T

H
E Original Internist
C•O•N•T•E•N•T•S
CALENDAR OF EVENTS ................................................................................................... 178

FROM THE EDITOR’S DESK ........................................................................................... 179

Jack Kessinger, DC, ND, DABCI

FUNCTIONAL ENDOCRINOLOGY PHILOSOPHY

FOR THE PRACTICING INTERNIST ............................................................................ 180
Datis Kharrazian, DC, DHSc, MS, MNeuroSci, FAACP, DACBN, DIBAK, CNS

THE LEGACY CONTINUES .............................................................................................. 183

A. Jay Kessinger IV, DC, ND, DABCI

THE TOXICITY OF METALS ........................................................................................... 185

E. Blaurock-Busch, PhD

IMMUNE BOOSTING COMPONENTS TO ARREST COLDS AND FLU ................... 189

Rachel Olivier, MS, ND, PhD

LIVER FLUSH: HELP OR HOAX ...................................................................................... 193

E. W. McDonagh, DO

UTILITY OF AN ORAL PRESENTATION OF HCG

(HUMAN CHORIOGONADOTROPIN) FOR THE MANAGEMENT
OF OBESITY: A DOUBLE BLIND STUDY ....................................................................... 197
Daniel Oscar Belluscio, MD, Leonor Ripamonte, MD, Marcelo Wolansky, PhD

BLOOD TRANSFUSIONS ARE VERY DANGEROUS.................................................... 211

Dr. James A. Howenstine

CLINICAL RELEVANCE OF NEUROTRANSMITTER TESTING .............................. 218

Dr. Scott Theirl

ABSTRACTS OF INTEREST .............................................................................................. 222

DABCIs AND WHERE THEY ARE ................................................................................... 227

CLINT PUBLICATIONS

VOL. 16, NO. 4 · ISSN 1529-4722 · DECEMBER 2009

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 THE ORIGINAL INTERNIST
Clint Publications Editor-in-Chief

720 Oak Knoll Jack Kessinger, DC, ND, DABCI

Rolla, MO 65401 Managing Editor

Production Manager
Telephone: (573) 341-8448 Virginia Kessinger
Fax: (573) 341-8494
E-mail: virginia@drkessinger.com Director of Advertising & Marketing
Annette Copeland
www.clintpublications.com
Editorial Staff
The Original Internist is published quarterly. Publication
months are March, June, September and December, barring Jay Kessinger, DC, ND, DABCI
any unusual or unforeseen circumstances. Kimberly Foster
News items and/or letters pertaining to natural health care
are welcome. The editorial staff reserves the right to edit
and/or reject all material received. Letters to the editor Research Editors
may be condensed in order to fit the allotted space. An
Debasis Bagchi, PhD, FACN
address and telephone number where the author may be
Paul Basile, DC
reached during normal business hours should also be
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included for verification purposes. Deadline for article
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submission is the 15th of the month preceding publication.
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SUBSCRIPTION & ADDRESS CHANGES Jerome Block, MD, FACP
A subscription to The Original Internist is $50. A free one- Harold M. Chalker, DC, DABCI
year subscription will be given to anyone who submits a Dallas Clouatre, PhD
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Please notify Clint Publications if you change your address Charlyn Marcusen, PhD
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Advertising deadline is the 5th of the month preceding Harry G. Preuss, MD, FACN, CNS
publication. For advertising rates or information, contact Oscar Rasmussen, PhD
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DISCLAIMER Charles Rudolph, DO
The opinions expressed in The Original Internist are Sidney Stohs, PhD, FACN, FATS, FASAHP
presented for the purpose of providing an open forum for Edward C. Sullivan, DC, PhD, Dipl Ac (IAMA), BCIAC,
unbiased case studies, contemporary ideas and discussion DAPA
of matters relevant to natural health care. Its primary Jon A. Sunderlage, DC, Dipl Ac (NCAOM)
mission is to educate and inform those especially interested Sharon A. Vallone, DC, DICCP
in promoting natural health care as a primary treatment. Steve Watterson, ATC
The opinions expressed in The Original Internist do not Michael Whitehead, DC, DACBR
necessarily reflect the opinions and policies of Clint David Wickes, DC, DABCI
Publications or The Original Internist. Jonathan V. Wright, MD

THE ORIGINAL INTERNIST DECEMBER 2009 177

 CALENDAR OF EVENTS
FOR ALL DABCI SEMINARS ….. VISIT OUR NEW WEBSITE
December 12-13, 2009 (Chicago, IL)
Reports, Clinical Documentation & Drug Reactions
GRADUATION
Instructor: Jack Kessinger, DC DABCI
January 9-10, 2010 (Dallas, TX)
Facts of Neoplastic Process & Examining the
Cancer Patient
Instructor: Jack Kessinger, DC DABCI
January 16-17, 2010 (Los Angeles, CA)
Multi Channel Blood Chemistries, CBC, Thyroid
Panel, TSH
Instructor: Jack Kessinger, DC DABCI
January 23-24, 2010 (Portland, OR)
Pharmacognosy (Herbal Therapy)
Instructor: Bill Kleber, DC DABCI
January 30-31, 2010 (Kansas City, MO)
Introduction to Chiropractic Family Practice
Instructor: Jack Kessinger, DC DABCI
February 6-7, 2010 (Hartford, CT)
Introduction to Chiropractic Family Practice
Instructor: Ben Bowers, DC DABCI
For more information on our 2009-2011 seminars
visit us online at
www.drkessinger.com
then click on ProHealth Seminars
178
THE ORIGINAL INTERNIST Spring 2006
www.DABCIdiplomate.com
February 13-14, 2010 (Kansas City, MO)
History Taking
Instructor: Jack Kessinger, DC DABCI
February 13-14, 2010 (Dallas, TX)
Malignant Diseases, AIDS, & Their Management
& Treatment
Instructor: Wayne Sodano, DC DABCI
February 20-21, 2010 (Los Angeles, CA)
Additional Blood Tests/Tumor Markers for Internal
Disorder Patient
Instructor: Ben Bowers, DC DABCI
February 27-28, 2010 (Portland, OR)
Chronic Degenerative Disease
Instructor: Bill Kleber, DC DABCI
March 6-7, 2010 (Hartford, CT)
History Taking
Wayne Sodano, DC DABC
March 6-7, 2010 (Kansas City, MO)
The General Examination and Associated Pathology
Ben Bowers, DC DABC
THE ORIGINAL INTERNIST 05
DECEMBER 2009

From the
Editor’s
Desk
by: Jack Kessinger, DC, ND, DABCI Dr. Jack Kessinger
jack@drkessinger.com
I have long questioned why mammograms are often
accepted to be the test of choice to diagnose breast
cancer, rather than the much less invasive tumor
markers, Cancer Antigen 15-3 (CA 15-3), and/or
Cancer Antigen 27-29 (CA 27-29). Now, with
healthcare reform looming, discussion is running
rampant and opinions are all over the place concerning
the frequency of mammograms.
One side of the mammogram issue argues that patients
should not be exposed to radiation annually. In 1977,
the US National Cancer Institute held its first
“consensus” conference and the topic was mamm-
ography screening of healthy women for the early
detection of breast cancer. Since that time, there have
been notable improvements in the imaging capabilities
of the x-ray units and an appreciable lowering of
radiation dose to breast tissue. One of the controversies
today surrounding the screening of healthy women is
whether the radiation exposures are hazardous, and
whether young women, under the age of 50 benefit
from mammograms.
Everyone is exposed to ionizing radiation from natural
and medical sources. In fact, ionizing radiation may be
the most studied cancer causing agent in humans with
scientific committees on radiation continuously re-
viewing and evaluating adverse health outcomes for
over 70 years. The female breast is known to be highly
susceptible to the cancer causing effects of radiation
when exposure occurs before menopause.
Recent reports say there are entirely too many false
positives reported with mammograms, which result in
unwarranted anxiety for patients. The current standard
THE ORIGINAL INTERNIST DECEMBER 2009
of cancer screening tests can frequently produce false
positive outcomes that may result not only in anxiety
and additional potentially painful testing, but also
additional economic costs as well, according to research
conducted by scientists at the Henry Ford Health
System, Detroit, Mich., and published in the December
14, 2004 issue of ” Cancer Epidemiology, Biomarkers
& Prevention.”
This causes me to ponder, how many false positives are
thrown into the scientific data of “cancer cures?” Are
the survivor rates skewed by these “false positives?”
Have we really improved the survivor rate of this
devastating disease, or do these numbers include the
results of women who never had cancer in the first
place?
It seems to me that a simple blood test like the CA 15-3
or CA 27-29 would be a much better screening option
for the women affected. They are non-invasive and the
answer is a clear yes or no. For a physician who is
required to read a mammogram and determine if a
shadow is truly something to be concerned about.
Wouldn’t the best answer be a solid negative or
positive? A tumor marker test returns a definitive
answer, and erases the need for further testing; such as
painful biopsies which require, at a minimum, an out
patient situation. Many times this potentially life
changing blood test is only done after a radical
mastectomy has been performed; to rule out the
existence of cancer. If this test is considered accurate
after disfiguring a woman for the rest of her life, why
wouldn’t it be a required test before a mastectomy is
considered as the only option? Often, women are opting
for mastectomies out of fear that the shadow on their
mammogram may eventually turn into cancer.
The opponents of “less mammogram testing” question
the reportedly successful treatment therapies of breast
cancer. Touting that what we have been doing is
working, but is it really? Is exposing women as early as
age 30 to radiation for a base line test, and then
annually after age 40 safe? More importantly does it
provide information that can be used with confidence? I
would hope that before one of your patients or family
members subject themselves to a mastectomy, that you
would recommend a simple blood test to confirm the
existence or non-existence of cancer with certainty.
Dr. Kessinger has a local weekly radio program called
“A Healthy Concept” every Tuesday morning from
9:30-10. The programs are available on his website
www.drkessinger.com or go directly to
www.drkessinger.com/radio.html ‹
179

Functional
Endocrinology
Philosophy for the
Practicing Internist
by: Datis Kharrazian, DC, DHSc, MS, MNeuroSci, FAACP, DACBN,
DIBAK, CNS
Functional Endocrinology Philosophy
In order to truly understand the philosophy of functional
endocrinology, we must first compare and contrast func-
tional endocrinology to standard pathological-centered
models. Secondly, we must compare the functional en-
docrinology model to the pharmaceutical-based models
and models of hormone replacement therapy. To put it
simply, the functional endocrinology approach does not
determine future clinical management based on the name
of the condition, but rather on the unique physiologic
expression of the patient. In addition, the functional en-
docrinology approach does not simply identify defi-
ciency of hormones and prescribe replacement, but
rather it attempts to find the mechanism of the hormone
imbalance and change its expression with diet, nutrition,
and lifestyle change whenever possible.
The functional endocrinology approach is physiology-
based, not condition-based. The functional endocrinolo-
gist does not determine treatment based on the ICD-9
diagnosis, but rather the patient’s unique phenotypic ex-
pression. For example, if a male has low libido and erec-
tile dysfunction in standard healthcare, he would be di-
agnosed with erectile dysfunction (799.89) and placed
on medications to stimulate the body to increase blood
supply to the genitals. He would follow the established
and published standard of care with a pharmaceutical
protocol. In the functional endocrinology approach, the
name and identification of the condition would be con-
sidered in the clinical work-up, but the mechanism for
their condition would be evaluated. A male with low
libido may have depressed testosterone, elevated estro-
gen, depressed luteinizing hormone (LH), elevated dihy-
drotestosterone creating androgen receptor site resis-
THE ORIGINAL INTERNIST
180 Spring 2006
tance, or elevated androstenedione competing with tes-
tosterone receptor sites. Each one of the patterns would
dictate different clinical management for the patient.
The traditional healthcare system is based on identifying
pathology or naming the condition. The name given to
the set of symptoms will then establish treatment. The
treatment is focused on the diagnosis, not on the pa-
tient’s specific physiological expression. On the other
hand, the functional approach is not based on treating the
name given to the set of symptoms, but rather on the
specific physiological shifts expressed by the patient.
The goal of functional endocrinology is to assess the
endocrine system and find the mechanisms for imbal-
ance. If a patient demonstrates a hormone imbalance, to
functional endocrinologists the first step is to identify the
mechanism. For example, if a 28-year-old female pre-
sents with depressed progesterone levels, the mechanism
for the deficiency must be evaluated rather than immedi-
ately considering progesterone replacement. The func-
tional endocrinologist will evaluate basic physiological
mechanisms first, identify the mechanism for the pattern,
and then consider the appropriate treatment. The patient
that presents with low progesterone may have depressed
LH levels, defects of the corpus luteum, a diminished
estradiol peak, suppressed follicle-stimulating hormone,
or she may have an autoimmune response against her
follicles. The goal of the functional endocrinologist is to
identify the mechanism. Let’s say further evaluation of
the 28-year-old patient identifies depressed LH. Since
the LH is depressed, the possibility of corpus luteum
defect is unlikely. The next question must be, “Why is
the LH low?” A healthy estradiol peak midcycle triggers
normal LH release. If the estradiol peak is normal, then
the focus is on the failure of the pituitary to release LH.
If the estradiol peak is abnormal then the functional en-
docrinologist must continue his or her assessment and
find out why the estradiol peak is abnormal. Let’s say
that in this patient we determine that the estradiol peak is
normal and the LH and progesterone are depressed. This
pattern clearly indicates that the low progesterone is re-
lated to the release of LH. The next step would be to
identify why the LH is suppressed, followed by strate-
gies to increase LH output. LH suppression is most com-
monly related to cytokines such as interleukin-6 released
during a chronic stress response, or a previous history of
exogenous progesterone overload. In this example, let’s
say the patient is in an active stress response because she
is hypoglycemic and has adrenal exhaustion. Therefore
clinical management will include lifestyle changes to
stabilize blood sugar imbalances and supplements to
help support adrenal function and glycemic stability. The
(Continued on page 182)
THE ORIGINAL INTERNIST DECEMBER 2009
05
 IODORAL®
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Available in tablets of 12.5 mg packaged Now available also in tablets of 50 mg
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Based on the collective experience of U.S. physicians who used Lugol solution extensively
in their practice for iodine supplementation over the past century, the recommended
daily intake for iodine supplementation was 0.1 to 0.3 ml containing 12.5 to 37.5
mg elemental iodine (1-3). We recently confirmed the keen observation of our medical
predecessors: this is exactly the range of iodine/iodide intake required for whole body
sufficiency, based on a recently developed iodine/iodide loading test (3). For non obese
subjects, whole body sufficiency for iodine can be achieved within 3 months with daily
intake of 12.5 to 50 mg (4,5).
1) Abraham, G.E., Flechas, J.D., Hakala, J.C., Orthoiodosupplementation: Iodine sufficiency of the whole human body. The Original Internist, 9:30-41, 2002.
2) Gennaro, A.R., Remington: The Science and Practice of Pharmacy, 19th Edition, 1995, Mack Publishing Co., 976 & 1267.
3) Abraham, G.E., The safe and effective implementation of orthoiodosupplementation in medical practice. The Original Internist, 11:17-33, 2004.
4) Abraham, G.E., The concept of orthoiodosupplementation and its clinical implications. The Original Internist, 11:29-38, 2004.
5) Abraham, G.E., The historical background of the iodine project. The Original Internist, 12(2):57-66, 2005.

For further information on:

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mechanism for LH suppression is identified and sup-
ported. In addition, the functional endocrinologist will
use compounds like vitex to enhance the stimulation of
LH release.
Note that in this example progesterone was not used,
because rather than providing exogenous support for low
progesterone, the mechanism of the imbalance was iden-
tified and treated appropriately. As a matter of fact, if
progesterone were to be used in this example, it would
actually further dampen LH and may cause long-term
dysregulation of LH-progesterone feedback loop coordi-
nation. Although a deficiency of progesterone was iden-
tified, it was related to primary pituitary output, not a
glandular defect. This patient may end up with long-term
dependency on progesterone replacement if her LH out-
put function becomes depressed. The outcome of this
may be infertility and inability to have proper healthy
and normally sequenced menstrual cycles after the pro-
gesterone replacement protocol.
In summary, the functional approach is “physiology-
based” and the traditional healthcare model is “condition
-based”. The functional approach uses diet, nutrition,
and lifestyle as tools to modulate the abnormal physiol-
ogic expression of the patient, and is therefore “nutrition
and lifestyle based.” The traditional model uses synthetic
agents and hormones as tools to manage the patient and
is therefore “pharmaceutical based.” Clinical compe-
tency in the traditional model of healthcare is based on
identifying the appropriate diagnosis and following the
standard of care flow chart. Competency in the use of the
appropriate drug is strongly emphasized, whereas diet,
nutrition, and lifestyle changes are ignored or not em-
phasized. In the functional model, competency in dis-
secting and evaluating physiological pathways and rec-
ommending nutrition, diet, and lifestyle change is
strongly emphasized, whereas drug therapy and hormone
replacement are not strongly emphasized. Lastly, it
should be made clear that not all conditions are amena-
ble to the functional approach, and the appropriate iden-
tification of pathology must always be conducted and
managed medically when appropriate.
PATHOLOGICAL MODEL PRINCIPLES
• Focused on establishing diagnosis (ICD.9 code). The
primary goal is to label the series of symptoms and
signs into an established category. The diagnosis
code name will be the indicator for management.
• Treatment and management is specific to the
diagnosis and not the patient.
• Dietary and lifestyle management is weakly
emphasized.
THE ORIGINAL INTERNIST
182 Spring 2006
• Treatment and management is virtually identical for
all patients.
• Diagnostic testing is used to establish the disease
process and is not unique to the patient’s physiologi-
cal expression.
• Clinically, competency in the model is based on
following standard of care management.
FUNCTIONAL MODEL PRINCIPLES
• Based on understanding the physiological imbal-
ances of the patient and not limited to identifying
diagnosis. The diagnosis is established, but not used
exclusively to determine management.
• Nutritional support is specific to the patient and not
the diagnosis.
• Diet and lifestyle management are strongly
emphasized.
• Management is different for virtually all individuals
with the same exact diagnosis.
• Diagnostic testing and monitoring is used to
establish physiological process.
• Competency in this model is based on reviewing and
managing altered physiology versus diagnosis.
Functional Endocrinology Clinical Applications
Three main attributes are necessary for functional
endocrinology. They include: (1) A detailed understand-
ing of physiological interactions, feedback loops, and
biochemistry; (2) A detailed understanding of laboratory
evaluation; and (3) A detailed understanding of the
specific influence of natural compounds on physiologi-
cal systems. Mastery of all three attributes is critical for
competence in the functional endocrinology approach. In
addition, the functional endocrinologist must be
competent in areas outside of endocrinology, such as
immunology, gastroenterology, neurology, and detoxifi-
cation. The endocrine system must not be evaluated in
isolation from other physiological systems. An
understanding of neuroendocrine-immune interactions is
critical for management of chronic metabolic disorders.
The intimate connections between these bodily systems
must be appreciated and evaluated clinically. Four
clinical priorities have been established in the functional
endocrinology model when it comes to balancing the
endocrine system without hormones, which include: (1)
Balancing blood sugar and adrenal abnormalities; (2)
Normalizing gastrointestinal function and decreasing
antigenic exposure to the gut; (3) Balancing essential
fatty acid metabolism; and (4) Enhancing the detoxifica-
tion capacities of the individual. ‹
THE ORIGINAL INTERNIST DECEMBER 2009
05

