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The
Oxygen Model of Diabetes
Majid Ali,
MD
Diabetes Type 2
is, first and foremost, an oxygen problem. This view
of diabetesThe oxygen Model of Oxygen stated in
simple wordshas two primary strengths: (1) In
understanding then nature of the disorder, it shifts
the focus away from raised blood glucose levels and
to the insulin receptor dysfunction caused by
oxygen-blocking toxicities of foods, environment,
and thoughts; and (2) It provides scientific sound
treatment plan for de-diabetization. I present in
detailed the various aspects of this view in various
tutorials of the Insulin toxicity Series.
Insulin receptor
dysfunction is caused by "plasticized" (chemicalized)
and hardened cell membranes that immobilize the
insulin receptors embedded in them. In the Oxygen
Model of Diabetes, the metabolic syndrome is
visualized as a "gummed-up matrix state and
prediabetes is 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.
Strong clinical,
epidemiologic, and experimental evidence links the
epidemics of obesity with those of diabetes in an
ever-increasing number of countries.9-11 That 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, the
hormonal output of adipocytes 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
* Pperoxisome
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,
* Plasminogen
activator inhibitor (PAI-1),
* Adipsin
(complement D),
* Acylation-stimulating
protein (ASP) 39-42
* Heat shock
protein 60, voltage-dependent anion channel 1
(VDAC-1),
* Grp7543; and
* Hypercoagulable
platelets44
These factors
constitute an enormous network of molecular and
cellular cross-talk, nearly all aspects of which are
linked to oxygen signaling and provide support for
the dysox model of diabetes. To cite some examples,
overexpression of several antioxidant and oxystatic
systems including superoxide dismutase, catalase,
and glutathione peroxidase in various tissue-organ
systems of diabetic animals and humans has been
documented.45 Later in this column, I furnish direct
evidence for impaired bioenergetics altered Krebs
cycle chemistry, glycolytic pathways, and
mitochondrial functions in individuals with
diabetes, by presenting personal data.
Angry Diabetes
Genes Getting Angrier by the Decade
Is diabetes a
genetic problem? No. My answer is likely to surprise
most readers. I recognize that diabetes runs in
families. However, the story of genetics unravels
rapidly when we consider the epidemics of diabetes
all over the world. Consider the following: on
January 9, 2006, the New York Times projected the
rising incidence of diabetes with the following
words: "If unchecked, it is expected to ensnare
coming generations on an unheard-of scale: One in
every three Americans born five years ago. One in
two Latinos." One in two Latinos! That is likely to
surprise only those unfamiliar with the sad story of
the galloping incidence of diabetes among the Pima
Indians of the Southwestern US. A single case of
diabetes was recorded among the tribes by a
traveling physician in 1908. Then Elliot Joslin (the
founder of Joslin Clinic for diabetes in Boston)
found 21 cases in the early 1930s. The number of
individuals with diabetes among the tribes had
increased to 283 cases in 1954 and to over 500 in
1965. By mid-1990s, the prevalence of diabetes among
the Pima Indians had risen to over 60%.44 As for
diabetes among children and adolescents, consider
another quote from the Times article cited above:
"So-called type 2 diabetes, the predominant form and
the focus of this series, is creeping into children,
something almost never heard of two decades ago."
Much-needed light
on the genetics of diabetes is also shed by newer
data concerning the epidemics of diabetes in Papua
New Guinea (PNG), Ceylon, Africa, and India. For
example, some years ago, the prevalence of diabetes
in PNG population was reported to be "virtually 0%,"
whereas recent surveys showed that type 2 diabetes
has become a common disease.45 In March 2006, the
Ceylon Medical Journal reported that in 1990, the
prevalence of type 2 diabetes was 2.5%, and it had
risen to 14.2% among males and 13.5% among females
by 2005.46 Similar data concerning epidemics of
diabetes are being reported from various African and
Asian countries. Most notable in this context is the
epidemic of low-body-weight diabetes in India. The
core questions here are the following: (1) Why did
the diabetes genes become angry during the last
century? and (2) Why are those genes getting angrier
by the decade? Genes not unlike physicians are
not solo performers. Genes do not exist and function
in a vacuum, nor do they serve their roles in the
essential injury-healing-injury cycle of life as
independent agents. Genes continuously recognize and
respond to changes in their environment. A new field
of "ecogenomics" is what is sorely needed, not only
to understand the true nature of the disease
processes we collectively designate as diabetes, but
also for designing integrative therapies for the
prevention of diabetes and the process that may be
called "de-diabetization" complete (see
illustrative case study below) or partial in
clinical practice.
