical, microscopic, and bioenergetic findings concerning the essential roles of oxygen signaling and insulin homeostasis in the pathobiology of chronic diseases. Specifically, his work extended to the fields of general histopathology,22,23  pathophysiology of aging,24,25 gut immunopathology,26-28  bowel ecology,29,30mitochondrial dysfunction1-3 molecular biology of oxygen,4-8 insulin homeostasis,9-15 cancer,31,32 autism,33dysautonnomia,33 and the science and philosophy of holism in health and healing.34  This work led to the recognition that oxygen signaling and insulin signaling are so inextricably intertwined throughout the kaleidoscopic mosaic of human biology that they cannot be considered as discrete entities in any field of study the of the health/dis-ease/diseases continuum.
 
The author and his colleagues in integrative medicine the clinical oxygen-insulin view, as illustrated by insulin studies in this column, to be very valuable for understanding the scientific underpinnings of diverse disease processes as well as for treating them.35 For optimal long-term clinical outcome, all relevant oxygen and insulin issues for a given patients need to diligently addressed. Treatment of chronic diseases that is confined to pharmacologic agents can be considered neither scientific nor ethical. Readers are invited to closely examine case studies presented in this column. They are drawn from the author’s personal insulin database of over 1100 post-glucose challenge insulin profiles. They can then determine if there is merit to his case for diligence in assessing insulin homeostasis with such laboratory tests.  The matters of keeping oxygen homeostasis at the therapeutic center stage for every patient with chronic disease with documentation of clinical outcomes have been covered at length in Darwin and Dysox Triology, the 10th, 11th, and 12th volumes of the Principles and Practice of Integrative Medicine.35-37  
To facilitate a critical review of the case studies and highlight core clinical aspects of the profile under consideration, the author offers explanatory notes at www.alidiabetes.org.  (For free rapid access, use the search box of the website with the search words: “Townsend Insulin Case Studies”).
Here, the author sees a glaring clinical deficit: a near-complete neglect of relevant oxygen and insulin issues in patient care in doctor offices and clinics in the prevailing medical model in the U.S.  To assess the scope of this issue, the author conducted an informal survey of his patients who had seen two or more physicians (primary physician, internists, endocrinologists, diabetologists, and others) during the year prior to visiting me. None of them recalled any visit in which relevant issues of insulin homeostasis or oxygen signaling in were discussed and appropriate tests were performed. Nearly of all them complied with my request to review their prior medical records. I did not find 3-hour post-glucose challenge insulin studies in any patients.

Hyperinsulinism As Body’s Energy Response to Cellular Injury
In the author’s oxygen-insulin view of insulin dysregulation-to-diabetes continuum, hyperinsulinism results from the response of the pancreas to meet increased energy needs of stressed and injured cells anywhere in the body during the repair processes. This perspective does not challenge the established knowledge of dynamics of hyperglycemia and hyperinsulinism, nor does it abandon any of the regulatory roles of pro-insulin and anti-insulin hormones like glucagon, glucagon-like peptides, and others. The explanatory power of the model, however, reaches far beyond the prevailing understanding of insulin functions and their clinical significance.
The inferences drawn from the author’s large personal database and presented here form the scientific basis and rationale for his view that incremental hyperinsulinism develops as a result of growing pancreatic-bioenergetic response for meeting increasing cellular demands for energy, except in cases of ectopic insulin production in hormone-producing neoplasms.29 Additional evidence for this view is drawn from an extensive body of clinical observations concerning improved clinical results of treatment of diverse disorders when hyperinsulinism accompanying them was detected  and duly addressed with integrative hyperinsulinism modification plans. It is anticipated that readers, who diligently study the diverse case studies presented here and critically examine the included insulin and glucose data will find them compelling and  convincing.