The
Legacy
Continues
by: A. Jay Kessinger IV, DC, ND, DABCI
jay@drkessinger.com
Dr. Jay Kessinger
Someone once told me, “You can’t expect those that set
the rules to rule in your favor if you make them look
foolish.” I took that as a fundamental lesson in politics;
i.e., Politics 101. Within my first year of practice I
realized that I was not in a good location for myself.
Distraught, I remember telling Grandad, Dr. A. J.
Kessinger II, “I thought I was entering the ‘living
happily ever after’ portion of my life, but I’m just not
getting there.” He explained to me that there’s always
one major problem, sometimes three or four that simul-
taneously have to be dealt with, and a whole host of
little ones that need to be taken care of at all times. I
recall thinking, “there are only glimpses of utopia this
side of heaven. So much for my short sighted idealistic
view of the post collegiate world I was now a part of.”
I took that as a fundamental lesson in life; i.e., Life
101.
The current political climate consists of many
governmental corrections for the private sector. One
such correction our federal government is fervently
grappling to attain is within the health provisionary
system. National health care, many have touted, may
very well have little to do with individual attainment of
the tools necessary to prevent disease, nor the freedom
to receive all the necessary aspects of care needed to
treat each persons’ diseased/injured/infected state of
unhealth. Rationing of governmental resources has
been sited as a potential problem with nationalized
health care as well. The health care consumers will
most assuredly be affected by many of the proposed
changes, as will their employers.
The other side of the coin is how the proposed
nationalized health insurance plan will affect the
providers. Of course, as American citizens and em-
ployers, this will affect us more than most, it appears.
This has the feel of a mandated federal HMO, where
non-physicians will determine how often, how much,
THE ORIGINAL INTERNIST DECEMBER 2009
and what type of care individual patients will be able to
receive. The art of health care will potentially be
degraded to technical applications of prepackaged
protocols with the fundamental purpose of cost and
resource containment for the greater good of the
masses. No longer will the health care consumer be in
the authoritative position of employer, but they will be
another subservient cog in the wheel of the bureau of
our governments’ new social health provision division.
Of course, that will put you and I on the bottom of that
food chain. I don’t mind being employed directly by
those I’ve chose to serve, I understand the whole
employer/employee concept and I’m comfortable with
it; however, when the patient, the one we have the
privilege to serve, no longer has the last word, much
less signs our paycheck, I wonder how this will effect
our psyche/drive and bottom line, our ability to provide
for them and our families.
I’ve gathered, the rift against the “nay sayers” of
national health care, is that we complain about the(ir)
solution given, but we contribute no new ideas to solve
the division in this country between the haves’ and
have nots’. First, I’d like to point out that we do not
have anyone in this country so destitute that they are
beyond receiving emergency and life continuing types
of health care, from before and including child birth to
diabetic, cardiac and even cancer medical care. Most
importantly, I hope to illustrate our need for a paradigm
shift in health care delivery, not in its payment system.
It is true that the pharmaceutical companies appear to
have a strangle-hold on the health care industry, with
both its consumers and providers alike; however, this is
capitalism at work. Curbing pharmaceutical appeal is
what they did in New Zealand when television
advertising of prescription medications was halted.
Let’s face it, when people can go to a prescribing
physician and eagerly accept and expect the side effects
so they can enjoy the superficial benefits without the
full understanding of the pathophysiology involved in
the treatment of their disorder and then, if serious
unknown complications arise, join a class action
lawsuit for damages incurred, there is an egregious
work of capitalism at play. Health care is by definition
to care for health, and not to be disregardent of it.
The paradigm shift we really need of our health care is
in its provision, not in its payment. The answers to
most health loss and the enhancing longevity dilemmas
are presently known; i.e., diet, exercise, and other
healthy, life style habits; but are too often ignored and
made unattainable for most through the advertising
media. The proposed nationalized health care system
will not give this human touch we need. ‹
183
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The Toxicity
of Metals
by: E. Blaurock-Busch, PhD
(the following is an unpublished excerpt from the
not-yet published: Antidota-Handbook of Chelation
Therapies. 2007 MTM, Germany/USA)
Any metal capable of disrupting essential physiological
processes is considered toxic. Examples of this are
cadmium, lead and mercury. Other metals in the wrong
form can be toxic. For example, chromium as the Cr+3
ion is an essential trace element important for
maintaining correct blood sugar levels, but as the Cr+6
ion, it is a known human lung carcinogen.
The toxic effects of most metals can be traced to their
ability to disrupt the function of essential biological
molecules; such as proteins, enzymes and DNA. In some
cases this involves displacing chemically related metal
ions that are required for important biological functions;
such as cell growth, division and repair. We have to
acknowledge that our present knowledge regarding
metal toxicity is much greater than a century ago, but
will be regarded insufficient decades from now.
Proteins, in particular, play an astounding number and
variety of roles in living organisms. They are used as
structural elements, for sending signals both within and
between cells, and as enzymes for the synthesis and
degradation of other biological molecules. If a metal ion
binds to the amino acids of a protein, the resulting metal-
protein complex may lack the protein's original
biological activity.
One metal may also substitute for another similar metal.
For example, the toxic metal, cadmium, can substitute
for the essential metal, zinc, in certain proteins that
require zinc for their structure or function. This can lead
to alterations in that protein that can have toxic
consequences. In the same way, lead can substitute for
calcium in bone, and in other sites where calcium is
required.
Metal ions can also remove an electron from the amino
THE ORIGINAL INTERNIST DECEMBER 2009
acids of a protein in a redox reaction that disrupts its
ability to carry out its biological function. Metal ions can
also remove an electron from the bases of DNA. Such
oxidative damage to these biological molecules is
implicated in the cumulative effects associated with
aging and in the mutations associated with cancer. 1
Are heavy metals the same as toxic metals?
In short, the answer is no, as "heavy" refers to the atomic
weight of an element, not its tendency to behave as a
biological bully. While the heavy metals cadmium, lead
and mercury are toxic, molybdenum is a heavy but
essential metal, while beryllium is a light but very toxic
metal.
Heavy metals have always been present in the earth's
ecosystem, but since the Industrial Revolution there has
been a massive redistribution of metals on the surface of
the earth. What has changed, is the relative availability
and the forms in which metals are being dispersed.
The problem with certain heavy metals is that they tend
to form very stable and long-lasting complexes with
sulphur in biological molecules, which can disrupt their
biological function. In some cases this allows these
metals to become concentrated at higher levels of the
food chain.1
Metals in Environmental Medicine
While some European countries enforce strict reg-
ulations, the Asian countries, by comparison, are more
relaxed about enforcing international standards. Overall,
the World Health Organization (WHO) tries to oversee
that regulations are followed and holds workshops in
various parts of the world, regarding environmental
health. Several heavy metals have become of concern to
countries, such as India, where arsenic in water has
affected the health of large number of people. Cadmium
in rice has been a concern, or mercury in fish near
(Continued on next page)
185
mining areas in Indonesia and other parts of the world.4
Just recently, Micro Trace Minerals under the direction
of Dr. E. Blaurock-Busch tested hair and urine analysis,
before and after oral DMPS provocation. The majority
of the nearly 150 test persons included in the study were
physically and mentally challenged children, many
suffering from cerebral palsy.
Unusually high hair levels of manganese, strontium and
uranium were seen in over 80% of the patients. Urine
testing before and after DMSA chelation substantiated
these findings. The final test results are now statistically
evaluated. Visit http://chelattherapie.blogspot.com for
more information.
The Toxicity of Metals in General Health Care
In the US, the Agency for Toxic Substances and Disease
Registry (ATSDR), based in Atlanta, Georgia, is a
federal public health agency of the U.S. Department of
Health and Human Services. ATSDR serves the public
by incorporating and reflecting on academic and medical
knowledge, taking responsive public health actions, and
providing official health information to prevent harmful
exposures and diseases related to toxic substances.5
The World Health Organization (WHO) provides
recommendations regarding the industrial and
environmental use of potentially hazardous substances.
It also provides international standards regarding ex-
posure and recommends reference ranges for human
biomonitoring.
European countries have their individual Environmental
Health Protection Agencies, which govern use and
exposure of toxic substances. Laboratory diagnostics and
reference ranges are based on these agencies recom-
mendations.6
The Toxic Metal Information below is based on ATSDR
official toxic facts and covers only toxic metals with a
history of toxicity as recognized by governmental and
academic sources. Additional information can be
obtained by e-mailing: cdcinfo@cdc.gov
The information on chelation and the tables (graphs)
listed, refer only to synthetic chelating agents and are
largely based on laboratory data from Micro Trace
Minerals, Germany/USA. For details and specifics
regarding Chelation Protocols see Chapter 5 and for
information on non-synthetic chelation agents and
specific protocols are listed in Chapter 6 of my book.
THE ORIGINAL INTERNIST
186 Spring 2006
The CERCLA Priority List
ATSDR and the EPA prepare a list, in order of priority,
ranking substances that are most commonly found at
facilities on the National Priorities List (NPL) and which
are determined to pose the most significant potential
threat to human health due to their known or suspected
toxicity and potential for human exposure at these NPL
sites.
This CERCLA priority list is revised and published on a
2-year basis, with a yearly informal review and revision.
This priority list is based on an algorithm that utilizes the
following three components: frequency of occurrence at
NPL sites, toxicity, and potential for human exposure to
the substances found at NPL sites. This algorithm
utilizes data from ATSDR's HazDat database, which
contains information from ATSDR's public health
assessments and health consultations.
It should be noted that this priority list is not a list of
"most toxic" substances, but rather a prioritization of
substances based on a combination of their frequency,
toxicity, and potential for human exposure at NPL sites.
Of the 275 substances listed, only some are listed and
discussed here. Ranking is shown in the column on the
left i.e. Arsenic is ranked as Toxin #1; Sodium Arsenite
is ranked as #241. (see next page)
References
1. Dartmouth Toxic Metals Research Program © 2001.
http://www.dartmouth.edu/~toxmetal/TX.shtml
2. OSHA
3. Messeter A. Lunds University, Faculty of Medicine.
Public health effects of exposure to toxic metals – a
new study. http://www.med.lu.se/english/research/
evaluation_of_research
4. Report of Environmental Health Impacts from
Exposure to Metals. 1-3 June 2005, Simla, India.
WHO 2005
5. ASTDR
6. Blaurock-Busch E. Antidota-Handbook of Chelation
Therapies. 2007 MTM, Germany/USA ‹
ADVERTISE IN
THE ORIGINAL INTERNIST
Call (573) 341-8448
e-mail: virginia@drkessinger.com
Website: www.drkessinger.com
THE ORIGINAL INTERNIST DECEMBER 2009
05
2007 RANK SUBSTANCE NAME TOTAL POINTS 2005 RANK CAS #

1 ARSENIC 1672.58 1 007440-38-2

2 LEAD 1534.07 2 007439-92-1
3 MERCURY 1504.69 3 007439-97-6
7 CADMIUM 1324.22 8 007440-43-9
18 CHROMIUM, HEXAVALENT 1149.98 18 018540-29-9
42 BERYLLIUM 1046.12 40 007440-41-7
49 COBALT 1015.57 50 007440-48-4
53 NICKEL 1005.4 55 007440-02-0
65 CHROMIUM(VI) OXIDE 969.58 66 001333-82-0
74 ZINC 932.89 74 007440-66-6
77 CHROMIUM 908.52 77 007440-47-3
109 BARIUM 813.46 109 007440-39-3
117 MANGANESE 807.9 115 007439-96-5
123 METHYLMERCURY 806.39 121 022967-92-6
125 LEAD-210 805.9 124 014255-04-0
128 COPPER 804.86 133 007440-50-8
147 SELENIUM 778.98 147 007782-49-2
180 PALLADIUM 700.66 177 007440-05-3
187 ALUMINUM 688.13 186 007429-90-5
198 VANADIUM 651.7 198 007440-62-2
214 SILVER 612.19 213 007440-22-4
215 CHROMIUM TRIOXIDE 610.85 218 007738-94-5
219 ANTIMONY 605.37 222 007440-36-0
223 ARSENIC ACID 604.45 226 007778-39-4
224 ARSENIC TRIOXIDE 604.36 227 001327-53-3
234 ARSINE 602.42 237 007784-42-1
241 CALCIUM ARSENATE 601.45 244 007778-44-1
241 MERCURIC CHLORIDE 601.45 244 007487-94-7
241 SODIUM ARSENITE 601.45 244 007784-46-5