There is an
essential relatedness of the above epidemiologic,
genetic, biochemical, and clinical observations. I
address by: presenting personal data showing
impaired altered Krebs cycle chemistry and
mitochondrial functions; (2) summarizing a large
body of recent experimental and clinical data that
shed light on the subjects of disrupted molecular
bioenergetics and impaired detox mechanisms in
diabetes; and (3) presenting some illustrative case
studies to underscore the potential for de-diabetization.
Impaired
Mitochondrial Function in Diabetes
Diabetes, first
and foremost, is a disorder of impaired molecular
bioenergetics and oxygen signaling. Mitochondrial
electron transfer events form the foundation of
human molecular energetics.47 This is where
respiration is coupled with oxidative
phosphorylation for ATP generation, which serves as
the energy currency of the body. If one were to
accept that diabetes is primarily a molecular
bioenergetic disorder, one would expect to find in
it clear evidence of dysfunctional mitochondrial
uncoupling proteins. That, indeed, is the case.
I draw evidence to
support my view from a large body of clinical,
biochemical, and experimental data. Clinically, it
is noteworthy in this context, the initial clinical
presentation of diabetes in poor countries is often
unexplained fatigue. In Table 1, I present
biochemical evidence of the existence of impaired
Krebs cycle and glycolysis, as well as biotoxins (mycotoxins
and others) in a series of 17 patients with type 2
diabetes. The average age of 11 males in the study
was 65 years (range 36 to 80), while those of six
females was 68 years (range 66 to 71). The data
presented show increased urinary excretion of
intermediates of Krebs cycle and glycolysis, which
serve as direct evidence of defects in those
pathways. The data concerning increased urinary
excretion of biotoxins (mycotoxins and others)
which are known to uncouple respiration from
oxidative phosphorylation, interfere with
mitochondrial electron transfer, and so impede or
block Krebs cycle provide indirect evidence for
the same.
The data in Table
1 validate my observations concerning the clinical
management of diabetes made over a period of two
decades. For three decades, on clinical grounds, I
became convinced that altered bowel flora affect the
energy homeostasis of the body and that obesity
alters the nature of the bowel microbiota.
Specifically, I recognized two sets of factors that
play crucial roles both in the optimal control of
blood sugar levels and the prevention of diabetic
complications: (1) the issues of bowel ecology,
which include untreated mold allergy and adverse
food reactions, altered bowel flora, mycotoxicosis,
increased bowel permeability, and
digestive-absorptive dysfunction, essentially in
that order of importance; and (2) impaired hepatic
detoxification and metabolic pathways. Note that all
diabetic individuals in the study showed clear
evidence of bowel-related biotoxins that directly or
indirectly uncouple respiration from oxidative
phosphorylation. More than half of the patients (10
of 17) had increased urinary excretion of hippuric
acid, indicating impaired hepatic enzymatic
detoxification functions. I discuss the therapeutic
implications of the data in Table 1 in the section
"De-Diabetization Strategies."
Immunology of Beta
Islet Cells and Insulin
Insulin is itself
a potent autoantigen that initiates autoimmune
(juvenile-onset, type 1) diabetes.1-3 What are the
conditions under which insulin, a hormone without
which life is not possible for more than a few days,
becomes an autoantigen that unleashes diabetes? This
is one of the central issues to be addressed in the
dysox model of diabetes. Before attempting to answer
this question, I briefly review here the immunology
of pancreatic beta cells and insulin.