The Crank and Crank-Shaft Model of Insulin  Resistance
In a 2006 column, the author put forth the crank and crank shaft model of insulin resistance, focusing on insulin receptor dysfunction resulting from impaired mitochondrial function.31   In this model, the “crank of insulin” fails to turn the “crank-shaft of insulin receptor” protein embedded in the cell membrane. This occurs when peroxidized lipid, misfolded proteins, and sugar addicts stagnate in cell membranes within accumulations of excess molecular waste and cellular debris as consequences of mitochondrial malfunction and respiratory-to-fermentative shift in ATP generation.32,33 The cell membrane is thickened with grease and glue — so to speak — and the crank-shaft of insulin receptor protein is rusted, turned, and twisted, so rendering the crank of insulin ineffective. Microscopically, such membrane changes can be visualized in some instances, for example, in diabetic nephropathy.34
The crank-crankshaft model of insulin dysfunction has robust explanatory power for the metabolic aspects of the dysfunction (sharp glycemic and insulin shifts, insulin resistance, and others), as well as for its non-metabolic disruptions outlined above. Specifically, it sheds light on how: (1) glucose spikes trigger insulin sharp spikes; (2) insulin  spikes create hypoglycemic troughs; (3) glucose lows set the stage for ‘carb-cravings’; (4) carbohydrate remedies create secondary cycles of glucose-insulin spikes, eventually leading to insulin dysregulation, hyperinsulinism, weight gain, Type 2 diabetes, and diabetic complications.
Hyperinsulism Fans Its Own Fires 
As put forth here, hyperinsulinism developing as pancreatic insulin response to increased tissue demands for energy comes at a cost: a “hyper-insulin” state – so to speak – which results from metabolic and non-metabolic insulin overdrive. This insulin state is fattening, fermenting, inflaming, and self-perpetuating. Simply stated, excess insulin begets excess insulinism.  From these aspects of pathophysiology of insulin dysfunction and overdrive,  abundantly documented by case studies included here and published previously,35,36 hyperinsulinism is expected to play central roles in the pathogenesis and progression of most, if not all chronic metabolic, developmental, inflammatory, infectious, autoimmune, degenerative, and malignant diseases.37-41  This, indeed, is observed when insulin homeostasis is assessed in individual patients with appropriate carbohydrate challenges. This is what the author and his colleagues observed in a large survey of hyperinsulinism in a general population in metropolitan New York area. Insulin dysfunction with varying levels of hyperinsulinism was found and documented in all chronic diseases so investigated – acne to dermatitis, psoriasis to sarcoidosis, autism to Alzheimer’s disease, liver steatosis to heart amyloidosis,  bronchiectasis to pulmonary fibrosis, lupus to scleroderma, rheumatoid arthritis to Lyme polyarthralgia, interstitial cystitis to recurrent prostatitis, and malignant tumors.42,43  

Optimal Insulin Homeostasis
What is optimal insulin homeostasis? Most regrettably, this crucial question has been almost totally ignored in endocrinology, diabetology, bariatrics, and internal medicine. On September 11, 2017, a Google search for optimal insulin homeostasis revealed only seven entries which listed the three words in that order; all of them concerned the author’s own texts. Notably missing were websites of the American Diabetes Association, the European Foundation for the Study of Diabetes, Diabetes Ca (Canada),  The American Congress of Obstetricians  and Gynecologists, and the World Health Organization. 
In the context of healthful aging, the author’s view of the evolutionary bioenergetic ideal of human metabolism is:  (1) the lower the blood insulin concentrations following a glucose challenge accompanied by unimpaired glucose tolerance, the greater the efficiency of insulin; (2) the greater the efficiency of insulin, the closer the insulin homeostasis to its ideal; (3) hypoinsulinism by itself is of no clinical consequence since there are no known adverse effects of very low blood insulin concentrations when accompanied by unimpaired glucose tolerance; (4) hyperinsulinism sets the stage of metabolic overdrive in all cellular populations of the body; (5) insulin in excess has hepatic, endothelial, myocardial, neural, ovarian, renal, and other adverse effects; (6) the growth factor roles of insulin intensify and perpetuate inflammatory, autoimmune, and neoplastic processes.
In a survey of insulin homeostasis in 684 patients (506 of them with known T2D, (Table 1) in the general New York metropolitan area,  the author and his colleagues reported a prevalence rate of hyperinsulinism in 75.1%.37   A subgroup of twelve participants was designated ‘exceptional insulin homeostasis’ for two reasons: (1) they showed an extremely low fasting insulin value of <2 uIU/mL (mean 14.3 uIU/mL) and peak insulin concentrations <20 uIU/mL accompanied by unimpaired glucose tolerance, and (2) ten of the twelve had no family history of diabetes (parents, siblings, grandparents, children, uncles or aunts), while the mother of the eleventh subject developed T2D in the closing months of her life at age 74 and both parents of the twelfth subject had T2D. This subgroup appears to reflect ideal metabolic efficiency of insulin in the larger evolutionary context.
Insulin Homeostasis Categories in 506 Study Subjects Without Type 2 Diabetes
Insulin Category*
Percentage of Subgroup
Mean Peak Glucose  mg/dL
(mmol/mL)
Mean Peak Insulin (uIU/mL)
Exceptional Insulin Homeostasis         N =  12**
1.7%
110.2     (6.12)
14.3
Optimal Insulin Homeostasis                N =  126
24.9 %
121.2     (6.73)
26.7
Hyperinsulinism, Mild                             N =  197
38.9 %
136.5   (7.58)
58.5
Hyperinsulinism,  Moderate                  N =  134
26.5 %
147.0    (8.16)
109.1
Hyperinsulinism,  Severe                        N =  49
9.7 %
150.0    (8.33)
231.0
#   Correlation coefficient, r value, for means of peak glucose and insulin levels in the five insulin categories is 0.84.
*Criteria for classification: (1) Exceptional insulin homeostasis, 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