THE ORIGINAL INTERNIST DECEMBER 2009 187


Immune Boosting
Components to Arrest
Colds and Flu
by : Rachel Olivier, MS, ND, PhD
Submitted by: Biotics Research Corporation
During this time of the year, our nutritional focus
typically spotlights the cold and flu season. Nutrients to
support the ramifications of such immune disturbances
are an important component of the nutritional arsenal.
This topic becomes especially pertinent this year in light
of the new H1N1 flu. It is well known in the alternative
healthcare industry that keeping the immune system
healthy contributes significantly to the prevention of
seasonal illnesses. In light of this, components noted to
have a beneficial effect on the immune response, and to
aid in keeping the immune system healthy are discussed.
Larch Arabinogalactans
Arabinogalactans derived from the Western Larch, Larix
occidentalis consist of highly branched nondigestible
polysaccharides, composed primarily of galactose and
arabinose in a 6:1 ratio. In addition to the Larch, many
edible plants are also a rich source of arabinogalactans,
including; among others carrots,1,2 pears,3 tomatoes,4 and
maize.5
The immune-enhancing properties of Larch arabin-
ogalactans suggest that it possesses an array of clinical
applications, both in preventive medicine, due to its
ability to build a more responsive immune system, and
in clinical medicine, as a therapeutic agent in conditions
associated with lowered immune function, decreased NK
activity, or chronic viral infection.6 Its use has also been
demonstrated to enhance the cytotoxicity of natural killer
(NK) cells,7 implying an additional benefit in immune
support. In one cell culture study, the pretreatment of
cells with arabinogalactan from Larix occidentalis was
demonstrated to induce a moderately increased release of
TNFα, interleukin 1β (IL-1β), interferon gamma (IFN-γ)
and interleukin 6 (IL-6).8
The cells involved in both innate and adaptive immune
responses, including macrophages, dendritic cells, T
cells and B cells, are known to express the vitamin D
receptor (VDR) on the cell surface, and can both
produce and respond to vitamin D (1,25(OH2)D3).9
THE ORIGINAL INTERNIST DECEMBER
SEPTEMBER2009
2008
Additionally, the comprehensive vitamin D system
exerts a cumulative effect on the immune response.
Consequently, immune responses are exceedingly depen
-dent upon an adequate vitamin D status. Vitamin D has
also been associated with the activation of toll-like
receptors (TLRs), specifically TLR2. Toll-like receptors
provide defense against pathogens, by virtue of their
response to “conserved pathogen-associated molecular
patterns derived from bacteria, mycoplasma, fungi or
viruses.”10 In light of epidemiological data, Cannell and
colleagues have proposed that the production of vitamin
D elicits a “seasonal stimulus” which underlies the
seasonality of epidemic influenza.11,12,13 Cumulatively,
vitamin D’s specific response has been correlated with
an enhancement of innate immunity, coupled with
multifaceted regulation of adaptive immunity.14
Neonatal Thymus glandular
The thymus gland is the initial migratory place of the T
lymphocytes following their origination in the bone
marrow. In the thymus, the T lymphocytes gain further
specificity, forming either helper T-cells (CD4) or
cytotoxic T-cells (CD8). The helper T-cells function in
aiding other cells of the immune system by promoting
their activation, while the cytotoxic T-cells act directly
on infected or diseased cells. Epithelial cells of the
thymic cortex express both class I and class II MHC
antigens,15,16 which function in the development of T
lymphocytes within the thymus.17
In a study with children, oral consumption of thymus
glandular was demonstrated to result in a significant
decrease in the frequency of recurrent respiratory in-
fections. Additionally, in the supplemented group a
statistically significant increase in the level of salivary
IgA (P<0.02) was observed.18 The beneficial attributes
of thymus glandular in this capacity was attributed to a
“restorative" effect.19 Other studies have concurred the
beneficial attributes of thymus glandular extract, which
included accelerated bone marrow recovery and
normalization of the peripheral blood count.20, 21, 22, 23
Intake has also been shown to benefit recurrent
respiratory tract infections, resulting in a lowered
frequency of infection, a shortened time of infection
(mean = 3 days), and a diminished severity of re-
currences.24
Neonatal Bovine Trachea
Trachea tissue is a powerful immune modulator, whose
use was historically examined by John Prudden, MD of
Harvard University. Trachea tissue has been specifically
referred to as an “immunoregulator,” functioning to both
stimulate the immune system, as well as to repress it, as
in instances of an overactive immune response. It is said
(Continued on next page)
119
189
to resemble fetal mesenchyme, which is the primordial
tissue from which muscle, bone, bone marrow, tendons,
ligaments, and skin develop.25 The antigen presenting
capacity (APC)26 of trachea tissue is well established,
with it demonstrating the ability to secrete IL-1 and to
express MHC class II antigens.27 Its action was also
observed to result in an increase in the activation of
both macrophages and cytotoxic T cells, along with a
stimulation of B cells, resulting in an increase in
immunoglobulins A, G and M, with an overall increase
in antimitotic activity.25 An immunostimulatory
response to viruses has also been demonstrated,
resulting in viral resistance.28 Given the fact that the
entire respiratory tract contains dendritic cells, capable
of functioning in antigen presentation, it is hypo-
thesized that these cells play an important role in the
immune responses of the entire respiratory system,29
including the thoracic cavity, the nasal cavity, the
pharynx, the larynx, as well as both the bronchi and
alveoli.
Vitamin A
Vitamin A is directly involved in protein synthesis,
both at the transcriptional and translational level.30 In
addition to these roles, it is also known to play a
functional role in gene activation.31 The immune
supporting properties of vitamin A are well established,
including its ability to enhance natural killer (NK) cell
activity,32 as well as its ability to decrease bacterial
adhesion to the respiratory epithelium.33 In addition to
these attributes, it is also speculated that vitamin A
contributes to the immune response by virtue of its
"anti-infective" properties, specifically by contributing
to both the maintenance and differentiation of the
intestinal and respiratory epithelium.34 In animals a
deficiency in Vitamin A was demonstrated to
drastically impair the secretory IgA (sIgA) response to
influenza infection, with a corresponding modest
increase in the serum IgG.35 The sIgA-mediated
response is considered a “crucial step in achieving
efficient protection of the epithelial barrier,”36 while
IgG aids in the preparation of the antigen to the
phagocytic cells, thus enhancing phagocytosis.37
Vitamin C
Leukocytes are known to contain a high concentration
of vitamin C. Preventative trials utilizing 1 gram of
vitamin C have shown that daily use reduces the
duration of colds in adults by 8% and in children by
14%.38 In a review of trials by Hemilä et al., it was
determined that supplemental vitamin C (average dose
of 1g/day) reduced the duration of colds by about 23%,
and ameliorated symptoms, although consistent effects
THE ORIGINAL INTERNIST
190 Spring 2006
were absent.39 A separate long-term trial (five years)
reported evidence of a 66% decrease in the common
cold with a daily 500 mg dose of vitamin C, compared
to a daily low dose (50 mg).40
Echinacea
Echinacea use for upper respiratory tract infections is
well recognized. As a member of the aster family
(Asteraceae), its primary components include poly-
saccharides, glycoproteins, alkamides, volatile oils, and
flavonoids. The roots contain a high concentration of
volatile oils, while the above-ground parts of the plant
tend to contain a higher percentage of polysaccharide
components, which serve in triggering an immune
activation. The above ground components are approved
in Germany for the treatment of colds, upper
respiratory tract infections, urinary tract infections, and
slow-healing wounds, while the root components are
approved for the treatment of flu-like symptoms.41 In a
meta-analysis examining the effect of Echinacea on the
deterrence and management of the common cold, a
58% decrease in the odds of developing the common
cold was demonstrated (p<0.001), in addition to a
decrease in the duration by 1.4 days (p=0.01).42 It is
also approved by the German Commission E expert
panel as an adjunct therapeutic in influenza-like
infections.43
Broad Spectrum Vitamin/Mineral Combination
In addition to the products discussed above, immune
protection may also be accomplished by the use of a
broad spectrum multi vitamin/mineral supplement, con-
taining immune supporting nutrients. Immune
supporting components, which provide beneficial
attributes, include citrus bioflavonoids, Echinacea,
Capsicum annuum, chlorophyllins and a source of
methyl donors and acceptors, which serves to assist
with various metabolic conversions, including free
radical conversion. Glandular components including
adrenal, thymus, spleen, liver, pancreas, parotid, lymph
and placenta also serve to provide both organ and
immune support.
It is well documented that multiple factors, including
age, stress, and dietary insufficiencies can negatively
impact the immune system. Inadequate nutrition along
with a poor diet makes one more susceptible to
succumbing to illnesses. The combined use of select
nutrients or combination thereof, as noted above,
provides support to strengthen the immune system, and
subsequently the immune response, making one less
susceptible to seasonal illnesses.
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009
05
References
1. Pennell RI, Knox JP, Scofield GN, Selvendran RR,
Roberts K. A family of abundant plasma membrane-
associated glycoproteins related to the
arabinogalactan proteins is unique to flowering
plants. J Cell Biol. 1989 May;108(5):1967-77.
2. Baldwin TC, McCann MC, Roberts K. A Novel
Hydroxyproline-Deficient Arabinogalactan Protein
Secreted by Suspension-Cultured Cells of Daucus
carota (Purification and Partial Characterization).
Plant Physiol. 1993 Sep;103(1):115-123.
3. Chen CG, Pu ZY, Moritz RL, Simpson RJ, Bacic A,
Clarke AE, Mau SL. Molecular cloning of a gene
encoding an arabinogalactan-protein from pear (Pyrus
communis) cell suspension culture. Proc Natl Acad
Sci USA. 1994 Oct 25;91(22):10305-9.
4. Related Articles, LinksPogson BJ, Davies C.
Characterization of a cDNA encoding the protein
moiety of a putative arabinogalactan protein from
Lycopersicon esculentum. Plant Mol Biol. 1995
May;28(2):347-52.
5. Kieliszewski MJ, Kamyab A, Leykam JF, Lamport
DT. A Histidine-Rich Extensin from Zea mays Is an
Arabinogalactan Protein. Plant Physiol. 1992 Jun;99
(2):538-547.
6. Kelly GS. Larch arabinogalactan: clinical relevance
of a novel immune-enhancing polysaccharide. Altern
Med Rev. 1999 Apr;4(2):96-103.
7. Hauer J, Anderer FA. Mechanism of stimulation of
human natural killer cytotoxicity by arabinogalactan
from Larix occidentalis. Cancer Immunol
Immunother. 1993;36(4):237-44.
8. Hauer J, Anderer FA. Mechanism of stimulation of
human natural killer cytotoxicity by arabinogalactan
from Larix occidentalis. Cancer Immunol
Immunother. 1993;36(4):237-44.
9. Adorini L, Penna G. Control of autoimmune diseases
by the vitamin D endocrine system. Nat Clin Pract
Rheumatol. 2008 Aug;4(8):404-12. Epub 2008 Jul 1.
10. Liu PT, Krutzik SR, Modlin RL. Therapeutic
implications of the TLR and VDR partnership. Trends
Mol Med. 2007 Mar;13(3):117-24. Epub 2007 Feb 5.
11. Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant
WB, Madronich S, Garland CF, Giovannucci E.
Epidemic influenza and vitamin D. Epidemiol. Infect.
2006 134:1129–1140.
12. Cannell JJ, Zasloff M, Garland CF, Scragg R,
Giovannucci E. On the epidemiology of influenza.
Virol. J. 2008 5:Art 29.
13. White JH. Vitamin D Signaling, Infectious Diseases,
and Regulation of Innate Immunity. Infection and
Immunity. Sept. 2008 76(9):3837–3843
14. Bikle DD. Vitamin D and immune function:
understanding common pathways. Curr Osteoporos
Rep. 2009 Jul;7(2):58-63.
15. Rouse RV, Parham P, Grumet FC, Weissman IL:
THE ORIGINAL INTERNIST DECEMBER 2009
Expression of HLA antigens by human thymic
epithelial cells. Hum Immunol. 1982 5:21.
16. Van Ewijk W, Rouse RV, Weissman IL: Distribution
of H-2 microenvironments in the mouse thymus,
lmmunoelectron microscopic identification of I-A and
H-2K bearing cells. J Histochem Cytochem. 1980
28:1089.
17. Jenkinson EJ, van Ewijk W, Owen JJT. Major
histocompatibility complex antigen expression on the
epithelium of the developing thymus in normal and
nude mice. J Exp Med. 1981 153:280.
18. Fiocchi A, Borella E, Riva E, Arensi D, Travaglini P,
Cazzola P, Giovannini M. A double-blind clinical trial
for the evaluation of the therapeutical effectiveness of a
calf thymus derivative (Thymomodulin) in children
with recurrent respiratory infections. Thymus. 1986 8
(6):331-9.
19. Longo F, Lepore L, Agosti E, Panizon F. [Evaluation
of the effectiveness of thymomodulin in children with
recurrent respiratory infections]. [Article in Italian]
Pediatr Med Chir. 1988 Nov-Dec;10(6):603-7.
20. Skotnicki AB, Dabrowska-Bernstein BK, Dabrowski
MP, Gorski A, Czarnecki J, Aleksandrowicz J.
Biological properties and clinical use of calf thymus
extract TFX-Polfa, in Goldstein A L (ed): Thymic
Hormones and Lymphokines, pp. 545-564, New York,
Plenum Press (1984).
21. Aleksandrowicz J, Blicharski J, Janicki K, Lisiewicz J,
Skotnicki A B, Sliwczynska B, Turowski G, Szmigiel
Z, Wazewska-Czyzewska M: Effect of the thymus
extract on congenital hypogamma-globulinaemia and
immunological deficiency accompanying the
proliferative and aplastic haematological diseases, in
van Bekkum D K (ed). Biological Activity of Thymus
Hormones. Rotterdam, Kooyker. 1975 pp. 37-39.
22. Skotnicki A B, Blicharski J, Lisiewicz J, Sasiadek U,
Janik J, Wolska T, Zdunczyk A, Aleksandrowicz J:
Calf thymus extract TFX-Polfa in the treatment of
patients with secondary leukopenia. Ther Drugs. 1987
37(95).
23. Zeromski J, Siowik-Gabryelska A, Krzysko R. The
preliminary evaluation of TFX administration in
advanced bronchogenic carcinoma, in Seminar on
Cellular and Humoral Immunity in Lung Diseases.
Poznan (1976). pp. 44-46.
24. Stankiewicz-Szymczak W, Moszynski B, Dabrowski
MP, Dabrowska-Bernsztein BK, Stasiak A. The initial
results of TFX-Polfa application in patients with
chronic recurrent infections of upper respiratory tract.
Pol J Otolaryng. 1986 2:350.
25. Kriegel H. Dr. John Prudden and Bovine Tracheal
Cartilage Research. Alternative & Comp Therapies.
April/May 1995. pp. 187-189.
26. Holt P, Schon-Hegrad MA, Oliver J. MHC class II
antigen-bearing dendritic cells in pulmonary tissues of
the rat. J . Exp. Med. 1988 167:262-274.
(Continued on next page)
191

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THE ORIGINAL INTERNIST
192 Spring 2006
27. Sertl K, Takemura T, Schachler T et al. Dendritic cells
with antigen presenting capability reside in airway
epithelium, lung parenchyma and visceral pleura. J Exp
Med 1986;163:436–451
28. Rosen J, Sherman WT, Prudden JF, Thorbecke GJ.
Immunoregualtory effects of catrix. J Biol Response
Modifiers. 1998 7:498-512.
29. Sertl K, Takemura T, Tschachler E, Ferrans VJ,
Kaliner MA, Shevach EM. Dendritic cells with antigen
presenting capability reside in airway epithelium, lung
parenchyma, and visceral pleura. J. Exp. Med. 1986
163 :436.
30. Berdanier CD. Advanced Nutrition Micronutrients.
CRC Press. 1998 p. 33.
31. Semba RD. Vitamin A, immunity, and infection. Clin
Infect Dis. 1994 Sep;19(3):489-99.
32. Goldfarb RH, Herberman RB. Natural killer cell
reactivity: regulatory interactions among phorbol
esters, interferon, cholera toxin, and retinoic acid.
Journal of Immunology. 1981 126:2129-2135.
33. Chandra, RK. Increased bacterial binding to respiratory
epithelial cells in vitamin A deficiency. British Medical
Journal. 1988 297:834-835.
34. Stephensen CB, Blount SR, Schoeb TR, Park JY.
Vitamin A deficiency impairs some aspects of the host
response to influenza A virus infection in BALB/c
mice. J Nutr. 1993 May;123(5):823-33.
35. Stephensen CB, Moldoveanu Z, Gangopadhyay NN.
Vitamin A deficiency diminishes the salivary
immunoglobulin A response and enhances the serum
immunoglobulin G response to influenza A virus
infection in BALB/c mice. J Nutr. 1996 Jan;126(1):94-
102.
36. Phalipon A, Cardona A, Kraehenbuhl JP, Edelman L,
Sansonetti PJ, Corthésy B. Secretory component: a
new role in secretory IgA-mediated immune exclusion
in vivo. Immunity. 2002 Jul;17(1):107-15.
37. http://pathmicro.med.sc.edu/mayer/IgStruct2000.htm
38. http://lpi.oregonstate.edu/infocenter/vitamins/
vitaminC/
39. Hemilä H, Chalker E, Treacy B, Douglas B. Vitamin C
for preventing and treating the common cold. Cochrane
Database of Systematic Reviews 2007, Issue 2. Art.
N o . : C D 0 0 0 9 8 0 . D O I :
10.1002/14651858.CD000980.pub3
40. Sasazuki1 S, Sasaki S, Tsubono Y, Okubo S, Hayashi
M, Tsugane S. Effect of vitamin C on common cold:
randomized controlled trial. EJCN. 2006 60:9–17.
41. http://www.umm.edu/altmed/articles/echinacea-
000239.htm
42. Shah SA, Sander S, White CM, Rinaldi M, Coleman
CI. Evaluation of echinacea for the prevention and
treatment of the common cold: a meta-analysis. Lancet
Infect Dis. 2007 Jul;7(7):473-80.
43. http://www.naturalstandard.com/monographs/ ‹
THE ORIGINAL INTERNIST DECEMBER 2009
05

Liver Flush:
Help or Hoax?
by: Dr. E. W. McDonagh, DO
Reprinted with permission: Townsend Letter October
2009, www.townsendletter.com
I am submitting the case history of my patient Lyle
Hanson for Publication. Mr. Hanson wants more people
to learn about the benefits of liver flush. Perhaps his
experience will stimulate interest.
Mr. Hanson is a 62-year-old overweight, caucasian man
with diabetes. In 1994, he had a nephrectomy. During
the work-up for kidney surgery, the radiologist
discovered several stonelike densities in the liver and
gallbladder. The patient refused surgery for these stones.
Several years later during a follow-up MRI, stones were
again seen in his liver area.
Mr. Hanson discovered a book at a health food store that
outlined a procedure purported to eliminate liver/
gallbladder stones. The regimen included apple juice,
Month 1
Month 4
THE ORIGINAL INTERNIST DECEMBER 2009
grapefruit juice, Epsom salts, and olive oil. It was to be
administered over six days monthly.
He followed the procedure. Stones of various densities,
colors, and amounts were produced monthly. Mr.
Hanson screened, washed and photographed them for 15
months. (There was no further stone excretion after the
14th Treatment.) some floated in water and some sank.
He stated that his fatigue is gone, energy has increased,
digestion is now normal, cholesterol is lowered, and
vision is sharper.
I have been aware of various recipes that might flush out
liver stones for at least 30 years. Stories, anecdotal at
best, never offered proof of effectiveness, or it was
scanty, indeed. Monthly treatments until no more stones
appear is crucial.
Treatment contraindications might include intestinal
diseases such as duodenal ulcers, ulcerative colitis, and
other medical problems. Please seek doctor’s advice if
contemplating this procedure.
Further details can be had by reading the Timeless
Secrets of Health and Rejuvenation, by Andreas Motitz,
an expert practitioner of Ayurvedic medicine.
Experienced readers’ comments are encouraged and
requested to be sent to me at DrMcDonagh@aol.com.‹
Month 5
Month 6
(Continued on next page)
193
 Month 7 Month 11

Month 8 Month 12

Month 9 Month 13

Month 10 Month 14

THE ORIGINAL INTERNIST

194 Spring 2006 THE ORIGINAL INTERNIST DECEMBER 2009
05
 NEW
HCG
Human Chorionic Gonadotropin

Now Available From

Professional Health Products ®

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Homeopathic HCG eliminates the need for daily

injections and is a more cost effective form for
patients.