In type 1
diabetes, lymphocytes react against and destroy the
beta cells in the pancreas of genetically vulnerable
individuals. The loss of insulin-producing cells
leads to insulin deficit, which, in turn, causes
hyperglycemia (diabetes in the prevailing sense of
that disease). Lymphocytes are expected to recognize
other autoantigenic targets as beta-cell destruction
proceeds with a process that has been termed
"antigenic spreading."48 Specifically, it is known
that reduced expression of some islet cell
autoantigens, or elimination of the lymphocytes that
recognize them, can reduce the degrees of glucose
dysregulation. However, beta-cell-specific
autoimmune attacks cannot be aborted by such
interventions.49,50 It is known that
insulin-reactive lymphocytes from healthy
individuals exert healthful regulatory functions by
producing some needed signaling molecules. By
contrast, insulin-reactive lymphocytes from
diabetics assume destructive roles by releasing
molecules that are harmful to beta cells.51
About 50% of the
lymphocytes isolated from the pancreatic draining
lymph node of diabetic patients recognized a segment
of the insulin A chain. Healthy control subjects, by
contrast, do not show a similar accumulation of
insulin segment-recognizing lymphocytes.52 A type of
immune cell called an antigen-presenting cell plays
an important role in such immune-recognition
processes. Specifically, it captures protein
fragments from dying beta cells and "displays" it to
the convening lymphocytes in the pancreatic-draining
lymph nodes. In 2006, it was reported that the
cell-surface protein that binds to and displays the
insulin A fragment on the antigen-presenting cells
is encoded by a gene known to confer genetic
susceptibility to diabetes.53
At the level of
adipocytes and myocytes, insulin can be visualized
as a crank a device that transmits rotary motion
and the insulin receptor protein as a crankshaft
embedded in the cell membrane. In the dysox model of
diabetes, insulin resistance can then be seen as a
rusted crankshaft of insulin receptor, which is
impacted in a "hardened" cell membrane and so cannot
be turned by the insulin crank.
Diabetes as a
Dysfunction of Mitochondrial Uncoupling Proteins
Mitochondrial
uncoupling proteins (UCPs) are a family of proteins
that serve as "metabolic brakes" located within the
cellular powerhouses.19-21 These proteins uncouple
respiration from oxidative phosphorylation and
provide counterregulatory mechanisms operating at
the very foundational levels of human bioenergetics
a cooling system, so to speak, in times of
"overheated" electron transfer events. (What an
elegant example of Nature's preoccupation with
complementarity and contrariety in its management of
energy economy!) If one were to accept that diabetes
is first a bioenergetic dysfunction, one would
expect to find in it clear evidence of dysfunctional
mitochondrial uncoupling proteins. That, indeed, is
the case.
The production of
mitochondrial uncoupling protein 2 (UCP2) in beta
cells is increased in obesity-related diabetes,19
indicating increased mitochondrial response to
factors that accelerate the electron transfer
reactions an effect predicted by the dysox model
of diabetes. Another dimension of the role of UCP in
the pathogenesis of diabetes is revealed in
experimental animals in which UCP2 overexpression is
associated with impairment of glucose-stimulated
insulin secretion (GSIS). I might add that a nuclear
receptor called the short heterodimer partner (SHP)
is also involved with GSIS, as well as with some key
cell membrane channels. For example, SHP
overexpression increases the glucose sensitivity of
ATP-sensitive K+ (KATP) channels and increases the
ATP/ADP ratio.54 In healthy animals, overexpression
of SHP enhances GSIS in normal islets and restores
this function in animals with UCP2-overexpressing
islets. This represents another mechanism by which
overwrought molecular "braking systems" can be
loosened up.
There are yet
other noteworthy aspects of SHP. Methylpyruvate is
an energy fuel that bypasses glycolysis and directly
enters the Krebs cycle. SHP overexpression also
corrects the impaired sensitivity of
UCP2-overexpressing beta cells to methylpyruvate.