Table 3 shows the prevalence rates of the categories of optimal insulin homeostasis, and hyperinsulinism of mild, moderate, and severe degrees in 178 survey subjects with Type 2 diabetes. By contrast to the group without Type 2 diabetes, the means of peak glucose levels in this group with Type 2 diabetes do not correlate with means of peak post-glucose insulin concentrations. The fourth category of diabetic insulin depletion in this group indicates varying degrees of pancreatic failure to produce sufficient insulin to override insulin receptor resistance, drive glucose into the cells, and keep glucose in the normal range. The significance of this finding is discussed in the Discussion section of this report.
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
Illustrative Case Studies of Insulin Responses to Glucose Challenge
Tables 4 to 8 present five illustrative sets of insulin and glucose profiles with brief clinical notes. The insulin profiles in Tables 4 and 8  represent the two extremes of insulin peaks (18 uIU/mL and 718.2 uIU/mL) encountered in this survey. The first of the two profiles (Table 4) is reflective of ideal metabolic efficiency of insulin in a larger evolutionary perspective of energy economy in the body. Notable findings here are: (1) a very low fasting insulin level of <2 uIU/mL reflecting efficient insulin conservation during the fasting state; (2) low insulin peak value (18 uIU/mL) indicating high insulin efficiency following a substantial glucose challenge; and (3) a very low insulin level in the 3-hour sample (<2 uIU/mL) reflects optimal beta cell response to glucose level falling below the fasting level.
Table 4. Example of Insulin and Glucose Profiles In Exceptional Insulin Homeostasis Category*
 
Fasting
½ Hr
1 Hr
2 Hr
3 Hr
Insulin uIU/mL
<2
18
14
4
<2
Glucose mg/mL  (mmol/L)
77     (4.27)
168   (9.33)
109      (6.05)
74       (4.11)
59    (2.88)
*The Patient,  A  60-Yr-Old 5’ 7” Man Weighing 138 lbs. Presented for a Wellness Assessment. He Was Considered to be in Excellent Health By Clinical and Laboratory Evaluation Criteria.
Table 5.  Severe Hyperinsulinemia in A Subject With Previously Undiagnosed Type 2 Diabetes*
 