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Utility of an Oral
Presentation of HCG
(Human
Choriogonadotropin) for
the Management of Obesity:
A Double Blind Study
by: Dr. Daniel Oscar Belluscio, MD
Dr. Leonor Ripamonte, MD
Dr. Marcelo Wolansky, PhD
Reprinted with permission: Dr. Daniel Oscar Belluscio, MD
Abstract
Female obese volunteers participating in a double blind
study, and submitted to the administration of an oral
presentation of hCG (Human Choriogonadotropin) plus
a VLCD (Very Low Calorie Diet), decreased specific
body circumferences and skinfold thickness from
conspicuous body areas more efficiently than
Placebo+VLCD -treated subjects.
Since a significant fat proportion from total body fat is
subcutaneously located (50 to 65 percent, depending on
sex and fat distribution), this hCG metabolic activity
would result in a reduction of the total body fat mass, the
main cause for obesity. We suggested that the combina-
tion of a VLCD and oral hCG could not only trigger
clinically significant changes in subcutaneous fat stores
but simultaneously decrease body weight and modelate
body contour.
hCG oral administration proved to be a safe and
effective procedure on obese treated volunteers. No side
effects were observed during the study. There are no
reports in the literature regarding this administration
route to compare our findings.
Compared to placebo treated subjects, volunteers who
were managed with an oral administration of hCG coped
more efficiently with daily irritating situations, were in a
better mood, and handled home conflicts without
stepping up family discussions.
KEYWORDS: Gonadotropin(s), Chorionic; Obesity;
Adipose tissue metabolism; fat; overweight; beta-
endorphin; lypolisis; lipogenesis.
THE ORIGINAL INTERNIST DECEMBER 2009
Introduction
Few substances have been so neglected and misunder-
stood regarding its potential therapeutic actions as hCG,
the acronym for Human Chorionic Gonadotropin.
First discovered by Ascheim and Zondek as far back as
1927 in the urine from pregnant women2, thousands of
articles were published regarding its action on gonads,
but comparatively quite a few investigated its vast
therapeutics potentialities, encompassing Kaposi sar-
coma,34 asthma,20,66 psychoses,22 artheriopaties,14 thalas-
semia,57,7,19 osteopenia,57 glaucoma.54
hCG is the glycoproteic hormone normally secreted by
trophoblastic cells of the placenta during pregnancy.67 It
consists of two dissimilar, separately, but most presuma-
bly coordinately translated chains, called the alpha and
beta sub-units.12,26,47,27,18,30
The three pituitary hormones LH (Luteinising Hor-
mone), FSH (Follicle Stimulating Hormone) and TSH
(Thyroid Stimulating Hormone) are closely related to
hCG in that all fours are glycosilated and have a dimeric
structure comprising the alpha and beta chains as
well.31,35,79
The amino acid sequence of the alpha chain of all four
human glycoproteic hormones is nearly identical. The
amino acid sequence of the Beta subunits differs and
accounted for by the unique immunological and biologi-
cal activities of each glycoproteic hormone.63 Beta hCG
contains a carboxylic residue of 30 amino acids charac-
teristic to hCG.11,52
Its denomination; (Human Chorionic Gonadotropin)
dates back from the early days, when it was found. hCG
rendered mature infantile sex glands in experimentation
animals (Gonadotropin) and it was secreted by the pla-
centary chorion (Chorionic).2,91
However, recent data suggest both terms can be
misleading: normal human tissues from non-pregnant
subjects,88,74,48,86,87 trophoblastic and non-trophoblastic
tumors,33,6,90 bacteria,49 and plants46,69 express hCG or a
hCG-like substance.
The first report on hCG and obesity was published back
as 1954 in The Lancet, by a British physician, Dr.
A.T.W. Simeons.70 After its publication, hCG was advo-
cated for several years as a useful approach to obesity.
The pendulum of its popularity swang back and forth
(Continued on next page)
197
until a series of studies1,3,8,17,36 but three concluded hCG
was of no use to manage the disease.3,25,80
According to basic pharmacological postulates, the
administration route may influence the biological
activity of a drug. All previous studies were performed
with a hCG preparation administered by injections. One
of the authors of this study (DB) theorized that an
increase in dose and a shifting in hCG administration to
a sublingual-enteral route may modify the pharmacologi-
cal activity of hCG.
The purpose of this study was to assess the utility of an
oral presentation hCG for the management of obesity.
Materials and methods
The study design was of the double-blind type: neither
treating physician nor patient knowing who was
receiving hCG, or an inert substance (placebo). Female
patients for the study were selected, since the clinic
where the study was performed specializes in the
diagnosis and treatment of gynecologic disorders.
Details of the protocol were explained to eighty-three
volunteers, who were solicited through a written
announcement. Before entering the study, they signed an
informed consent in front of a neutral witness.
Inclusion criteria
We required selected volunteers to meet the following
criteria: being at least 25% BMI (Body Mass Index),
overweight, and in general healthy condition. If taking
medication for obesity, such as anorectics or
amphetamines, they should discontinue the medication
at least one month prior the initiation of the study. Drugs
to control their clinical diseases (hypertension, hypothy-
roidism, etc.) were allowed. No patients under steroid,
diuretics or hormones were entered the study. During the
study, volunteers were also asked about starting the use
of medical prescribed drugs or pharmaceutical prepara-
tions during the trial period.
Exclusion criteria
No teenagers or patients over 75 y.o. were admitted to
the study. No patients with severe and/or uncontrolled
clinical diseases (cancer, IDDM, heart attacks, infarcts
sequelae) were accepted. After applying the inclusion/
exclusion criteria, we counted on 70 subjects to divide in
treatment groups. These women were randomly assigned
to groups Placebo (P, N=26) or hCG (N=44) by a simple
randomized sampling method. This latter group was in
turn split in two subgroups: G1 (N=36) and G2 (N=8),
according to the hCG dose administered (see below).
THE ORIGINAL INTERNIST
198 Spring 2006
Patients were Caucasian, ages ranging from 23 to 73
y.o. (group P: 41 ± 13; group G1: 42 ± 12; group G2: 41
± 14), a range of heights of 162 cm. to 181 cm., and
overweight ranging from 25 to 499 on BMI Tables.
Since there were no published reports on the oral use of
hCG, except for one study posted by D.B. and L.R. on
the Internet (http://indexmedico.com/obesitv/hcg.htm),
group G2 was administered twice the dose of G1, to
assess if hCG concentration may affect obtained results.
The pharmacist prepared two types of vials: one
containing saline solution (Na Cl 0,9% w/v), and the
other containing a diluted solution (saline) of commer-
cial, standardized hCG (from Gonacor, Massone
Pharmaceutical Industry). HCG Solution was prepared
buffering the drug with Sodium Bicarbonate and
glycerin.
Notice: after uploading this report to the Internet, further
research we have performed on oral hCG preparations
demonstrated that the addition of certain diluents, de-
grades hCG molecule, partially inactivating its activity.
Therefore, we have reverted to the use of saline solutions
instead. Our results have significantly improved since
then.
Vials were randomly labeled, each number correspond-
ing to a patient. The pharmacist kept the codes in a
sealed envelope. They were opened after completing the
protocol.
Volunteers from group G1 were administered a diluted
solution of hCG (125 IU) b.i.d. (twice daily; total: 250
IU). One of the doses was taken before breakfast
(fasting). The remaining was administered 1 hr before
dinner.
Volunteers from group G2 were given twice the
amount of group G1: 250 IU b.i.d. (a total of 500 IU
daily).
Patients were advised to maintain the solution at least
two minutes in the oral cavity before swallowing
(sublingual, to profit from the rich venous plexus exist-
ing in this region, also bypassing the liver). They were
also told that medication has to be maintained under re-
frigeration at all times.
Diet plan
The same Very-Low-Calorie-Diet (VLCD), specific and
detailed, was prescribed to all groups.
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009
05
Breakfast: tea or coffee in any quantity without sugar.
Only one tablespoonful of milk allowed in 24 hr.
Saccharin or other sweeteners could be used.
Lunch: 100 grams. of veal, beef, chicken breast, fresh
white fish, lobster, crab or shrimp. All visible fat was
carefully removed before cooking, and the meat weighed
raw. Salmon, tuna fish, herring, dried or pickled fish was
not allowed.
The chicken breast was removed raw from the bird. One
type of vegetable could be only chosen from the
following: spinach, chard, chicory, beet-greens, green
salad, tomatoes, celery, fennel, onions, red radishes,
cucumbers, asparagus, and cabbage. One breadstick
(grissini) or one Melba toast was allowed, and an apple
or an orange, or a handful of strawberries or one-half
grapefruit.
For dinner: The same four choices as lunch.
The juice of only one lemon daily was allowed for all
purposes. Salt, pepper, vinegar, mustard power, garlic,
sweet basil, parsley, thyme, marjoram, etc., could be
used for seasoning, but no oil, butter or dressing. Tea,
coffee, plain water, mineral water were the only drinks
allowed, but they could be taken in any quantity and at
all times.
Clinicometric controls
Volunteers assisted twice weekly at the clinic to be
controlled and weighed. The following evaluations were
completed once a week:
I. Height and Weight, performed on a medical scale.
Volunteers were weighed using normal underwear.
II. Body circumferences. Using a flexible, non elastic
metric tape, the following anatomic areas were assessed:
• Wrist (WRT), at the level of flexion fold (wrist-
forearm);
• Breast (BRE), submammary fold;
• Waist (WAT): at the hypogastric region level;
• Abdominal (ABD), at the navel level;
• Hips (HIP): pubic line;
• Thighs (THI): 8 cm. below pubic line;
• Suprapatelar (ROT), at the patella upper border;
• Ankle (ANK), at the flexion fold (peroneal protuber-
ance).
THE ORIGINAL INTERNIST DECEMBER 2009
III. Skinfold thickness. Using a Lange Skinfold Caliper
(Cambridge Scientific Industries, Cambridge,
Maryland), the following folds were examined:
• Tricipital (TRI), arm midline, posterior region and
tricipital muscle zone;
• Anterior Axilar line (AXA), at the fold created when
pinching the skin region at the level of the pectoralis
muscle extending to the arm;
• Subscapular (SCA (i)): inferior scapular spine;
• Thoracic (TOR): at the fold created when pinching
the region located immediately below the ribs, at the
level of an imaginary line extending from anterior
axilar line;
• Suprailiac (ILI), at the fold created 4 cm above the
anterior superior iliac spine;
• Supraumbilical (UMB(u)), 3 cm above navel;
• Infraumbilical (UMB(i)), 3 cm below navel;
• Thighs (THI), internal aspect of thighs, eight cm
below the pubic area;
• Patellar area (ROT), at the fold created when
pinching the region located 6 cm medial to the
internal patellar border.
IV. Bioelectrical impedance. Using Tetrapolar Bioelec-
trical Impedance (TBI) with a body fat analyzer Maltron,
model BF-905 (Maltron International Ltd., Rayleigh,
Essex).
Volunteers voided previous to the evaluation, placed on
supine position, and allowed to rest half an hour before
determination. Self-adhering electrodes were placed on
extremities. Every determination was performed with a
separate set of electrodes, discarded after single use.
The following TBI determinations were assessed:
1. Fat weight (FW)
2. Lean weight (LW)
3. Water weight (WW)
4. Calories (CAL)
V. ß-hCG determinations: all subjects enrolled in the
trial were studied for plasmatic ß-hCG levels by an
ELISA test (64) on 0-15-30 study days.
VI. Mood questionnaire: from the first study week on,
patients were given weekly self-administered
questionnaires to be completed at home. It consisted of
twenty-four questions related to their mood changes in
the course of the study, plus four questions related to
adverse drug effects. They returned the data at the time
of the subsequent visit to the clinic.
(Continued on page 201)
199
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Data Analysis
Variables were split as follows for a better data
processing and statistical results presentation:
• Category I, BW plus four bioelectrical impedance
records (FW, LW, WW and CAL),
• Category II, eight anthropometrical measurements
(corporal circumferences WRT, BRE, WAT, ABD,
HIP, THI, ROT and ANK).
• Category III, nine skinfold assessments (TRI,
AXA, SCA (i), TOR, ILI, UMB(u), UMB(i), THI,
ROT) (see long names and definitions for the
studied variables at the beginning of this section).
Each set was analyzed with a two-way multivariate
analysis of variance (MANOVA), comparing the
obtained Wilks-lambda' F with the corresponding critical
value.
TREATMENT (VLCD diet plus group-specific
pharmacological intervention) was considered the
between-subject factor with three levels (P, G1, G2), and
WEEK of clinicometric control served as an additional
within-subject factor with six levels: weeks 0 to 5.
To estimate how the differences between treatment
groups depended on the trial time elapsed since week
zero (comparison of pattern trend changes in function of
treatment time) we obtained the MANOVA result for the
effect of the INTERACTION (also displayed in the text
as TREATMENT x WEEK).
Moreover, to prevent any possible influence of acute
effects specifically associated to any VLCD program in
the adaptation phase (first 5-7 days), we additionally
evaluated with separate MANOVA analyses the differ-
ences between groups and within subjects in the course
of the last four treatment's weeks.
After obtaining a statistically significant multivariate test
for a particular main effect or interaction, we further
examined the univariate F tests for each dependent
variable. When parameters from these tests displayed
significant modifications, data were further analyzed to
ascertain which group (P, G1 or G2) was responsible for
the previous p values obtained. We also compared data
basal values from each group against those obtained in
subsequent weeks (e.g., records of week 0 against week
1, thereafter against week 2, and so on). These pain/vise
comparisons were statistically assessed applying post
hoc Scheffé F tests.
THE ORIGINAL INTERNIST DECEMBER 2009
Questionnaire responses were converted into percentages
and submitted to a chi-square (2%) test to compare
between-groups and within-groups (pairing off final vs.
initial data) statistic results.
To attenuate the natural source of within-subject
variation, inherent to all assessments of subjective
symptoms, we averaged data results from identical ques-
tionnaires completed weekly during the initial first two
study weeks. Thus, we obtained a more precise "initial
questionnaire" (avoiding the potential "adaptation effect"
common to any VLCD regime in the first treatment
week).
To obtain the final mood behavior results over the last
two treatment weeks, they were averaged using the same
schema as detailed before. Criteria for significance was
p<0.05. Statistica 4.2 (from StatSoft, Inc.) for Windows
software was used in all processing.
Results
All volunteers were submitted to the same VLCD
schedule lasting five weeks. The objective of this work
was to gather data on the potential synergism between
hCG administration and a VLCD plan. At the end of the
study we counted a total of 4.3 % missing data due to
the absence of subjects in control days (no one absent in
more than two opportunities) as a consequence of per-
sonal situations not associated with the experimental
conditions. No statistic differences were obtained be-
tween Placebo and hCG groups regarding missing data.
No statistic differences were obtained among Placebo
and hCG groups regarding missing data.
1. Regarding weight loss, similar results (with/