Diabetes as a
Dysfunction of Paracrine and Endocrine Roles of
Adipocytes
Adipose tissue
governs the body's energy economy (homeostasis) in
many important ways.55 Specifically, it modulates
all aspects of human metabolism by releasing a host
of signaling, hormonal, appetite-modifying, and
proinflammatory substances called cytokines,
including:
· NEFAs
· glycerol
· leptin
(generally an appetite-suppressing hormone)27,28
· suppression of
cytokine signaling (SOCS) proteins36
· inducible nitric
oxide synthase (iNOS)18
· proinflammatory
cytokines22-24
· retinol-binding
protein-4 (RBP4), which induces insulin resistance
through reduced phosphatidylinositol-3-OH kinase
(PI[3]K) signaling37
· over-expression
in muscle of gluconeogenic enzyme
phosphoenolpyruvate carboxykinase in a
retinol-dependent mechanism56
· adiponectin, an
insulin sensitizer,30 which stimulates fatty acid
oxidation in an AMP-activated protein kinase (AMPK)
and peroxisome proliferator-activated receptor- (PPAR-)-dependent
manner.32-34
In health, all the
above molecular pathways play Dr. Jekyll roles and
regulate the cellular energy economy with
physiological limits. In obesity and diabetes, those
Dr. Jekylls turn into molecular Mr. Hydes and set
the stage for incremental accumulation of fats in
adipocytes. For example, nonesterified fatty acids
in excess induce insulin resistance and impair
beta-cell function. Stated simply, fat becomes
fattening.
Diabetes as a
Dysfunction of Molecular Signaling
In diabetes, there
is abnormal expression of several important
signaling molecules. One of the best-studied of such
molecules is the transcription factor peroxisome
proliferator-activated receptor (PPAR-?).32-34,57
Impaired activity of this factor disrupts molecular
energetics in many ways, including diminished
glycolysis, impaired citric acid cycle, and
gluconeogenesis. In obesity and diabetes, PPAR-alpha
is weakly expressed in adipose tissue and is
associated with profound metabolic derangements
across all tissues. There is an increase in lactate
and a profound decrease in glucose and a number of
amino acids, such as glutamine and alanine.58 The
SHP dynamics appear to be independent of the role of
PPAR-gamma, since a PPAR-gamma antagonist did not
block it. Another line of experimental evidence that
supports the dysox model of diabetes concerns a
protein called nuclear respiratory factor-1
(NRF-1).35 Insulin resistance and diabetes are
associated with reduced expression of multiple
NRF-1-dependent genes, which encode several key
enzymes involved with oxidative phosphorylation and
some mitochondrial function.
Diabetes as a
Disorder of Glycation
Sugars adduct to
nearly all normal cellular constituents proteins,
enzymes, fats, redox-restorative, and oxystatic
substances and render them dysfunctional. Beyond a
certain point, this process produces irreversible
permutations of those molecules to produce the toxic
advanced glycation end-products (AGEs).59,60 The
rate of such transformations the "sugarization" of
nonsugars of the body is useful for patient
education increases with rising intracellular
levels of sugars. Glycosylation of hemoglobin (the
basis of the HbA1C test for monitoring the results
of diabetes treatment) is the best-known example of
sugarization of a vitally important protein, which
renders it functionally impaired. AGEs form by
several chemical reactions, some of which are
blocked by thiamine and nenfotiamine (via reactions
facilitated by transketolase and related enzymes61),
and inflict oxidative damage on endothelial, neural,
and other cellular populations. I discuss this
crucial process at length in Integrative Cardiology,
the sixth volume of The Principles and Practice of
Integrative Medicine.62 Here in the context of the
dysox model of diabetes, the crucial point is this:
all abnormalities of mitochondrial electron transfer
reactions, the Krebs cycle, the glycolytic pathways,
and critical detox mechanisms encountered in
diabetes and presented above occur more in
endothelial, neural, retinal, and renal tissues than
in other tissues of the body. I draw support for
this statement from the established facts of much
higher susceptibility of those tissues to impaired
molecular bioenergetics seen in diabetes.
Diabetes as an Inflammatory Disorder
Injury is
inevitable in an organism's struggle for survival.