Fasting
½ Hr
1 Hr
2 Hr
3 Hr
Insulin uIU/mL
23.8
19.3
36.9
114.7
75.2
Glucose mg/mL  (mmol/L)
112     (6.21)
158   (8.77)
214      (11.76)
241    (13.38)
129   (7.16)
* The Patient,  A 64-Yr-Old 5’ 4” Woman Weighing 164 lbs. Presented With Hypothyroidism, History of Coronary Artery Stent Insertions, Fatty Liver, Memory Concerns And Without Previous Diagnosis of Type 2 Diabetes.
Table 6. Hyperinsulinism 18 Years After the Diagnosis of Type 2 Diabetes*
Fasting
½ Hr
1Hr
2Hr
3Hr
Insulin uIU/mL
  12.9
27.2
29.2
36.2
25.4
Glucose mg/mL  (mmol/L)
128      (7.10)
224   (12.43)
278    (15.42)
297    (16.48)
249     (13.81)
*The Patient,  A 74-Yr-Old 5’ 6” Woman Weighing 155 Lbs. Presented With Bronchiectasis, Rheumatoid Arthritis, Prehypertension, and Inhalant Allergy.
Table 7. Brisk Insulin Response With A “Flat” Glucose Tolerance Profile*
Fasting
½ Hr
1Hr
2Hr
3Hr
Insulin uIU/mL
3
23
22
8
<2
Glucose mg/mL  (mmol/L)
72      (3.39)
44     (2.44)
63    (3.49)
58     (3.21)
65   (3.90)
*The Patient,  A 47-Yr.Old  5’ 5” Woman Weighing 170 Lbs. Presented With Polyarthralgia, Recurrent Sinusitis, and Fatigue.
Table 8. Severe Hyperinsulinism In A 13-Yr-Old With Lupus Erythematosus*
Fasting
½  Hr
1Hr
2Hr
3Hr
Insulin uIU/mL
27.9
362.5
424.0
718.2
571.7
Glucose mg/mL  (mmol/L)
      70   (3.88)
  140     (7.77)
   157     (8.71)
   150    (8.33)
   111   (6.16)
Insulin and Glucose Profiles Obtained After Four Months of Robust Integrative Therapies
Insulin uIU/mL
7.2
125.1
238.5
208.0
132.0
Glucose mg/mL  (mmol/L)
81     (4.49)
154   (8.54)
181     (10.04)
130     (7.21)
97      (5.38)
*The Patient,  A 13-Yr-Old Girl With a History of Three Hospitalizations In One Year for Systemic Lupus Erythematosus, Recurrent Pneumonia, Thrombocytopenia, and Severe Optic Neuritis Resulting In Complete Loss of Vision In Right Eye. The Peak Insulin Fell from 718 to 238.5 In Four Months of Robust Integrative Treatment.
Majid Ali

 


References
1.    Ali M: RDA:Rats, Drugs, and Assumptions. Denville, New Jersey, Life Span Books 1995. Pp 277-280.
2.    Ali M. Respiratory-to-Fermentative (RTF) Shift in ATP Production in Chronic Energy Deficit States. Townsend Letter for Doctors and Patients. 2004;253:64-65.
3.    Ali M. Oxygen and Aging. (2nd ed.) New York, Canary 21 Press. 2004.
4.    Ali M. Epidemic of Dysoxygenosis and the Metabolic Syndrome. In: The Principles and Practice of Integrative Medicine. Volume 5. Pp 246-256. Canary 21 Press. New York. 2005.
5.    Ali M. Dr. Ali’s Plan for Reversing Diabetes. New York, Canary 21 Press. Aging Healthfully Book 2011. Pp 107-205.
6.    Ali M. Altered States of Bowel Ecology. (monograph). Teaneck, NJ, 1980.
7.    Ali M. Mercury Toxicity and Detox. Volume XIII. New York The Principles and Practice of Integrative Medicine New York (2013).
8.    Ali M.Darwin, Dysox, and Integrative Protocols. Volume XII . The Principles and Practice of Integrative Medicine New York (2009). Institute of Integrative Medicine Press.