without hCG administration) were obtained. Bioelec-
trical impedance exhibited discrete modifications in
tested groups.
As expected, for all types of clinicometric assessments,
significant results were obtained through MANOVA
analysis on factor WEEK. Figures 1 and 2 (bioelectrical
impedance and anthropometrical data, respectively)
show that the time-dependent changes were uniformly
present in all tested groups. We therefore estimated that
the decreasing observed patterns were the consequence
of VLCD acting on overweight patients. However, re-
garding skinfold thickness findings (Figures 3 and 4), we
detected in P group a noticeable tendency to attenuation
of the within-subject variation during the last (third to
fifth) study weeks. The data suggested us that this latter
period might be the focus of our interest).
(Continued on next page)
201
Figure 1 (see page 209) shows data patterns resulting in
all groups from three representative variables (BW, FW
and LW) of the variable category I. The MANOVA
analysis revealed nearly significant differences for the
INTERACTION (TREATMENT x WEEK) [F(50,58)
=1.35, p=0.13] without statistical significance on analy-
sis of TREATMENT as main effect [F(10,98)=1.22,
p=0.29].
When all groups were submitted to multivariate and
univariate analyses taking exclusive data from weeks 2-
5, we observed no significant difference result for the
INTERACTION among group P and hCG-treated
groups. This finding could be related to differences in
mean basal body weights and treatment-dependent
responses to the acute effects of VLCD during former
weeks.
When the post hoc Scheffé test was applied to compare
the result from each weekly record (weeks 1-5) to it's
corresponding basal value (week zero), we found
similar patterns for all groups concerning analysis of
BW and TBI records (compare P vs. hCG-treated
groups in every panel of Figure 1).
However, regarding the analysis of FW and BW data,
we detected significant differences for the effect of the
INTERACTION (p<0.005 and p<0.05, respectively).
Comparing FW patterns from groups P and G1: F
(5,230)=4.55, p<0.001. For the comparison P vs. G2,
(BW and FW data), we obtained: F(5,140)=4.20 and
2.97, respectively (p<0.01 for both cases).
2. hCG+diet significantly decreased more waist
and abdominal circumferences than diet alone.
Figure 2 shows the results for three (category II) body
circumference assessments (WAT, ABD and HIP).
MANOVA analysis showed significant differences for
factor TREATMENT as main effect [F (16,92)=1.92,
p<0.04], which we do not consider relevant due to the
presence of higher basal records in group G2 when
compared to the rest of the studied groups.
As a whole, the effect of the INTERACTION did not
reveal statistical significance.
Nevertheless, significant differences were obtained
after further analysis for the effect of the INTERAC-
TION on variable WAT [F (10,265)=2.44, p<0.01, see
panel A].
Data assessments from other circumferences did not
show statistical differences for this effect among
THE ORIGINAL INTERNIST
202 Spring 2006
groups [as representative examples, see ABD (p=0.35)
and HIP records in panels B and C, respectively].
When the records of weeks 0-1 were subtracted from
MANOVA analysis, almost all p values were slightly
affected. WAT and ABD measurements demonstrated
to still be more affected by the INTERACTION: for
WAT, p<0.003; for ABD, p<0.08. The INTERAC-
TION significance increased when P controls were
compared to subjects from group G2: comparing P vs.
G2, and considering data from weeks 0-5, we obtained:
F (5,140)=2.87 (p<0.02) for WAT, and F(5,140)=1.80,
(p=0.12) for ABD. But when we analyzed data from
weeks 2-5, we found the following: for WAT, F (3,84)
=3.43 (p<0.02), for ABD, F (3,84)=2.73 (p<0.05).
3. Weak effects of hCG on a series of skinfold thick-
ness reduction patterns.
Figures 3-4 show results from subcutaneous fat
evaluations, as assessed by skinfold thickness, on nine
selected skinfolds. Figure 3 presents three representa-
tive folds [TRI, SCA (i), ILI (U)3 out of five (those
previous mentioned plus AXA and TOR)] that demon-
strated to be slightly affected by the pharmacological
treatment.
Analyzing skinfold data from weeks 0 to 5, the main
effect TREATMENT showed statistical significance (F
(10,98)=2.39, p<0.02). However, prevailing higher
basal records in group G2 might account for this statis-
tical significance. After studying the effect of the IN-
TERACTION on skinfold results, statistics were as
follows: TRI (see panel A), p<0.08; AXA, p=0.98;
SCA(i) (see panel B), p<0.005; ILI (see panel C),
p=0.23; TOR, p=0.35.
Performing pairwise comparisons between control P
and hCG-treated groups, we observed that the higher
significances obtained for SCA (i) and TRI skinfolds
derived mainly from the comparison between P and
G2: for TRI, F (5,140)=2.55, p<0.04, for skinfold SCA
(i), F (5,140)=6.02, p<0.0001. MANOVA analyses run
on weeks 2-5 data resulted in a significance increase
for TREATMENT as main effect [F (10,98)=2.55,
p<0.009]. In addition, the INTERACTION was en-
hanced on data from SCA(i) assessment (p<0.00005):
by comparing data from groups P and G2 during weeks
2 to 5: for TRI, F (3,84)=2.08 (p<0.04), for SCA(i), F
(3,84)=9.31.
4. Higher response rates in a different skinfold
series by treatment with hCG plus a VLCD.
In Figure 4 we display skinfold thickness results
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009
05
obtained from another series of four examined skin-
folds [UMB (U), UMB ^ THI, ROT(U)]. MANOVA
analysis resulted in a nearly significant INTERAC-
TION [F (40,68)=1.55, p<0.06] in the absence of statis-
tical significance for TREATMENT as main effect [F
(8,100)=1.43, p=0.20].
When the specific effect of the INTERACTION was
evaluated for each skinfold, highly significant differ-
ences were found. By computing F (10,265) values, we
obtained the following results: UMB (U) (see panel A),
p<10-3; UMB (U) (see panel B), p<10-5; ROT (see
panel C), p<0.05; THI (see panel D), p<10-6. When we
restricted the data analysis from weeks 2 to 5, we found
nearly significant results for factor TREATMENT as
main effect [F (8,100)=1.75, p<0.1] and for the effect
of the INTERACTION [F (24,84)=1.55, p<0.06]. The
INTERACTION was further studied pairing P group
against each hCG-treated group in separate multivariate
analyses.
By comparing P vs. G1, we found: for UMB(i), p<0.04,
and for RQT , p<0.03 (UMB(U) and THI achieved
nearly significant p values). Again, the strength of the
INTERACTION [TREATMENT x WEEK] was higher
when group G2 was selected for the comparison.
From the obtained data, it becomes clear that skinfolds
determinations in Q2 subjects showed a differential
response to VLCD schedule with respect to that of P
controls (for INTERACTION, in these points of skin-
fold assessment, p<0.0005).
5. Selective response of some skinfolds to hCG was
dependent on dose.
The experimental design of this investigation was not
intended to determine the dose-response curve for hCG
acting on diet-induced effects.
However, the effects of hCG on some of these skin-
folds seemed to be dependent on dose, significant dif-
ferences for the effect of the INTERACTION after the
comparison between G1 vs. G2 groups for UMB (u)
(p<0.001) and UMB (i) (p<0.005), and a nearly signifi-
cant p value for THI (p=0.11).
Figure 4 also displays the percentages of skinfold thick-
ness reduction from the beginning to the end of the
clinical trial. We found skinfolds decreases for group
G1 ranging from over 22% (for UMB (u), see panel A)
up to over 115% (for THI, see panel D) over respective
decreases in P group. These differences were still
higher when G2-subjects were compared to P controls:
THE ORIGINAL INTERNIST DECEMBER 2009
by computing the ratio between decrease percentages,
G2 had over twice (for UMB (u), see panel A) to over
four-fold (for THI, see panel D) the skinfold records
drops observed in group P (see each actual percentage,
group by group, in Fig. 4).
Most of the differences among hCG-treated subjects
and P controls regarding skinfold reduction rates were
enhanced when data corresponding to week five was
compared to records of week two instead week zero
(data not shown).
6. Improvement in mood-related parameters by
hCG.
In Figure 5, we display the responses to four represen-
tative questions asking about the occurrence frequency
for specific mood-related events, according to a multi-
ple choice designed questionnaire completed every
treatment week by all the subjects enrolled in the trial.
Panels A to D display the initial and final questionnaire
results, expressed as percentages for each optional
response (covering a four-option frequency scale from
never to frequent).
Using this procedure, we expected to find, in tested
volunteers, skewness towards either sense concerning
their behaviors and feelings in response to a diet and a
pharmacological intervention. For all these questions,
and compared to control subjects, hCG-treated volun-
teers (G1+G2) showed a trend to improvement of inter-
personal contacts and mood control when confronting
upsetting or conflicting situations. Pairing off final (f)
vs. initial (i) distribution of percentages for optional
responses, we particularly found statistical significance
in two of these questions in group G (after\test:
2
X3=16.3, p<0.002, and 2X3=7.82, p<0.05; see right
sectors of panel A and B, respectively).
P group-subjects did not present temporal differences
(see panel A), or were adversely affected in their mood
during the trial 2X3=14.4, p<0.002 (compare in panel B
corresponding initial and final values for group P and
G).
Furthermore, group P exhibited, in two other questions,
certain skewness to the impairment of its mood (see left
half of panels C and D, p<10-5 ); for group G we
obtained the 2X3 values 1.51 and 3.98, respectively
(p>0.3), showing the absence of temporal mood
changes.
For all other mood-related questions, no statistical sig-
(Continued on next page)
203
nificant difference among groups was found (data not
shown).
We also included some questions intended to evaluate
the potential occurrence of treatment-dependent clinical
anomalies regarding hormonal, physiological or
metabolic disorders. We found no significant difference
after final vs. initial records' comparison (data not
shown).
7. No detectable ß-hCG plasmatic levels in all tested
groups.
On treatment days 0, 15 and 30 we have tested all
volunteers, screening for the presence of plasmatic
p-hCG. Concentrations were undetectable in all cases
(data not shown).
Discussion
Concerning hCG and its utility for the management of
obesity, this study introduces two new aspects, and
adds new data for a third:
I. This is the first report assessing variables not
included in previous reports;38,51,68,89
II. We report a new administration route for hCG
management of obesity, the oral approach,
which has never been reported before;
III. We have detected mood changes in hCG treated
patients, regarding a better confrontation of
daily emotionally conflicting situations.
I) Skinfold thickness (SKF) and Tetrapolar
Bioelectric Impedance (TBI) records.
Both approaches have been extensively discussed in the
literature. It was shown that the correlation between the
values obtained with the two methods to be linear and
highly significant for both sexes.42,81,27
There is general agreement that skinfolds calipers are
particularly useful in the clinical setting,56,82,16,76,10,65,
9,15,75
particularly in view of the fact that measurement
of subcutaneous body fat at different body sites is
becoming increasingly important for the characteriza-
tion of risk of certain disease states.55
When comparing skinfold assessments to body circum-
ference estimates, some data suggests that the latter
approach appears to be more sensitive in the determina-
tion of subcutaneous body fat,53 this procedure is in our
opinion subjected to clinical variables (bloating syn-
drome after a meal, premenstrual water retention, etc.)
that may affect negatively on the final estimate’s re-
THE ORIGINAL INTERNIST
204 Spring 2006
sults. Also, when comparing SKF to body contour as-
sessments, some data suggest that the pattern of fat
thickness body distribution measured over several spe-
cific sites by one method of measurement is unlikely to
be duplicated by of the other method on the same indi-
vidual.40,41
Adipose tissue patterns show great variability, showing
the importance of using skinfold caliper readings from
a variety of different anatomic sites including upper
limbs, lower limbs and trunk.30,65
According to the above conclusions from several
authors,72,13,60, 25,73,62 we would like to suggest that
former studies on hCG and obesity lacked of sufficient
data to estimate accurately the modifications of adipose
tissue distribution in tested volunteers. Consequently
we designed the study to assess as many variables as
possible .
As far as our study concerns, we subjected each
volunteer enrolled in the trial to four bioelectrical
impedance, eight anthropometrical plus nine SKF
evaluations. Performing this multiple site determina-
tions, our results show that specific SKF are highly
responsive to hCG pharmacological intervention (upper
and lower umbilical). The greater response was
obtained in those regions where the corresponding
circumference assessments resulted in nearly signifi-
cant or significant decreases through the trial period
(see waist and abdomen records in Fig. 2 and the above
detailed description of statistical results for the effect of
the interaction).
II) Oral hCG is an valuable alternative administra-
tion route.
No data appear on the scientific literature regarding an
oral administration of hCG in humans. But results from
this study suggests hCG may be used by the sublingual-
enteral route. Despite plasmatic, ß-hCG remained
undetectable both in Placebo and hCG groups
throughout the study, an oral administration of hCG
proved to possess therapeutic activity.
Since commercial preparations of hCG contains
ß-endorphin, it may be tempting to hypothesize that
this pentapeptide might account for the pharmacologi-
cal activity observed on mood stability during the Pro-
tocol.
III) Volunteers treated with hCG coped better with
daily irritating situations.
As can be seen on Figure 5, hCG-treated groups
(Continued on page 206)
THE ORIGINAL INTERNIST DECEMBER 2009
05
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handled better their irritability, their mood at home, and
were less prone to episodes of extreme nervousness
capable of provoking violent discussions. Several
reports proposed hCG might be used for the treatment
of psychoses or neurosis.29,61,24 Our study appears to
corroborate these proposals.
To conclude, this study poses several still unanswered
questions:
1. hCG absorption. We have tested all volunteers,
screening for the p-hCG in plasma. Concentrations
were undetectable in all cases.
Therefore, which hCG fraction is responsible for
the pharmacological activity observed in our study?
hCG’s molecular size (alpha chain -14,500 KD;
beta chain -22,200 KD) makes it highly improbable
that the entire molecule has been absorbed. Our
hypothesis is that only a fraction of the entire hCG
molecule is absorbed through this administration
route.
2. hCG and lipid metabolism. We do not know pre-
cisely how hCG acts on adipose tissue metabolism.
However, some reports32,84,85,83 suggest hCG
possesses a metabolic activity on adipose tissue
(i.e. decrease lipogenesis). These actions are not
directly exerted on adipocytes, since fat cell mem-
branes have no receptors for hCG.32
3. hCG and mood. A stable mood and lack of attri-
tion characterized the hCG-treated group.
It is well known that VLCD's are associated with
mood changes, particularly attrition78 during the
dieting period. In one study, disinhibition and hun-
ger were significantly related to anxiety and de-
pression while restraint was not.44 Another study
concluded that elevated levels of anxiety persist in
female patients throughout a VLCD course of treat-
ment.45
Also many patients complain about fatigue during a
VLCD.4
Conversely, our data suggest that hCG-treated