Healing is the intrinsic capacity of the organism to
repair damage inflicted by that injury. Inflammation
is the energetic-molecular mosaic of that intrinsic
capacity. This energetic view of inflammation
extends far beyond the classical and wholly
inadequate notion of it being a process
characterized by edema, erythema, tenderness, pain,
and infiltrate of inflammatory cells. In my May 2005
Townsend Letter column, I marshaled a large body of
clinical and experimental data to show that all
molecular and cellular components of the
pathophysiology of inflammation are directly or
indirectly governed by oxygen signalling.63 In this
column, I extend that concept of inflammation to the
pathogenesis of both obesity and diabetes by
pointing out that all information presented in the
preceding sections supports the view. Specifically,
in both obesity and diabetes, impaired oxygen
signaling is a phenomenon common to all aspects of
impeded Krebs cycle and glycolytic pathways, altered
free radical dynamics, impaired molecular signaling,
proinflammatory cytokines, AGEs, and the immunology
of insulin presented above.
The crucial
clinical significance of the above "inflammatory
view" of obesity and diabetes is this: All elements
that cause chronic inflammation must be recognized
as "obesitizing" and "diabetizing" influences.
Equally important is the recognition that no
strategies for the prevention of diabetes and de-diabetization
can be considered complete if they do not
effectively address all proinflammatory influences,
such as insidious subclinical infections,
undiagnosed and untreated mold and allergies, toxic
metal burden, xenobiotic load, and impaired hepatic
detoxification pathways.
The Oxygen Model of Diabetes
Simply stated,
there are three primary sets of elements that create
the complex conditions that are simplistically
labeled as diabetes: (1) toxic environment; (2)
toxic foods; and (3) toxic thoughts. This is the
only way it is possible to make some sense of
spreading diabetes epidemics in all countries of the
world the greater the degrees of toxicity produced
by those elements in any given country, the wider
the epidemic. The US has the lamentable distinction
of being the front-runner in the world. From those
toxicities arise all the known molecular and
cellular disruptions of diabetes, which are shown
schematically in Figure 1.
In 1998, I
proposed the dysox model of disease as a unifying
concept of dysfunctional molecular bioenergetics
that are clinically expressed as diverse disease
states on the basis of varying environmental,
nutritional, stress-related, and genetic
factors.64-66 This model has two primary strengths:
(1) It focuses on quantifiable abnormalities of
molecular bioenergetics as the basis of cellular and
tissue injury; and (2) It provides clear scientific
basis and/or rationale for integrative plans for
arresting and/or reversing chronic disease. In 2001,
I published an extensive review of the
epidemiological, clinical, bioenergetic, and
experimental aspects of insulin resistance and
diabetes in a three-part article titled "Beyond
Insulin Resistance The Oxidative-Dysoxygenative
Model of Insulin Dysfunction (ODID)" published in
Townsend Letter (available at www.jintmed.com). In
that series, I discussed altered dynamics of nitric
oxide, inducible nitric oxide synthase, resistin,
leptin, TNF-a, PPAR-?, and some proinflammatory
cytokines. Above, I reviewed some recent advances in
the knowledge of the immunology of insulin and beta
cells of the pancreas, mitochondrial uncoupling
proteins (UCPs), altered paracrine and endocrine
functions of adipocytes, and advanced glycation end
products (AGEs) to shed additional light on the
dysox model of diabetes.
De-Diabetization
Strategies
In my view, the
four crucial components of the de-diabetization
regimens, for complete or partial success, are: (1)
choices in the kitchen; (2) fat-burning exercises
(presented at length in my book The Ghoraa and
Limbic Exercise);67 (3) restoration of bowel
ecology; and (4) optimization of the hepatic
metabolic and detoxification functions. Beyond that,
it is important to investigate and address other
coexisting endocrine and neurotransmission
dysfunctions. As to the third element of restoring
bowel ecology, in December 2006, Nature published
two landmark reports and an accompanying commentary
that documented the impact of gut microbiota on the
body's energy balance in mice and humans.68-70
Specifically, obese human and mice showed an
increase in the gut population of Firmicute species,
while those of Bacteroides species normally
accounting for more than 50% of microbial species of
human microbiome were decreased. These
observations shed some light on the mechanisms that
underlie the observed weight loss with therapies
that restore the digestive-absorptive dysfunctions
and restore the gut mictobiota.