Additional Citation
1.       Ali. M. Oxygen and Aging. 2000. (Ist ed.) New York, Canary 21 Press. Aging Healthfully Book 2000.
2.       Ali M. Respiratory-to-Fermentative (RTF) Shift in ATP Production in Chronic Energy Deficit States. Townsend Letter for Doctors and Patients. 2004;253:64-65.
3.       Chouchani ET, Victoria R. Pell VR, Edoardo Gaude E, et. al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature. 2014; 515:431–435.
4.       Ali M. Succinate Retention. In: Chouchani ET, Victoria R. Pell VR, Edoardo Gaude E, et. al. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS. Nature. 2014;515:431–435. Data after references).
5.       Ali M. Dysox Model of Diabetes and De-Diabetization Potential. Townsend Letter-The examiner of Alternative Medicine. 2007; 286:137-145.
6.       Ali M. Oxygen, Insulin Toxicity, Inflammation, and  the Clinical Benefits of Chelation. Part I. Townsend Letter-The examiner of Alternative Medicine. 2009;315:105-109. October, 2009.
7.       Ali M. Insulin Reduction and EDTA Chelation: Two Potent and Complementary Approaches For Preventing and Reversing Coronary Disease. Oxygen, Insulin Toxicity, Inflammation, and the  Clinical Benefits of Chelation – Part II. Townsend Letter-The examiner of Alternative Medicine. 2010;323:74-79. June 2010.
8.       Ali M. Beyond insulin resistance and syndrome X: The oxidative-dysoxygenative insulin dysfunction (ODID) model. J Capital University of Integrative Medicine. 2001;1:101-141.
9.       Ali M.Epidemic of Dysoxygenosis and the Metabolic Syndrome. In: The Principles and Practice of Integrative Medicine. Volume 5. Pp 246-256. Canary 21 Press. New York. 2005.
10.    Ali M. Dr. Ali’s Plan for Reversing Diabetes. New York, Canary 21 Press. Aging Healthfully Book 2011.
11.    Ali M. Ali Fayemi AO, Shifting Focus From Glycemic Statsu to Insulin Homeostasis. Ali M, Fayemi AO, Ali O, Dasoju S, Chaudhary D, Hameedi S, Amin J, Ali K, and Svoboda B. Shifting focus from glycemic status to insulin homeostasis for stemming global tides of hyperinsulinism and Type 2 diabetes. Townsend Letter – The examiner of Alternative Medicine. 2017;402:91-96.
12.    Ali M. Shifting Focus From Glycemic Status to Insulin Homeostasis. E-comments In Nature. 2017;542:191.Re: Kobayashi T, Yamaguchi T, Hamanaka S, et al. Generation of rat pancreas in mouse by interspecies blastocyt injection of pluripotent stem cells. Cell. 2010;142:787-799.
13.    Ali M. Importance of Subtyping Diabetes Type 2 Into Diabetes Type 2A and Diabetes Type 2B. Townsend Letter-The Examiner of Alternative Medicine. 2014; 369:56-58.
14.    Ali M. Dasoju S, Karim N, Amin J, Chaudary D. Study of Responses to Carbohydrates and Non-carbohydrate Challenges In Insulin-Based Care of Metabolic Disorders.  Townsend Letter-The Examiner of Alternative Medicine. 2016; 391:48-51.
15.    Ali M. Darwin, Oxygen Homeostasis, and  Oxystatic Therapies. Volume X, 3 rd. Edi The Principles and Practice of Integrative Medicine (2009) New York. Institute of Integrative Medicine Press.

 


 

Selected Insulin Homeostasis Data

 

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)
231.0
#   Correlation coefficient, r value, for means of peak glucose and insulin levels in the five insulin categories is 0.84.
*Criteria for classification: (1) Exceptional insulin homeostasis, 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
Table 3 shows the prevalence rates of the categories of optimal insulin homeostasis, and hyperinsulinism of mild, moderate, and severe degrees in 178 survey subjects with Type 2 diabetes. By contrast to the group without Type 2 diabetes, the means of peak glucose levels in this group with Type 2 diabetes do not correlate with means of peak post-glucose insulin concentrations. The fourth category of diabetic insulin depletion in this group indicates varying degrees of pancreatic failure to produce sufficient insulin to override insulin receptor resistance, drive glucose into the cells, and keep glucose in the normal range. The significance of this finding is discussed in the Discussion section of this report.
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
Illustrative Case Studies of Insulin Responses to Glucose Challenge
Tables 4 to 8 present five illustrative sets of insulin and glucose profiles with brief clinical notes. The insulin profiles in Tables 4 and 8  represent the two extremes of insulin peaks (18 uIU/mL and 718.2 uIU/mL) encountered in this survey. The first of the two profiles (Table 4) is reflective of ideal metabolic efficiency of insulin in a larger evolutionary perspective of energy economy in the body. Notable findings here are: (1) a very low fasting insulin level of <2 uIU/mL reflecting efficient insulin conservation during the fasting state; (2) low insulin peak value (18 uIU/mL) indicating high insulin efficiency following a substantial glucose challenge; and (3) a very low insulin level in the 3-hour sample (<2 uIU/mL) reflects optimal beta cell response to glucose level falling below the fasting level.
 