volunteers rather improved their attitude towards their
environment, in the sense of an enhanced well-being,
less irritability and lack of fatigue. Since commercial
preparations of hCG contains 3-endorphin39 and this
neuropeptide has been demonstrated to affect the func-
tion of limbic-emotional circuits,21,58,5,28 we hypothe-
THE ORIGINAL INTERNIST
206 Spring 2006
sized that the p-endorphin fraction present in commer-
cial preparations of hCG might account for the activity
observed regarding mood control.
Additional studies remain to be performed to test the
validity of this hypothesis.
Conclusions
1. Female obese volunteers participating in a double
blind study, and submitted to the administration of
an oral presentation of hCG plus a VLCD,
decreased specific body circumferences and skin-
fold thickness from conspicuous body areas more
efficiently than Placebo+VLCD-treated subjects.
Since a significant fat proportion from total body fat is
subcutaneously located (50 to 65 percent, depending on
sex and fat distribution), this hCG metabolic activity
would result in a reduction of the total body fat mass,
the main cause for obesity. We suggested that the com-
bination of a VLCD and oral hCG could not only
trigger clinically significant changes in subcutaneous
fat stores but simultaneously decrease body weight and
modulate body contour.
2. hCG oral administration proved to be a safe and
effective procedure on obese treated volunteers. No
side effects were observed during the study. There
are no reports in the literature regarding this
administration route to compare our findings.
3. Compared to placebo treated subjects, volunteers
managed with an oral administration of hCG coped
more efficiently with daily irritating situations,
were in a better mood, and handled home conflicts
without stepping up family discussions.
This study appears to contradict former conclusions on
the issue of hCG and obesity. We attribute those differ-
ences to a different approach, including variables not
assessed in former publications.
Acknowledgements:
One of the authors of the report (Dr. Belluscio, Daniel)
was granted with a staying period at the Bellevue
Klinik, Zurich, Switzerland, to be trained on the
clinical management of the hCG method. He would
like to thank Dr. Trudy Vogt (Clinic Director) for her
generous contribution through this grant to part of the
ongoing Research Program performed at her Institu-
tion.
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009
05
References
1) Albrink MJ. Chorionic gonadotropin and obesity? Am J
Clin Nutr 1969 Jun;22(6):681-5
2) ASCHEIM S; ZONDEK B. Die Shwangerschafts Diag-
nose aus dem Harn durch nachweis der Hypophysovor-
derlappenhormone. Klin. Wochschr. 7:1401-1411. 1928
3) Asher WL. Harper HW. Effect of human chorionic go-
nadotrophin on weight loss. hunger. and feeling of well-
being. Am J Clin Nutr 1973 Feb;26(2):211-8
4) Astrup A.. VLCD compliance and lean body mass. Int J
Obes 1989;13 Suppl 2:27-31
5) Atkinson JH. et al., Plasma measures of beta-endorphin/
beta-lipotropin-like immunoreactivity in chronic pain
syndrome and psychiatric subjects. Psychiatry Res. 1983
Aug;9(4):319-27
6) Bagshawe KD. et al., Pregnancy beta1 glycoprotein and
chorionic gonadotrophin in the serum of patients with
trophoblastic and non-trophoblastic tumors. Eur J Can-
cer. 1978 Dec;14(12):1331-5
7) Balducci R. et al., Effect of hCG or hCG+ treatments in
young thalassemic patients with hypogonadotropic hy-
pogonadism. J Endocrinol Invest. 1990 Jan;13(1):1-7
8) Ballin JC. White PL. Fallacy and hazard. Human chori-
onic gonadotropin-500-calorie diet and weight reduc-
tion. JAMA 1974 Nov 4;230(5):693-4
9) Bastow MD. Anthropometrics revisited. Proc Nutr Soc
1982 Sep;41(3):381-8
10) Berry JN. Use of skinfold thickness for estimation of
body fat. Indian J Med Res 1974 Feb;62(2):233-9
11) Birken S. et al., Isolation and amino acid sequence of
COOH-terminal fragments from the beta subunit of hu-
man choriogonadotropin. J Biol Chem. 1977 Aug
10;252(15):5386-92
12) Birken S.. Chemistry of human choriogonadotropin.
Ann Endocrinol (Paris). 1984;45(4-5):297-305
13) Birmingham CL. et al., Human chorionic gonadotropin
is of no value in the management of obesity. Can Med
Assoc J. 1983 May 15;128(10):1156-7
14) Bonandrini L. et al., Chorionic gonadotropin (HCG) in
the therapy of chronic peripheral obliterating arteriopa-
thy (CPOA) of the lower extremities caused by arterio-
sclerosis. Minerva Chir. 1970 Mar 15;25(5):368-83
15) Borkan GA et. al., Comparison of ultrasound and skin-
fold measurements in assessment of subcutaneous and
total fatness. Am J Phys Anthropol 1982 Jul;58(3):307-
13
16) Borkan GA, Hults DE, Gerzof SG, Burrows BA, Rob-
bins AH. Relationships between computed tomography
tissue areas, thicknesses and total body composition.
Ann Hum Biol. 1983 Nov-Dec;10(6):537-45.
17) Bosch B. et al., Human chorionic gonadotrophin and
weight loss. A double-blind. placebo-controlled trial. S
Afr Med J 1990 Feb 17;77(4):185-9
18) Bousfield GR. et al., Structural features of mammalian
gonadotropins. Mol Cell Endocrinol. 1996 Dec 20;125
(1-2):3-19
19) Bozzola M. et al., Effect of human chorionic gonadotro-
pin on growth velocity and biological growth parame-
THE ORIGINAL INTERNIST DECEMBER 2009
ters in adolescents with thalassemia major. Eur J Pedi-
atr. 1989 Jan;148(4):300-3
20) Bradley P. Human chorionic gonadotrophin [letter].
Med J Aust Sep 25;2(13):510-1 1976
21) Brambilla F. et al., beta-Endorphin and beta-lipotropin
plasma levels in chronic schizophrenia. primary affec-
tive disorders and secondary affective disorders. Psy-
choneuroendocrinology. 1981 Dec;6(4):321-30
22) Bujanow W. Hormones in the treatment of psychoses.
Br Med J Nov 4;4(835):298 1972
23) Bujanow W.Letter: Is oxytocin an anti-schizophrenic
hormone? Can Psychiatr Assoc J. 1974 Jun;19(3):323.
24) Cairella M.. Drug therapy of obesity. Clin Ter. 1978
Mar 31;84(6):571-92
25) Canfield RE. et al., Studies of human chorionic gonad-
otropin. Recent Prog Horm Res. 1971;27:121-64
26) Cole LA. Immunoassay of human chorionic gonadotro-
pin. Its free subunit and metabolites. Clin Chem. 1997
Dec;43(12):2233-43
27) Emrich HM. Endorphins in psychiatry. Psychiatr Dev
1984 Summer;2(2):97-114
28) Ferrari C. Use of a testosterone-gonadotropin combina-
tion in the treatment of pathological syndromes in adult
males. Minerva Med. 1972 Jun 2;63(42):2399-408
29) Fiddes JC. et al., Structure. expression. and evolution of
the genes for the human glycoprotein hormones. Recent
Prog Horm Res. 1984;40:43-78
30) Fiddes JC. et al., The gene encoding the common alpha
subunit of the four human glycoprotein hormones. J Mol
Appl Genet. 1981;1(1):3-18
31) Fleigelman R. Metabolic effects of human chorionic
gonadotropin (HCG) in rats. Proc Soc Exp Biol Med
1970 Nov;135(2):317-9
32) Gailani S. et al., Human chorionic gonadotrophins
(hCG) in non-trophoblastic neoplasms. Assessment of
abnormalities of hCG and CEA in bronchogenic and
digestive neoplasms. Cancer. 1976 Oct;38(4):1684-6
33) Gallo RC. Bryant J. Antitumor effects of hCG in KS. Nat
Biotechnol Mar;16(3):218 1998
34) Giudice LC. et al., Glycoprotein hormones: some as-
pects of studies of secondary and tertiary structure.
Monograph. 1979 May 23
35) Greenway FL. et al., Human chorionic gonadotropin
(HCG) in the treatment of obesity: a critical assessment
of the Simeons method. West J Med 1977 Dec;127
(6):461-3
36) Grzonkowski S. Analysis of the results of the measure-
ments of adipose tissue in the human body based on the
study of skinfold thickness. Przegl Epidemiol 1989;43
(3):272-82
37) Gusman HA. Chorionic gonadotropin in obesity. Fur-
ther clinical observations. Am J Clin Nutr 1969 Jun;22
(6):686-95
38) Hashimoto TK. Chorionic gonadotropin preparation as
an analgesic. Arch Intern Med 1981 Feb;141(2):269
39) Hayes PA. Sub-cutaneous fat thickness measured by
magnetic resonance imaging, ultrasound , and calipers.
Med Sci Sports Exerc 1988 Jun;20(3):303-9
(Continued on next page)
207
40) Weiss LW, Clark FC. Three protocols for measuring
subcutaneous fat thickness on the upper extremities. Eur
J Appl Physiol. 1987;56(2):217-21.
PMID: 3552659; UI: 87190331
41) Heitmann BL et al., Evaluation of body fat estimated
from body mass index, skinfolds and impedance. A com-
parative study. Eur J Clin Nutr 1990 Nov;44(11):831-7
42) Hermans P. Clumeck N. Picard O. et. al., AIDS-related
Kaposi's sarcoma patients with visceral manifestations.
Response to human chorionic gonadotropin prepara-
tions. J Hum Virol Jan-Feb;1(2):82-9. 1998
43) LaPorte DJ. Predicting attrition and adherence to a very
low calorie diet: a prospective investigation of the eat-
ing inventory. Int J Obes 1990 Mar;14(3):197-206
44) LaPorte DJ. Treatment response in obese binge eaters:
preliminary results using a very low calorie diet (VLCD)
and behavior therapy. Addict Behav 1992;17(3):247-57
45) Leshem Y. et al., Gonadotropin promotion of adventi-
tious root production on cuttings of Begonia semper-
florens and Vitis vinifera. Plant Physiol. 1968 Mar;43
(3):313-7
46) Lustbader JW. et al., Structural and molecular studies of
human chorionic gonadotropin and its receptor. Recent
Prog Horm Res. 1998;53:395-424
47) Malkin A. The presence of glycosilated, biologically
active chorionic gonadotropin in human liver. Clin Bio-
chem 1985 Apr;18(2):75-7
48) Maruo T. et al., Production of Choriogonadotropin-like
factor by a microorganism. Proc Natl Acad Sci U S A.
1979 Dec;76(12):6622-6
49) McGarvey ME. Tulpule A. et. al., Emerging treatments
for epidemic (AIDS-related) Kaposi's sarcoma. Curr
Opin Oncol Sep;10(5):413-21 1998
50) Miller R. et al., A clinical study of the use of human
chorionic gonadotrophin in weight reduction. J Fam
Pract. 1977 Mar;4(3):445-8
51) Morgan FJ. et al., Chemistry of human chorionic gonad-
otropin. Monograph. 1976 May 25
52) Mueller WH. Relative reliability of circumferences and
skinfolds as measures of body fat distribution. Am J
Phys Anthropol 1987 Apr;72(4):437-9
53) Niebroj TK. et al., Effect of chorionic gonadotropins
administration on water metabolism in glaucomatous
women. Endokrynol Pol. 1971 May-Jun;22(3):251-5
54) Orphanidou C. Accuracy of subcutaneous fat measure-
ment: comparison of skinfold calipers. ultrasound, and
computed tomography. J Am Diet Assoc 1994 Aug;94
(8):855-8
55) Orphanidou CI, McCargar LJ, Birmingham CL, Belz-
berg AS. Changes in body composition and fat distribu-
tion after short-term weight gain in patients with ano-
rexia nervosa. Am J Clin Nutr. 1997 Apr ; 65 (4) :1034-
41
56) Perniola R. et al., Human chorionic gonadotrophin ther-
apy in hypogonadal thalassaemic patients with os-
teopenia: increase in bone mineral density. J Pediatr
Endocrinol Metab. 1998;11 Suppl 3:995-6
57) Pickar D et al., Clinical studies of the endogenous opioid
system. Biol Psychiatry 1982 Nov;17(11):1243-76
THE ORIGINAL INTERNIST
208 Spring 2006
58) Pierce JG.. Eli Lilly lecture. The subunits of pituitary
thyrotropin--their relationship to other glycoproteic
hormones. Endocrinology. 1971 Dec;89(6):1331-44
59) Rabe T. et al., Risk-benefit analysis of a hCG-500 kcal
reducing diet (cura romana) in females. Geburtshilfe
Frauenheilkd. 1987 May;47(5):297-307
60) Reiss M.. Stunted growth and the mechanism of its
stimulation in mentally disturbed adolescents. Int J Neu-
ropsychiatry. 1965 Aug;1(4):313-7
61) Rivlin RS.. Therapy of obesity with hormones. N Engl J
Med. 1975 Jan 2;292(1):26-9
62) Ross GT.. Clinical relevance of research on the struc-
ture of human chorionic gonadotropin. Am J Obstet
Gynecol. 1977 Dec 1;129(7):795-808
63) Sanders S, Norman AP. Chorionic gonadotrophin in
male growth-retarded adolescent asthmatic patients.
Practitioner. 1973 May;210(259):690-2.
64) Sarma JM. Houghten RA. Enzyme linked immunosor-
bent assay (ELISA) for beta-endorphin and its antibod-
ies. Life Sci 1983;33 Suppl 1:129-32
65) Sarria A et al., Skinfold thickness measurements are
better predictors of body fat percentage than body mass
index in male Spanish children and adolescents. Eur J
Clin Nutr 1998 Aug;52(8):573-6
66) Scaffidi A. Data on the pathogenesis and therapy of
bronchial asthma in patients with secondary hypo-
gonadism. Minerva Med Dec 1;65(86):4473-6 1974
67) Segal SJ (ed.). Chorionic Gonadotropin. Plenum Press:
NY. 1980
68) Shetty KR. et al., Human chorionic gonadotropin
(HCG) treatment of obesity. Arch Intern Med. 1977
Feb;137(2):151-5
69) Shomer-Ilan A. et al., Further evidence for the presence
of an endogenous gonadotrophin-like plant factor:
"phytotrophin."Isolation and mechanism of action of the
active principle. Aust J Biol Sci. 1973 Feb;26(1):105-12
70) Simeons ATW. The action of chorionic gonadotropin in
the obese. Lancet II:1954: 946-947
71) Simeons ATW.. Pounds and Inches: A new approach to
obesity. Private Printing (1976)
72) Stein MR. et al., Ineffectiveness of human chorionic go-
nadotropin in weight reduction: a double-blind study.
Am J Clin Nutr. 1976 Sep;29(9):940-8
73) Stern JS. Weight control programs. Curr Concepts Nutr.
1977;5:137-55
74) Suginami H. et al., Immunohistochemical localization of
a human chorionic gonadotropin-like substance in the
human pituitary gland. J Clin Endocrinol Metab. 1982
Dec;55(6):1161-6
75) Tagliabue A et al., Application of bioelectric impedance
measurement in the evaluation of body fat. Recenti Prog
Med 1989 Feb;80(2):59-62
76) Talbot LA et al., Assessing body composition: the skin-
fold method. AAOHN J 1995 Dec;43(12):605-13
77) Tavio M. Nasti G. Simonelli C. et. al., Human chorionic
gonadotropin in the treatment of HIV-related Kaposi's
sarcoma. Eur J Cancer Sep;34(10):1634-7 1998
78) Torgerson JS et al., VLCD plus dietary and behavioral
support versus support alone in the treatment of severe
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009
05
 obesity. A randomised two-year clinical trial. Int J Obes
Relat Metab Disord 1997 Nov;21(11):987-94
79) Vaitukaitis JL. Glycoprotein hormones and their sub-
units--immunological and biological characterization.
Monograph. 1979 May 23
80) Veilleux H. et al., Gonadic and extragonadic effects in
humans of 3.500 I.U. of HCG (human chorionic gonad-
otropin) in fractional doses. Vie Med Can
b) Vogt T, Belluscio D. Controversies in plastic surgery:
suction-assisted lipectomy (SAL) and the hCG (human
chorionic gonadotropin) protocol for obesity treatment.
Aesthetic Plast Surg. 1987;11(3):131-56. Review.
81) Wattanapenpaiboon N. et al., Agreement of skinfold
measurement and bioelectrical impedance analysis
(BIA) methods with dual energy X-ray absorptiometry
(DEXA) in estimating total body fat in Anglo-Celtic Aus-
tralians. Int J Obes Relat Metab Disord. 1998 Sep;22
(9):854-60
82) Weits T. et al., Comparison of ultrasound and skinfold
caliper measurement of subcutaneous fat tissue. Int J
Obes 1986;10(3):161-8
83) Yanagihara Y. Carbohydrate and lipid metabolism in
pregnant albino rats during hunger after loading with
gonad-stimulating hormones. Nippon Sanka Fujinka
Gakkai Zasshi 1966 Nov;18(11):1293-301
THE ORIGINAL INTERNIST DECEMBER 2009
84) Yanagihara Y. Carbohydrate and fatty acid metabolism
in pregnant albino rats simultaneously loaded with fat
emulsion and sex stimulating hormones during starva-
tion. Nippon Sanka Fujinka Gakkai Zasshi 1967 Jan;19
(1):8-14
85) Yanagihara Y. Carbohydrate and lipid metabolism in
pregnant albino rats during starvation after loading
with gonad-stimulating hormones. Nippon Sanka Fu-
jinka Gakkai Zasshi 1966 Dec;18(12):1379-84
86) Yoshimoto Y. et al.. Human chorionic gonadotropin--
like material: presence in normal human tissues. Am J
Obstet Gynecol. 1979 Aug 1;134(7):729-33
87) Yoshimoto Y. et al.. Human chorionic gonadotropin-like
substance in nonendocrine tissues of normal subjects.
Science. 1977 Aug 5;197(4303):575-7
88) Young RL. et al., Chorionic gonadotropin in weight
control. A double-blind crossover study. JAMA. 1976
Nov 29;236(22):2495-7
89) Zakut H. et al.. hCG as tumor marker in non-
trophoblastic neoplasms. Harefuah. 1985 Jan 15;108
(2):82-5
90) Zondek B. Sulman F. The mechanism of action and me-
tabolism of gonadotrophic hormones in the organism.
Vit Horm 1945 3:297-336 ‹
(Continued on next page)
209
 More photos are available at
http://hcgobesity.org/hcg_obesity_photographs.htm

