This article originally
appeared in the May 2007 issue of the Townsend
Published online May 2009.
Is diabetes mellitus a sugar problem?
No. The abnormalities of blood sugar seen in diabetes are the consequences
of the derangements of cellular energetics and toxicity that collectively
create what is commonly called diabetes. Is diabetes an insulin
problem? No. The abnormalities of insulin functions are the consequences
of plasticized (chemicalized) and hardened cell membranes that immobilize
the insulin receptors embedded in them. Is diabetes a problem of
blood vessels that causes blindness, kidney failure, stroke, heart
attacks, and neuropathy? No. The abnormalities of blood vessels
are the consequences of oxidizing and deoxygenizing influences in
In this column, I marshal evidence for my view that the state of
insulin resistance should be regarded as a "hardened cell membrane
state." The so-called metabolic syndrome should be visualized
as a "gummed-up matrix state." Prediabetes should be seen
as a "mitochondrial dysfunction state." The strategies
for the prevention and reversal of diabetes yield better long-term
clinical results if diabetes is recognized as a "dysfunction
oxygen signaling," or dysox, state.
In type 1 diabetes, insulin itself becomes a potent autoantigen
and initiates autoimmune injury to pancreatic islet cells.1-3 I
will show how this recently documented role of insulin in the pathogenesis
of diabetes fits in the dysox model of diabetes presented here.
In type 2 diabetes, insulin cannot function – insulin resistance,
in the common jargon – and hyperinsulinemia develops, which
triggers and amplifies the inflammatory response.4-6 In all types
of diabetes, the endothelial cells produce nitric oxide and other
bioactive factors in abnormal quantities and proportions.7,8 Diabetes
causes neuropathy, retinopathy, nephropathy, dementia, stroke, and
heart attacks. I will describe how those complications of diabetes
can be better understood when the problems are seen through the
prism of oxygen signaling.
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
· tumor necrosis factor-alpha (TNF-a)31
· peroxisome proliferator-activated receptor gamma (PPARgamma)32-34
· nuclear respiratory factor-1 (NRF-1)35
· suppression of cytokine signaling (SOCS) proteins36
· retinol-binding protein-4 (RBP4)37
· antibodies against glutamic acid decarboxylase38
· prothrombotic species, including fibrinogen, von Willebrand
factor, and plasminogen activator inhibitor (PAI-1), adipsin (complement
D), and acylation-stimulating protein (ASP) 39-42
· heat shock protein 60, voltage-dependent anion channel
1 (VDAC-1), and Grp7543
· hypercoagulable platelets44
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.
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.
In this column, I demonstrate the essential relatedness of the above
epidemiologic, genetic, biochemical, and clinical observations and
offer answers to questions I raise by (1) 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
Cycle and Glycolytic Pathways 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
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:
· 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 (PIK)
· 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
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
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
The Dysox Model
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
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.
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:
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.
Choices for Diabetes
· Large salad with goat cheese, chicken, or fish
· Uncooked, steamed, or lightly stir-fried vegetables
Use 4 to 6 ounces of Dr. Ali's breakfast mixture (prepared
in the morning and carried to work).
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.
Phytofactors of Special Value 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.
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
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
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.
I want to underscore the 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 Dysox 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
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
Majid Ali, MD, is president
of the Institute of Integrative Medicine in New York, NY, and Denville,
NJ. He is the author of the 12-volume series The
Principles and Practice of Integrative Medicine and editor
of the Journal of Integrative Medicine.
Dr. Ali was formerly associate professor of pathology at Columbia
University College of Physicians & Surgeons, New York, NY; president
and professor of medicine, Capital University of Integrative Medicine,
Washington, DC, and president and chief pathologist at Holy Name
Hospital, Teaneck, NJ.
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lymph nodes of type 1 diabetic subjects recognize an insulin epitope.
3.von Herrath M. Insulin trigger for diabetes. Nature.
4.Eisenbarth GS, et al. Insulin autoimmunity: Prediction/precipitation/prevention
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