Table 4. Example of Insulin and Glucose Profiles In Exceptional Insulin Homeostasis Category*
 
Fasting
½ Hr
1 Hr
2 Hr
3 Hr
Insulin uIU/mL
<2
18
14
4
<2
Glucose mg/mL  (mmol/L)
77     (4.27)
168   (9.33)
109      (6.05)
74       (4.11)
59    (2.88)
*The Patient,  A  60-Yr-Old 5’ 7” Man Weighing 138 lbs. Presented for a Wellness Assessment. He Was Considered to be in Excellent Health By Clinical and Laboratory Evaluation Criteria.
Table 5.  Severe Hyperinsulinemia in A Subject With Previously Undiagnosed Type 2 Diabetes*
 
Fasting
½ Hr
1 Hr
2 Hr
3 Hr
Insulin uIU/mL
23.8
19.3
36.9
114.7
75.2
Glucose mg/mL  (mmol/L)
112     (6.21)
158   (8.77)
214      (11.76)
241    (13.38)
129   (7.16)
* The Patient,  A 64-Yr-Old 5’ 4” Woman Weighing 164 lbs. Presented With Hypothyroidism, History of Coronary Artery Stent Insertions, Fatty Liver, Memory Concerns And Without Previous Diagnosis of Type 2 Diabetes.
Table 6. Hyperinsulinism 18 Years After the Diagnosis of Type 2 Diabetes*
Fasting
½ Hr
1Hr
2Hr
3Hr
Insulin uIU/mL
  12.9
27.2
29.2
36.2
25.4
Glucose mg/mL  (mmol/L)
128      (7.10)
224   (12.43)
278    (15.42)
297    (16.48)
249     (13.81)
*The Patient,  A 74-Yr-Old 5’ 6” Woman Weighing 155 Lbs. Presented With Bronchiectasis, Rheumatoid Arthritis, Prehypertension, and Inhalant Allergy.
Table 7. Brisk Insulin Response With A “Flat” Glucose Tolerance Profile*
Fasting
½ Hr
1Hr
2Hr
3Hr
Insulin uIU/mL
3
23
22
8
<2
Glucose mg/mL  (mmol/L)
72      (3.39)
44     (2.44)
63    (3.49)
58     (3.21)
65   (3.90)
*The Patient,  A 47-Yr.Old  5’ 5” Woman Weighing 170 Lbs. Presented With Polyarthralgia, Recurrent Sinusitis, and Fatigue.
Table 8. Severe Hyperinsulinism In A 13-Yr-Old With Lupus Erythematosus*
Fasting
½  Hr
1Hr
2Hr
3Hr
Insulin uIU/mL
27.9
362.5
424.0
718.2
571.7
Glucose mg/mL  (mmol/L)
      70   (3.88)
  140     (7.77)
   157     (8.71)
   150    (8.33)
   111   (6.16)
Insulin and Glucose Profiles Obtained After Four Months of Robust Integrative Therapies
Insulin uIU/mL
7.2
125.1
238.5
208.0
132.0
Glucose mg/mL  (mmol/L)
81     (4.49)
154   (8.54)
181     (10.04)
130     (7.21)
97      (5.38)
*The Patient,  A 13-Yr-Old Girl With a History of Three Hospitalizations In One Year for Systemic Lupus Erythematosus, Recurrent Pneumonia, Thrombocytopenia, and Severe Optic Neuritis Resulting In Complete Loss of Vision In Right Eye. The Peak Insulin Fell from 718 to 238.5 In Four Months of Robust Integrative Treatment.
Majid Ali

 

 

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s