THE ORIGINAL INTERNIST

210 Spring 2006 THE ORIGINAL INTERNIST DECEMBER 2009
05

BLOOD
TRANSFUSIONS
ARE VERY
DANGEROUS
by: Dr. James A. Howenstine
Excessive use of blood transfusions is a major cause of
death that has generally been overlooked. Conservative
study of blood transfusions estimates that at least 25%
are unnecessary. Ten percent of all patients entering
hospitals are given blood transfusions. Blood transfu-
sions are frequently given for anemia but their use may
cause greater problems than benefits.
Why Are Blood Transfusions Dangerous?
In the United States there are about 500,000 heart bypass
operations performed each year. Researchers at the
University of Michigan studied 9218 persons aged 65 or
older who had coronary bypass surgery. They learned
that patients who had received blood transfusions were
five times more likely to die2 within 100 days of the
surgery than patients who were not transfused. More
than 66% of the men having this operation and 88% of
the women having this operation receive a blood transfu-
sion. Women had a 9% death rate within 100 days of this
operation but only 6% of men die in the same time
interval. The primary cause for death in these bypass
patients is infection at a site unrelated to the operative
procedure.
The odds on developing an infection were three times
higher in bypass patients who had received a blood
transfusion when compared to patients who were not
transfused during the surgery. The more units of blood
transfused the greater the risk of infection. If transfu-
sions are dangerous it is easy to understand why more
women die than men because their smaller blood volume
causes them to receive proportionally more blood.
THE ORIGINAL INTERNIST DECEMBER 2009
Coronary artery bypass operations are a huge stress for
an elderly person. This major operation produces
profound immuno-suppression in the body. This means
that the body will not be able to do a good job fighting
off infections and the spread of cancer cells for several
months after this surgery.
Of even greater importance are the adverse effects of
transfusion itself. What are these transfusions doing to
the human body? Some undesirable effects of transfu-
sion include:
• The infections seen are not at the operative site but
are randomly scattered throughout the body suggest-
ing the immune system is not capable of preventing
serious infections. Something has injured the
immune system.
• Blood transfusions are placing an enormous burden
on the immune system in patients getting this
surgery.
• Every individual’s blood is unique. Each person’s
blood contains dozens of antigens capable of
producing adverse responses in the blood recipient
[(inhaled antigens, poorly digested proteins that
were able to be absorbed into the blood stream, tu-
mor antigens, and antibodies directed against parts
of the body perceived as foreign (auto antibodies to
islet cells, bronchial epithelium, synovial mem-
branes etc.)] Blood may also contain residue from
cigarette smoke, pesticides, herbicides, inhalant
cleaning substances, chemicals etc.
• We are all constantly fighting off infections.
Donated blood may also contain viral, bacterial,
spirochetal, parasitic and fungal organisms the donor
was battling. It is estimated that one in every six
persons3 in the world is currently infected with
Borrelia Burgdorfi spirochetes (Lyme Disease). This
means the person whose blood is given may have
pathogens in this blood capable of causing colds,
gingivitis, sinusitis or even a serious infection
(Lyme Disease, Chaga’s Disease) in the recipient.
All blood can and does transmit infectious agents
(viral, bacterial, fungal, parasitic, mycoplaasma,
spirochetal) present in donated blood. Given to a
healthy person this would usually not cause a fatal
problem but given to an immuno-suppressed patient
trying to recuperate from a major operation it may
become the proverbial straw that broke the camel’s
back.
• The most important pathogen in blood is probably
Borellia Burgdorfi (Bb) which causes Lyme Disease.
(Continued on next page)
211
 Borrelia is not tested for in transfused blood. It is
easy to understand how a patient seriously ill after
bypass surgery could be overwhelmed by the onset
of Lyme Disease postoperatively. Lyme Disease is
rampant because it is easily spread person to person.
Most patients with Lyme Disease have a silent
infection that does not become evident until some
serious incident damages their immune system
(major surgery, accident, infection, immune injury
from alcohol, drugs, insomnia, stress etc). This
means there are millions of persons walking around
whose blood would be dangerous to receive because
they look healthy but have blood containing Bb
spirochetes. Lyme disease is now impossible to be
accurately diagnosed because the two best tests for
the disease are no longer available (blood culture
Dr. Lyda Mattman, QIRBb Dr. JoAnne Whitaker).
These tests were fool proof because growing spiro-
chetes out of the blood or visualizing pieces of spiro-
chetes in blood samples constitutes undeniable proof
of diagnosis. Remember one in 6 persons has the Bb
spirochetes in their blood so if you receive six units
of blood you are probably getting Bb spirochetes.
We will never know how many postoperative deaths
in transfused patients are being caused by undiag-
nosed Lyme Disease because there are no longer
reliable tests available to diagnose this disease.
Chaga’s Disease (parasitic illness) from Latin
American citizens damages the heart and is certainly
being infused into unfortunate persons getting blood
transfusions. Neither Chaga’s Disease or Lyme
Disease is likely to be considered in the postopera-
tive period.
• Diagnosable transfusion reactions (chills, fever, skin
rash) occur in one out of every 100 transfused
persons.
A major operation like bypass surgery causes a
profound immuno-suppressive reaction. This damages
the body’s ability to kill bacteria and cancer cells for
several months. The immuno-suppressive state follow-
ing colon cancer surgery can be blocked by the use of
the drug Tagamet taken before or started shortly after
the colon operation. Patients treated with Tagamet for
one year have a significantly higher survival rate4 than
controls not receiving Tagamet.
What Are The Results Of Blood Transfusions In
Other Health Conditions?
Cancer Therapy
Chemotherapy and radiation suppress bone marrow
production of red blood cells. The resulting anemia is
THE ORIGINAL INTERNIST
212 Spring 2006
often treated with blood transfusions. These transfusions
in cancer patients come with a price.
In Holland, a study of colon cancer patients revealed that
only 48% of cases transfused were alive at 5 years
compared to 74% in non transfused patients. The results
for head and neck cancers are even worse.
Cancer of the larynx had only 14% survivors at 5 years
in transfused patients and 65% in non-transfused
patients. In cancers of the oral cavity the cancer
recurrence rate was 31% without transfusions and 71%
with transfusions.
A lung cancer study from Europe confirmed adverse
results5 with transfusions. Thirty day mortality rose from
2.4 percent for patients not transfused to 10.9 percent for
those getting 2 or less transfusions and to 21.9 percent in
patients receiving more than 2 units of blood. Other
studies in patients with colon cancer have confirmed the
more blood transfused6 the worse the results.
Hip Replacement Surgery
Patients undergoing hip replacement, who had received
transfusions, had a 35% greater risk of a serious bacterial
infection and a 52% greater risk7 of developing pneumo-
nia. Surgeons and other physicians often do not hesitate
to order blood transfusions because they do not realize
the real danger of transfusion.
These undesirable results are not limited to cancer
patients and patients having hip replacement. All
transfusions are dangerous. The risk of serious infections
goes along with transfusion therapy in general.
Can The Number Of Blood Transfusions Be Safely
Reduced?
Coronary artery bypass surgery is one of the principal
users of blood transfusions. There is an unrecognized
serious mortality from coronary artery bypass surgery
when patients are followed 100 days for the full morbid-
ity of blood transfusion damage to the immune system to
become manifest (9% deaths in women and 6% deaths in
men above age 65).
In addition between 1.5% and 5.2% of patients have a
stroke8 under anesthesia during coronary bypass surgery.
Other patients experience loss of memory and difficulty
focusing attention following coronary bypass surgery.
These problems are probably due to brain cell injury and
death from small emboli to the brain and reperfusion
acidosis following the surgery. Reintroduction of blood
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009
05
into the cerebral circulation after the bypass is completed
causes the rapid appearance of oxygen-deprived blood
containing free radicals which can damage the fat
containing brain cells. The propolis from honey can
protect9 the brain from this type injury by virtue of its
strong antioxidant effects, but this is probably only
rarely used in the United States where hospitals rely on
drugs.
A large population study disclosed that angioplasty
(forcible opening of narrowed heart arteries with a bal-
loon) performed 3 to 28 days after a heart attack failed to
prevent death,10 new heart attacks and heart failure.
Furthermore, in a four year follow-up of these patients
there were more new heart attacks in the patients who
received angioplasties than the group treated conserva-
tively without angioplasties.
Coronary bypass surgery has long had prominent
detractors but has steadily grown in use until it has
become a huge industry in the USA. In 1977, the first
extensive evaluation of cardiac surgery for arteriosclero-
sis was done. This evaluation of 596 patients treated
with bypass surgery or drug therapy revealed that
surgery was no better than drug therapy. Eugene
Braunwald,11 highly respected Chief of Cardiology at
Harvard Medical School, commented 30 years ago that,
“an industry is being built around this operation. It is
developing a momentum of its own, and as time passes it
will be progressively more difficult and costly to curtail
it.” In 1984, another large study involving 780 patients,
again disclosed no advantage for surgery over drug
therapy.
Natural therapies are far more effective than drugs
which are unable to reverse arteriosclerosis. Knowledge
of their existence has been systematically suppressed by
the power of the pharmaceutical industry which controls
what is published in conventional medical journals and
by the news media which conveniently ignores health
breakthroughs that would hurt the earnings of pharma-
ceutical companies. Nobel Prize winner Dr. Linus
Pauling proposed an effective new therapeutic program
using lysine and Vitamin C that reverses arteriosclerosis
in 6 to 8 weeks which remains largely unknown to U.S.
citizens.
Coronary artery repair by angioplasty, stent placement,
and coronary artery bypass are procedures that have
become routine in the United States. The reason that
surgery fails to improve the long-term results may be
that surgery is treating the symptoms of arteriosclerosis
(chest pain, heart attack), but not really reversing the
causes for arteriosclerosis.
THE ORIGINAL INTERNIST DECEMBER 2009
Alternative health therapies (eliminating toxic metals
from endothelium with long term oral chelation,
treating endothelial infections with tumeric, high doses
of vitamin C and lysine{Linus Pauling}, N-acetyl cys-
teine, L-arginine, lowering homocysteine values with
pyridoxine, folic acid, B12 and trimethylglycine,
curtailing sugar intake, Vitamin K2 [removes calcium
from arterial plaque and places calcium in bone] and
use of Mediterranean diet) would promptly heal
patients with arteriosclerosis. Excessive sugar intake12
is now regarded as the number one risk factor for heart
attacks in women and the number 2 risk factor in men.
Often the sales pitch that encourages patients to have
bypass surgery, angioplasties and stent placement is
based on fear (You are a walking time bomb. You
could drop dead any moment!!!). All decisions based
on fear are emotional rather than a rational considera-
tion of scientific truth. Frightened patients readily
accept dangerous surgical therapies particularly when
they are unaware there is an alternative.
A major factor preventing the switch by the public to
safer alternative health regimens is the fact that drugs
and surgery are covered by health plans and alternative
therapies are not. Linus Pauling’s high doses of vitamin
C and lysine can rapidly reverse anginal pain, hyperten-
sion and claudication. Dr. Julian Whitaker has seen
many patients with severe angina, positive treadmills
and dire warnings about impending death without
bypass surgery become asymptomatic and so far
removed from arteriosclerosis they are able to partici-
pate in marathon races and other stressful activities,
after embarking on a rational program to eliminate
arteriosclerosis. Dr. Garry Gordon often relates that he
has never seen a stroke or heart attack in 30 years in
those patients taking his long term oral chelation com-
bined with anticoagulation using the safe natural anti-
clotting substance (carrageenan {red algae} found in
Natural Cellular Defense).
Any therapy based on mechanical repair of narrowed
arteries is doomed to failure because it fails to deal
with the root cause for arteriosclerosis which is a
degenerative metabolic disorder caused by toxic
metals, infections, vitamin C and K2 deficiency, excess
sugar, dietary transfats, gingivitis and dangerous levels
of homocysteine.
Harvard cardiologist Dr. Thomas Graboys believes that
90% of the 740,000 coronary bypass operations and
600,000 angioplasties performed annually in the US
are unnecessary. There would be significant declines in
the death rate13 from cardiovascular disease if all by-
(Continued on next page)
213
pass, angioplasties and stents were replaced with effec-
tive natural therapies for arteriosclerosis.
If the general public became informed of the hazards of
coronary artery surgery and switched to natural options
for arteriosclerotic heart disease much less blood would
be used and many lives would be saved. This is not
likely to occur because this knowledge is not being
transmitted to the public by media that serve the pharma-
ceutical industry.
Important Information About Lyme Disease
(Borrelia Burgdorfi Infection)
Lyme Disease was originally regarded as an uncommon
illness caused by the spirochete Borrelia Burgdorfi Bb.
The disease transmission was thought to be solely by the
bite from a tick infected with this parasite. The Bb
spirochete is able to burrow into tendons, muscle cells,
ligaments and directly into organs. A classic bulls-eye
rash is often visible in the early stages of the illness.
Later in the illness the disease can affect the heart, nerv-
ous system, joints and other organs. It is now realized
that the disease can mimic amyotrophic lateral sclerosis,
Parkinson’s Disease, Bell’s palsy, reflex sympathetic
dystrophy, neuritis, all psychiatric illnesses including
schizophrenia, chronic fatigue, heart failure, angina,
irregular heart rhythms, fibromyalgia, dermatitis, auto-
immune diseases such as sclera-derma and lupus, eye
inflammatory reactions, sudden deafness, SIDS, ADD
and hyperactivity, chronic pain and many other con-
ditions.
Biology professor, Lida Mattman, author of Cell Wall
Deficient Forms: Stealth Pathogens, has been able to
recover live spirochetes of Bb from mosquitoes, fleas,
mites, semen, urine, blood and spinal fluid. A factor
contributing to making Bb so dangerous is that it can
survive and spread without having a cell wall (cell wall-
deficient (CWD). Many valuable antibiotics kill bacteria
by breaking down the cell wall. These antibiotics often
prove ineffective against Bb.
Lyme Disease is now thought to be the fastest growing
infectious disease in the world. Even with a current lack
of good diagnostic tests, at least 200,000 new cases are
diagnosed each year in the U.S. and some experts think
as many as one in every 15 Americans is currently
infected (20 million persons). Dr. Ralph Rowen knows a
family where the mother’s infection spread to 5 of her 6
children14 all of whom recovered with appropriate
therapy. It is difficult to believe that these children were
all bitten by ticks and seems more plausible that person
to person spread within the family caused this problem.
THE ORIGINAL INTERNIST
214 Spring 2006
Bacteriologist Lida Mattman states “I’m convinced
Lyme Disease is transmissible from person to person.”
In 1995 Dr. Mattman obtained positive cultures for Bb
from 43 of 47 persons with chronic illness. Only 1 of 23
control patients had a positive Bb culture. Dr. Mattman
has subsequently recovered Bb spirochetes from 8 out of
8 cases of Parkinson’s Disease, 41 cases of multiple
sclerosis, 21 cases of amyotrophic lateral sclerosis and
all tested cases of Alzheimer’s Disease. The complete
recovery of several persons with terminal amyotrophic
lateral sclerosis after appropriate therapy shows the great
importance of establishing the diagnosis of Lyme
Disease.
Some very important information has recently become
available about the spread and magnitude of the problem
with Lyme Disease. The severity of the disease is related
to the spirochete load in the patient. Few spirochetes
produce mild or asymptomatic infection. A study from
Switzerland in 1998 pointed out that only 12.5% of
patients testing positive for Bb had developed symptoms.
A German boy developed Lyme arthritis 5 years after
his tick bite.
Often, mycoplasma infections remain without symptoms
until the victim suffers a traumatic event (stress, injury,
accident, major surgery etc.) These stressing events
enable the mycoplasma to begin consumption of choles-
terol in the neural sheath, and symptoms (ALS) may
begin to present as these nerve cells die. The mechanism
of this deterioration is thought to be suppression of the
immune system secondary to stress. Lyme Disease may
have a similar delayed presentation as many persons
experience the onset of Lyme symptoms after stressful
events.
Dr. Jo Anne Whitaker relates that nearly every patient
with Parkinson’s Disease (PD) has tested positive for
Bb. Dr. Louis Romero reports that 3 patients with
Parkinson’s disease are 99% better after TAO-free cat’s
claw (Uncaria tomentosa) therapy.
When Dr. Mattman cultured 25 patients with fibromyal-
gia all subjects had positive cultures for the CWD Bb
which causes Lyme Disease. She relates that Bb can be
found in tears and could thus easily appear on the hands
where touching could spread Lyme Disease. Several
families are now documented where nearly every family
member is infected. How sick the individual patient
becomes relates to their initial spirochete dose, immune
system status, detoxification capability and stress level.
Transmission of the disease has been clearly doc-
umented after bites by fleas, mites, mosquitoes and ticks.
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009
05
There is compelling evidence that Lyme Disease (LD)
can be spread by sexual and congenital transfer. One
physician has cared for 5000 children with LD. 240 of
these children were born with the disease. Dr. Charles
Ray Jones, the leading pediatric specialist on Lyme
Disease, has found 12 breast fed children who have
developed Lyme Disease. Miscarriage, premature birth,
stillborn, birth defects and transplacental infection of the
fetus have all been reported. Studies at the Univ. of
Vienna have found Bb in urine and breast milk of LD
mothers.
Researchers at the Univ. of Wisconsin have reported that
dairy cattle can be infected with Bb, hence milk could be
contaminated. Bb can also be transmitted to lab animals
by oral intake such as food.
The Sacramento, California blood bank thinks that LD
can be spread by blood transfusions. The CDC (Center
for Disease Control) in Atlanta, Georgia states that their
data indicates that Bb can survive blood processing
techniques used for transfusions in the U.S.
Lyme Disease is the fastest growing epidemic in the
world. LD is grossly underreported so there are far more
than the 200,000 cases reported annually in the U.S.
Lyme Disease is thought to be a contributing factor in
50% of patients who have chronic disease.
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THE ORIGINAL INTERNIST DECEMBER 2009
Dr. Jo Anne Whitaker, a Lyme disease victim from
childhood, has developed a reliable test for the presence
of Lyme Disease. This test looks for the Bb organism,
not antibodies, and is able to identify pieces of the cell
wall deficient (CWD) form of the spirochete as well as
the actual Bb organism. Her test is called Q-RiBb which
stands for quantitative rapid identification of Bb. Dr.
Lida Mattman has confirmed that Dr. Whitaker’s test is
sensitive and accurate because there has been a 100%
correlation between a positive blood culture of Bb by
Dr. Mattman’s lab and a positive Q-RiBb test from Dr.
Whitaker’s laboratory.
Because 87.5% of patients incubating Lyme Disease
may not have symptoms, there is a huge pool of poten-
tial blood donors who present serious danger to any
patient who will need blood transfusions for an elective
surgical procedure. Therefore potential surgical patients
need to be certain that the risks of surgery and transfu-
sion warrant proceeding with the operation.
How To Protect Yourself From The Danger Of
Transfusions
Elective surgery often provides sufficient time to place
your own blood in reserve for your surgery. In the
Michigan study those who banked their own blood and
those who avoided transfusions had the lowest rates of
infection and the lowest risk of dying after bypass
surgery.
New surgical techniques save blood. Lost blood can be
saved, cleaned and recycled back to the patient during
the surgery. Lasers and cryotherapy can instantly stop
blood loss in the operating room. Drops of blood instead
of vials can be used to perform lab tests. Microsurgical
techniques minimize tissue trauma and blood loss. Hy-
perbaric oxygen chambers, drugs such as erythropoietin,
vitamins, iron, and hormones can be utilized to increase
red blood cell production before surgery.
It is estimated that 75,000 surgeons have been trained to
perform bloodless surgery in the USA. Many hospitals
have become equipped to perform this type surgery.
Check to learn if your local hospitals can provide this
care.
Continue to donate blood as properly used transfusions
can be life saving. Healthy individuals are allowed to
donate as often as every 8 weeks.
The danger of blood transfusions is real and not widely
appreciated by the general public and the medical
profession. Try to be certain that the risks of transfusion
(Continued on next page)
215
are exceeded by the benefits before accepting blood
transfusions.
Dr. James A. Howenstine is a board certified specialist
in internal medicine who spent 34 years taking care of
hospital and office patients. For more information visit
www.mynaturalhealthteam.com and by phoning 1-800-
416-2806. Dr. Howenstine can be reached by email at
dr.jimhow@gmail.com and by writing Dr. James
Howenstine, C/O Remarsa USA SB 37, P.O. Box 25292,
Miami, FL 33102-5292
References
1) Williams, David G. Alternatives Feb 2007 Volume
11 No. 20 pg 153.
2) Am Heart J 06;252(6): 1028-1034 Archiv Intern
Med 06;166(4):437-443
3) Harvey, W.T.M.D., Salvato, Patricia M.D. The
History of Lyme Disease Focus Newsletter Allergy
Research Group Breakthrough in Lyme Disease Oct
2003 pg 5
4) The Lancet Dec 31,1994 pg 1768-1769 The Lancet
July 8, 1995 pg 115
5) Eur Respir J 06;Nov 1{Epub]
6) Dis Colon Rectum 06;49(8):1116-1130
7) Transfusion 99;39(7): 694-700
8) Selnes Oa et al. Coronary artery bypass surgery and
the brain New England Journal Of Medicine
2001Feb 8;44(6):451-2.
9) CellBiochem Funct 03;21(3):283-9.
10) Hochman Js et al Coronary intervention for persis-
tent occlusion after myocardial infarction N Engl j
Me 2006 Dec 7;355;2395-2407.
11) Braunwald E. Coronary-artery surgery at the cross-
roads New England Journal Of Medicine 1977;297:
(12) 661-3.
12) Grant WB Reassessing the role of sugar in the etol-
ogy of heart disease. J Orthomolecular Med 1998;13
(2): 95-104
13) Whitaker, Julian Coronary Artery Disease Back to
Basics Health & Healing Feb 2007 Vol 12. No.2 pg
1-3.
14) Rowen, Robert If you have ANY chronic debilitat-
ing disease, you could be the victim of a Monste
Epidemic! Second Opinion Vol X111 No. 11 Nov
2003 ‹