In my Townsend
Letter column of October 2006, "Hurt Human Habitat
and Energy Deficit Healing Through the Restoration
of Krebs Cycle Chemistry,"71 I presented the
regimens that I prescribe for effectively addressing
the bowel- and liver-related issues in chronic
disorders. I find the same regimens equally
effective to address those issues for my patients
with diabetes. In that article, I also briefly
outlined my approach to addressing other existing
hormonal issues (concerning the thyroid, adrenals,
and neuroendocrine systems). I refer the readers
interested in detailed discussion of those subject
to Integrative Nutritional Medicine, the fifth
volume of The Principles and Practice of Integrative
Medicine (2002).72 My essential clinical priorities
are: (1) very low-carbohydrate diet; (2)
high-frequency, low-intensity, predominantly
lipolytic, limbic exercise (described and discussed
at length in Limbic Exercise); and (3) the
restoration of bowel, blood, and liver ecosystems.
Guidelines for Nutritional and Herbal Support for
De-Diabetization
In my October 2006
column, I presented my herbal, nutrient, and detox
choices for: (1) herbal protocols for restoring the
gut ecology; (2) castor oil packs and other measures
for liver detoxification; (3) adrenal, thyroid, and
gonadal support, when needed; (4) antioxidant and
oxystatic vitamin and mineral supplementation; (5)
slow, sustained limbic exercise; and (6) meditative
approach for coping with lifestyle stressors. In the
following paragraphs, I offer some menu suggestions
and guidelines for specific herbal remedies that I
have found to be especially valuable in achieving
optimal glycemic control:
Optimal Breakfast Choices for Diabetes
Dr. Ali's
breakfast on five to six days per week comprising:
· two tablespoons
of a protein powder containing 85%90% calories in
proteins and peptides;
· two tablespoons
of a granular lecithin;
· two tablespoons
of freshly ground flaxseed (the use of a coffee
grinder is recommended);
· 12 to 16 ounces
of organic vegetable juice (avoiding or minimizing
the use of carrots and red beets);
· 12 to 16 ounces
of water. A few ounces of seltzer water or a few
drops of lemon juice may be added to suit personal
taste.
I personally
consume this mixture in portions of 6 to 8 ounces
with my nutrient and herbal protocols during the
period of my morning exercise, meditation, and
preparation for work. I have not yet encountered any
negative impact of the protein content in this
breakfast on renal function. Still, individuals with
serum creatinine levels above the normal range need
to be monitored for renal function.
Optimal Lunch
Choices for Diabetes
· Large salad with
goat cheese, chicken, or fish
· Uncooked,
steamed, or lightly stir-fried vegetables
Mid-afternoon
Snack
Use 4 to 6 ounces
of Dr. Ali's breakfast mixture (prepared in the
morning and carried to work).
Optimal Dinner
Choices for Diabetes
First, take
uncooked, steamed, or lightly stir-fried vegetables.
Next add proteins (fish, poultry, turkey, lamb,
organic game meats, or beef). Pasta, bread, rice,
and other starches should be taken in minimal
amounts (just for taste). I ask my patients with
diabetes never to allow bread to appear on the table
(for them) before vegetables and animal proteins. In
my experience, de-diabetization plans with
vegetarian diets generally yield poor results.
Valuable Phytofactors for Diabetes
The use of herbs
for optimizing blood sugar control and for de-diabetizing
efforts requires considerable clinical experience.
As in the case of phytofactor remedies for chronic
disorders, it is my clinical practice to prescribe
herbal remedies for my diabetic patients in
rotation. My preferred phytofactors are these: neem
tree bark or leaves, bitter lemon, Gymnema sylvestre,
fenugreek, fennel seeds, licorice extract, green
tea, and pau d'arco. The following are other
options: aloe, banaba, bitter lemon, cinnamon herb
powder, cayenne, licorice extract, guggul,
huckleberry, juniper berries, yarrow, and yellow
gentian. I also liberally prescribe vanadyl sulfate
in my program.
An
Illustrative Case History of De-Diabetization
A 70-year-old man
presented to the Institute on June 5, 2003, with the
following health issues: uncontrolled diabetes of
22-years duration; gastroesophageal reflux disorder;
colonic diverticulitis; benign prostate hyperplasia;
and chronic fatigue. His HbA1c level was 11.1
despite the use of Glucophage and Glucontrol. Table
2 displays the data for four-hour glucose tolerance
and insulin profile.
Other pertinent
laboratory values were as follows:
· Hb, 14.7 gm/dL;
WBC, 5,200
· an abnormally
low value of T3-Uptake (0.7 units)
· homocysteine
value (11.4 umol/L)
· dysautonomia
(sympathetic-overdrive and parasympathetic deficit)
as determined by a power spectral scan of heart rate
variability
· PSA, 0.66 ng/mL
· Lead, aluminum,
arsenic, nickel, and tin overload (measured with
DMSA provocation)
· insulin-like
growth factor, 66 ng/mL
· cholesterol 177
mg/dL and HDL cholesterol 47 mg/dL
· Raised levels of
allergen-specific IgE and IgG antibodies to
Aspergillus, Penicillium, Alternaria, Candida, and
other mold species.
He complied well
to my de-diabetization regimen, but was unable to
follow my recommended exercise program for reason of
long-established work habits. Table 3 shows the data
for a period of follow-up of 28 months.
Concluding Comments
This tutorial has
two crucial messages of this column: first, a clear
understanding of the energetic consequences of the
respiratory-to-fermentative shift in the dysox state
is crucial to a complete comprehension of the Oxygen
Model of diabetes. The primary biochemical evidence
for that model presented here concerns increased
urinary excretion of metabolites of the Krebs cycle
and glycolytic pathways for generation of ATP. In
essence, the respiratory-to-fermentative shift with
waste of organic intermediates represents a costly
metabolic error that eventually affects all cell
populations in the body. That is the energetic basis
of all known complications of diabetes involving all
organ-systems of the body.
Second, and
equally important, is the understanding that no
interventional strategies for the prevention of
diabetes and de-diabetization can be considered
complete if they do not effectively address all
elements that threaten oxygen homeostasis and feed
the pathophysiology of diabetes, especially those
related to spiritual disequilibrium, lack of
exercise, and the bowel blood ecosystems. Thus, the
mere prescriptions for oral hypoglycemic agents and
insulin regimens along with carbohydrate
restrictions cannot be accepted as optimal
management of diabetes. In the context of the gut
ecology, consider the following quote from the
December 21, 2006 issue of Nature:70
Gordon and
colleagues' results tempt consideration of how we
might manipulate the microbiotic environment to
treat or prevent obesity. ... The two papers
nonetheless open up an intriguing line of scientific
enquiry that will ally microbiologists with
nutritionist, physiologists, and neuroscientists in
the fight against obesity.
There is something
profoundly ironic in the above statement. For
centuries, holistic physicians have cared for the
sick with a sharp focus on the bowel flora. In
recent decades, I have published more than 50
articles describing my clinical, pathologic, and
biochemical observations concerning the altered
states of gut ecology and their adverse
consequences. The readers can obtain a compendium of
many of those articles in my book Darwin, Dysox, and
Disease, the 11th volume of The Principles and
Practice of Integrative Medicine (2002).73
List of Related
Articles
*
The Insulin-Obesity-Diabetes
Continuum
*
Insulin-Wise-Eating
*
Insulin-Smart-Recipes
*
Less Insulin, More Life
*
Evidence for Insulin Toxicity
*
The Oxyegn Model of Diabetes
*
The Oxygen
Model of Obesity
*Insulin
Evolutionary
*
Seven Stages of
Insulin Toxicity
*
Prediabetes
*
Subtypes of
Diabetes Type 2
*
Less Insulin, More Life
*
Evidence for Insulin Toxicity
*
If Mice Can Reverse
Diabetes, Why Can't People?
*
Dysox Explains
the Exercise-Weight-Loss Disconnect
k
The Oxygen Models of Diseases
k
The Oxyegn Model of Diabetes
k
The Oxygen
Model of Obesity
k
Oxygen Model of
Coronary Heart Disease
k
Oxygen Models of
memory Loss and Alzheimer's Disease
k
Oxygen Model of Cancer
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