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THE ORIGINAL INTERNIST

216 Spring 2006 THE ORIGINAL INTERNIST DECEMBER 2009
05
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Clinical Relevance
of Neurotransmitter
Testing
by: Dr Scott Theirl
Submitted by: NeuroScience, Inc.
There are many differing professional opinions on the
subject of urinary neurotransmitter testing and the
subsequent use of amino acid supplements to help
optimize neurotransmitter stores in the body. I believe
these varied opinions are simply due to the newness of
the testing protocols and the debate will drive further
research and development much more quickly. This
push for research and development will ultimately
benefit patients, but in the meantime, practitioners are
left to decide which side of the debate they choose to
be on. This can be both confusing and frustrating as
science continues to sort out the most efficient ways of
helping our patients.
Basic facts concerning neurotransmitters
• Neurotransmitters are very important for overall
health and specifically for nervous system function.
• Urinary neurotransmitter measurement has existed
for decades.
• Amino acids are the building blocks of neurotrans-
mitters and some can cross the blood-brain barrier.
• Neurotransmitters are synthesized in many areas of
the body including the central nervous system, the
peripheral nervous system, the kidneys, the gas-
trointestinal tract, and the adrenal glands.
• Intact neurotransmitters are filtered by the kidneys
resulting in the ability to measure them in the urine.
• Adding specific amino acid supplements can alter
urinary neurotransmitter values.
• Adding specific amino acid supplements may
benefit patients by reducing neurologic symptoms.
Primary considerations regarding neurotransmitter
assessment
• Where are the neurotransmitters in the urine
coming from?
• Is there sufficient clinical correlation between
urinary neurotransmitter testing, patient symptoms,
and patient outcomes to support testing?
• Is there sufficient scientific correlation between
urinary neurotransmitter testing, patient symptoms
and patient outcomes to support testing?
THE ORIGINAL INTERNIST
218 Spring 2006
• What time of the day is it best to do the urine
collection?
• How do different supplements affect urinary
neurotransmitter values?
Urinary measurements reflect whole-body neuro-
transmitter production
Following are my own opinions regarding some of
these issues. I choose to start with the misconception
that urinary neurotransmitter testing examines brain
levels of neurotransmitters only. I have never
witnessed any reputable lab claim this. This claim only
comes from misguided clinicians and patients. Urinary
neurotransmitters are reflective of the entire physical
system. With the many sources of neurotransmitter
synthesis reviewed earlier, it is accepted that urinary
measurements are reflective of total body neurotrans-
mitter activity. Additionally, it has been observed that
urinary neurotransmitter measurements are correlated
with neurotransmitter activity in the central nervous
system.
Clinical observations regarding neurotransmitter
testing
Although there are studies supporting both sides of the
argument of clinical correlation, I have found time and
again, a strong clinical correlation between urinary
neurotransmitter levels and patient symptoms such as
depression, anxiety and insomnia. Urinary neurotrans-
mitter testing must be used in conjunction with a
detailed patient history and thorough physical examina-
tion at the time of testing. It is only upon alignment of
patient history, exam and laboratory testing that an
appropriate treatment plan can be recommended and
integrated. Urinary neurotransmitter values alone are
of limited significance. For example, if one wants to
define the value of urinary norepinephrine and epineph-
rine to peripheral output from the adrenal medulla
alone, this can still be of value to me as a clinician
demonstrating hyper versus hypo adrenal neurotrans-
mitter function. But these high/low values must be
considered in the context of the patient’s history of
stress (physical, emotional, and/or cognitive). Only
when all of the elements are used together can a clini-
cian make appropriate recommendations to their
patients. Science will continue to illuminate the
biochemical associations between urinary neurotrans-
mitter testing and central nervous system function, but
the clinical associations between urinary neurotransmit-
ter testing and patient’s symptoms are promising and of
benefit to many patients.
Scientific evidence supporting neurotransmitter
testing
Neurotransmitters have been measured in academic
settings for decades. The argument concerning whether
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009
05
or not neurotransmitters exist in the urinary pool is
irrefutable. Recent advances in clinical laboratory
technology now provide reliable, cost-effective, and
convenient methods for measuring neurotransmitters in
clinical settings. A brief review of scientific literature
yields a plethora of studies investigating urinary neuro-
transmitters as correlates of a wide variety of neuro-
logical and psychiatric disease states. A comprehensive
review of the literature is beyond the scope of this arti-
cle, however, those interested in more information
should contact NeuroScience, Inc. Visit
www.neuroscienceinc.com for a concise review of evi-
dence pertaining to the clinical relevance of urinary neu-
rotransmitter measurements.
Timing neurotransmitter collection
Neurotransmitter testing is not a “one-size-fits-all” treat-
ment protocol, rather it serves as a tool to assess a
patient’s individual biochemistry at that given moment
in time. So if you, as a clinician, desire to assess a
patient’s daytime symptoms such as fatigue, anxiety, or
attention difficulties, it is best to perform a morning
urine sample, but if your patient suffers from insomnia,
then a nighttime sample will be most helpful. As a clini-
cian I was always taught to examine, treat and then re-
examine in order to observe objective and subjective
changes, for better or worse. Consequently, I believe that
baseline neurotransmitter testing is helpful to clinicians
to understand where a patient was prior to intervention
and where they are headed after follow-up neurotrans-
mitter testing is performed. It is difficult to comprehend
where a treatment plan is going if you do not know
where you have come from. This is the value of a
detailed patient history and objective laboratory
measurements at the beginning of any new therapeutic
protocol.
Amino acids influence neurotransmitter synthesis
and excretion patterns
Amino acids, the precursors to neurotransmitters,
circulate both peripherally and centrally. Both the central
and peripheral nervous systems produce neurotransmit-
ters from the same common amino acids. Consequently,
supplementation with specific amino acids has the
ability to improve central and peripheral nervous system
neurotransmitter stores and support other neurotransmit-
ter synthesis sites including the intestine and adrenal
glands. I believe urinary neurotransmitter testing is the
best objective measurement we as clinicians currently
have available to guide amino acid supplementation
protocols.
Case Study
The following case is an example of both the power of
neurotransmitter/hormone biomarker testing as well as
the benefit of using specific amino acids to best support
your patients’ neurochemical balance.
THE ORIGINAL INTERNIST DECEMBER 2009
The patient was a 41 year old male, married, father of
two and self-employed. He presented to me with anxi-
ety, fatigue and various physical pain complaints. He
reported the anxiety began one year previously, initiated
by a panic attack that involved elevated heart rate,
elevated respiration, sweating and clammy skin. These
symptoms were severe enough to require hospitalization
five times in the past year for similar panic attacks. He
also stated that during these episodes, he was clear
headed and did not feel anxious, but his body was
clearly in “panic mode”. He detailed his energy levels as
“feeling good only a few hours per day” and then feeling
so fatigued that he wanted nothing more than to sleep.
He reported that his peak energy of the day was between
9pm and midnight. He has a history of chronic asthma,
chronic sinusitis with year-round allergies and three
nasal polyp surgeries in the last nine years. He also
reported irritable bowel syndrome and insomnia, and
explained that falling asleep was easy but he would
wake 3-4 times per night. He stated that it was currently
difficult to lose weight even if he ate less and dairy-free.
He had a full cardiac work-up, upper and lower GI scope
and a thyroid work-up which he reported were all nega-
tive. His medications included Advair, Allegra D,
Xanax, Paxil and Bisoprolol. He also commented that
he had taken prolonged antibiotics and nasal steroids
seasonally for years secondary to his sinusitis, but was
not currently on either type of medication. His NeuroEn-
docrine Panel results are on the next page.
These reports can be viewed from three angles:
androgen hormones, adrenal hormones and neurotrans-
mitters: excitatory/inhibitory. Each of these three areas
have the opportunity to present as optimal, low or
elevated. This information provides insight into a pa-
tient’s metabolic state. Is this patient experiencing acute
or chronic stress responses as evidenced by their bio-
markers? Is it best to support this patient’s androgen
hormones, adrenal hormones (DHEA and cortisol),
adrenal neurotransmitters (epinephrine and norepineph-
rine), or additional neurotransmitters (excitatory, Inhibi-
tory, or both)? Patients, such as with this example, who
have experienced anxiety/panic attacks, fatigue, pain
syndromes and insomnia can present with many differ-
ent biomarker combinations depending on their individ-
ual severity of metabolic fatigue. This clearly illustrates
why it is so beneficial to practitioner and patient alike
to perform an initial test.
With this patient I thought it best to support his DHEA
(15mg with breakfast), cortisol (Isocort-2 pellets with
breakfast), serotonin/GABA (Travacor 2 capsules at
bedtime), adrenal neurotransmitter support (Adrecor-
work up to 2 capsules BID prior to breakfast and lunch).
I also recommended 2-3 grams Omega-3 fish oils/day
and 100 billion multistrain probiotics/day.
(Continued on next page)
219
This patient followed up with me approximately seven
weeks later and reported his anxiety improved with some
“good days” that did not require any Xanax, improved
daytime energy that was “on and off day by day,” and
still present but improved overall physical pain. He also
reported his efforts to lose weight were beginning to pay
off. Of additional clinical interest, is that these sympto-
matic improvements happened at the same time as an
additional three rounds of antibiotics that were
prescribed for possible cellulitis.
I modified his supplement routine and added GABA
support (Kavinace-maximum 6 per day) as needed to
support anxious symptoms and further support healthy
sleep patterns. I also recommended catecholamine sup-
port for daytime energy (ExcitaPlus 1 capsule BID prior
to breakfast and lunch to be taken with his Adrecor). I
moved cautiously on his excitatory support due to his
history of anxiety.
During a telephone follow-up three weeks later, he
reported continued improved anxiety levels with no need
for medication in over a week and improved sleep
patterns, but he had experienced increased daytime
fatigue following an additional sinus polyp surgery six
days prior to the conversation. Follow up testing was
recommended in the near future and he was pleased with
his progress to date, as am I. This was a very positive
clinical response considering his additional medical
complications.
Summary
Imagine how exciting it will be when you can objec-
tively determine which parts of the neurotransmitter
puzzle need to be addressed specifically for your patient.
Having observed the positive outcomes in my patients
utilizing the testing that is currently available, I have
become extremely enthused about the future of
neurotransmitter optimization. I look forward to the day
when we have clinical tests to objectively assess neuro-
transmitter binding and uptake, enzymatic degradation
and receptor sensitivity therapies. In the interim, I
advocate the use of urinary neurotransmitter testing and
amino acid supplementation to optimize pre-synaptic
neurotransmitter stores.
Lastly, recognize that the future of neurotransmitter
testing and optimization will do much more than just
objectively measure levels of neurotransmitters in the
urine. Incorporation of the immune and endocrine
systems is essential to understanding how to best support
the entire system. Thyroid hormones, adrenal cortisol,
immune cytokines & antibodies, food sensitivities, and
environmental toxins are just some of the many compo-
nents that will intersect with neurotransmitter testing for
clinical application and improved patient outcomes.
Neuroendoimmunology is in its infancy but the future is
very bright.
With the combination of objective testing and subjective
findings, a more accurate and complete picture of your
patient’s current condition can be constructed and allow
for improved clinical applications. In the end, every
practitioner must decide their own personal clinical
strategies. Urinary neurotransmitter testing and amino
acid supplementation, coupled with a detailed patient
history and physical examination, have been essential to
my ability to help my patients achieve optimal function. ‹

Test Parameter Result Optimal Range

Estradiol 2.1 0.8-1.5
Estrone 2.3 1.0-2.5
Progesterone 0.032 0.070-0.150
Testosterone 60.1 75-95
Dihydrotestosterone 19.1 20-40
DHEA 84.5 250-450
Cortisol AM 2.2 7.0-10
Cortisol Midday 3.6 3-6
Cortisol Afternoon 6.9 2-4
Cortisol PM 1.3 <1.5
Epinephrine 8.5 8-11 daytime
Norepinephrine 36.5 35-45 daytime
Dopamine 76.4 125-175 daytime
Serotonin 60.5 125-175 daytime
GABA 3.9 1.5-4.0 daytime
Glutamate 38.1 15-35 daytime
PEA 108.6 30-70 daytime
Histamine 19.5 10-20 daytime

220
THE ORIGINAL INTERNIST Spring 2006 THE ORIGINAL INTERNIST DECEMBER 2009
05
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NeuROTRANsMITTeR TesT PROFIle (New ACCOuNTs ONly).

Abstracts
of Interest
Supplements plus Statins Reduce a Prime Indicator
of Atherosclerosis--a Finding not Associated with
Stand-Alone Statin Therapy
Author: Steve Austin, N.D.
Reference: Davis W, Rockway S, Kwasny M. Effect
of a combined therapeutic approach of intensive lipid
management, omega-3 fatty acid supplementation, and
increased serum 25(OH) vitamin D on coronary cal-
cium scores in asymptomatic adults. Am J Therapeutics
2009;16:326−32.
Design: Unblinded retrospective analysis of data from
clinical interventions
Participants: 45 adults with coronary calcium scores
(CCS) ≥50
Study Medication and Dosage: Subjects were
encouraged to eat a low saturated fat, high-fiber, low-
glycemic index diet. Statins doses were individually
tailored to reduce LDL levels to a maximum of 60 mg/
dL. (To meet this criterion, all female subjects and 77%
of male subjects required at least some use of statins.)
Most subjects also received time-release niacin at un-
specified doses.
Additional supplementation consisted of 2,000 IU/day
vitamin D3 initially, increased as needed to achieve 25
(OH)D3 serum levels between 50 and 60 ng/mL
(average dose of vitamin D: 3,590 IU/day). Fish oil was
supplemented in varying doses (4–10 g/day; average
dose: 4.8 g/day) to lower triglycerides (TG) to ≤60 mg/
dL. Fish oil supplements contained a minimum of 30%
omega-3 fatty acids. A mean of 18 months occurred
between the initial and final CT scan reports.
Primary Outcome Measures: Total cholesterol (TC),
low-density lipoprotein cholesterol (LDL), high-density
lipoprotein cholesterol (HDL), TG, and CCS (as
THE ORIGINAL INTERNIST
222 Spring 2006
calculated from before-and-after CT scans of the heart)
were measured at baseline and at the completion of the
trial.
Key Findings: As a function of the combined use of
statins plus supplements, TC declined by 24%, LDL
declined by 41%, TG declined by 42%, and HDL
increased by 19%. Except for the increase in HDL
observed in female subjects (11 mg/dL), these changes
attained statistical significance.
After 18 months, 20 of 45 subjects experienced an
average CCS decline (improvement) of 14.5%, and all
but three of the remaining subjects experienced either
no change in CCS or a relatively slow rate of progres-
sion (averaging 12%). A substantial decline in CCS
occurred in 44% of subjects and a slowed plaque
growth occurred in an additional 49%. These changes
in CCS were statistically significant when subjects
were divided into three subgroups based upon the rate
of change in CCS: “typical” progression (>29%
progression per year), “slowed” progression (<29%
progression per year), and the combination of subjects
showing no progression and those experiencing actual
regression.
Practice Implications: Increasingly, researchers are
accepting CCS as an indicator of coronary risk and,
more specifically, atherosclerotic progression. When
administered alone, statin drugs lower cholesterol but
have not been found to reduce CCS or even slow its
progression, suggesting that these drugs may not be
halting atherosclerotic plaque formation. Despite this
limitation, statin therapy has been shown to reduce
both the incidence of myocardial infarction and death
from coronary artery disease. Nonetheless, the apparent
inability of statins to improve CCS suggests that their
therapeutic effect may not be optimal.
And what triggered the inclusion of these particular
nutritional supplements? Vitamin D was added because
the principle investigator had previously observed that
supplementation with vitamin D improved insulin
sensitivity while reducing C-reactive protein and TG
(unpublished data). Related findings have also been
reported by other researchers. Fish oil was added
primarily because of its proven ability to lower TG
levels. Niacin is known to lower TC and LDL while
raising HDL. Niacin has also been reported to reduce
coronary disease morbidity and mortality.
We still lack firm proof that improvements in CCS that
appear to result from the addition of niacin, vitamin D,
and fish oil would translate into reductions in myocar-
(Continued on next page)
THE ORIGINAL INTERNIST DECEMBER 2009 05
dial infarction rates or cardiovascular mortality beyond
those expected to occur when statins are used as
stand-alone therapy. That said, however, the intriguing
findings of the new report suggest that such may well
be the case.
These new findings do not tell us which component or
components (niacin, fish oil, and/or vitamin D) are key
to halting the progression of atherosclerosis. Given that
heart disease remains the leading killer of Americans
and that improvements in CCS appear likely to reduce
cardiovascular disease risk, until we know more,
healthcare practitioners may wish to consider admini-
stration of this combined-therapy approach in the treat-
ment of patients with risk factors for (or a history of)
cardiovascular disease. ‹
Red Yeast Rice Extract Lowers M.I. Incidence and
Mortality from Coronary Disease
Author: Steve Austin, N.D.
Reference: Li J-J, Lu Z-L, Kou W-R, et al. Beneficial
impact of Xuezhikang on cardiovascular events and
mortality in elderly hypertensive patients with previous
myocardial infarction from the China Coronary
Secondary Prevention Study (CCSPS). J Clin Pharma-
col 2009;49:947–56.
Design: Randomized double-blind intervention trial
Participants: 1530 elderly (≥65 years of age)
hypertensive subjects with a history of myocardial in-
farction (MI)
Study Medication and Dosage: Subjects received
either Xuezhikang, a red yeast rice (RYR) extract,
administered as 600 mg b.i.d., or placebo for an
average of 4.5 years. Each 600 mg capsule of RYR
contained 2.5–3.2 mg of monacolin K plus “a small
quantity of lovastatin hydroxyl acid as well as
ergosterol and some other components.”
Primary Outcome Measures: Recurrent coronary
events
Key Findings: Compared with the placebo group, there
was a 38% reduced risk of suffering a coronary event
(primarily MIs) (P=0.0009). Similarly there was a 29%
reduced risk of dying from coronary disease during the
course of the trial (P=0.05). Secondary endpoints
revealed a 21% decline in LDL levels in the RYR
group (P=0.0001) and a 12% decline in triglyceride
THE ORIGINAL INTERNIST DECEMBER 2009
levels (P=0.003) compared with trivial declines in the
placebo group. Total mortality also declined by 36% in
the group receiving RYR (P=0.003).
Practice Implications: RYR extracts are known to
reduce cholesterol levels in humans and have been
traditionally used in China to treat people with
cardiovascular disease. RYR naturally contains the
same molecule found in the prescription drug lov-
astatin. Previous RYR research has focused primarily
on cholesterol reduction, though some evidence for
reduction in inflammatory markers has also surfaced.
The current trial goes several steps further, showing
clinically (and statistically) significant reductions in
coronary disease incidence and mortality. Hidden in the
data is a near-statistically significant (P=0.06) 37%
reduction in the risk of stroke and a statistically signifi-
cant (P<0.04) reduction in total cancer incidence when
compared with the placebo group. No current
understanding of the effects of RYR clearly explains
these additional positive findings.
One caveat requires mentioning: a previous report
studying the pharmacokinetics of a related statin drug
found that area-under-the-curve response was twice as
great in Chinese subjects compared with white subjects
(Clin Pharmacol Ther 2005;78:330–41). Should further
investigations confirm these findings in regard to
monacolins found in RYR, white (and potentially
black) patients might require significantly higher doses
of RYR to achieve the same clinical outcomes that
occurred in the new report, which studied Chinese
subjects. ‹
Green Tea Polyphenols lower PSA Levels in
Prostate Cancer Patients
Author: Steve Austin, N.D.
Reference: McLarty J, Bigelow RLH, Smith M, et al.,
Tea polyphenols decrease serum levels of
prostate-specific antigen, hepatocyte growth factor, and
vascular endothelial growth factor in vitro. Cancer
Prev Res 2009;2:674–82.
Design: Unblinded intervention trial
Participants: 26 men with recently diagnosed stage I,
II, or III prostate cancer (CA), all scheduled for radical
prostatectomy.
Study Medication and Dosage: Polyphenon E, a green
(Continued on next page)
223
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tea extract that delivered 1.3 g/day total polyphenols
including 800 mg/day epigallocatechin-3-gallate
(EGCG) was given to all subjects in the form of four
capsules taken during one meal each day up until the
time of surgery (a median of 34.5 days).
Main Outcome Measures: Prostate-specific antigen
(PSA), insulin-like growth factor I, and additional
biomarkers of prostate CA status
Key Findings: PSA levels declined by 10.4%
(P=0.01). In the subgroup of subjects taking the extract
for longer than the median time (>34.5 days), 85%
experienced a decline in PSA compared with 64% of
those taking the extract for shorter periods of time,
though this difference did not attain statistical signifi-
cance.
Insulin-like growth factor I declined by 11% (P=0.02).
Other prostate CA markers declined by 3 –19% and
each of these changes also attained statistical signifi-
cance (P values varying from 0.03 to <0.001).
Cases of hepatotoxicity have previously surfaced in
regard to green tea polyphenols. However, liver
enzymes and other markers of hepatic function (which
were tracked because of this concern) actually declined
during the trial; five of these reductions reached statisti-
cal significance.
Practice Implications: EGCG has inhibited prostate
CA cells in vitro. Though epidemiologic data remain
mixed, three years ago, an Italian research group
reported that consumption of green tea polyphenols
delayed progression of high-grade prostatic intraepithe-
lial neoplasia (Cancer Res 2006;66:1234–40).
Why might green tea polyphenols have anticancer ef-
fects? Hepatocyte growth factor (HGF)/c-Met signaling
pathway is disturbed in a wide variety of cancers
including prostate CA. Increasingly, researchers be-
lieve that inhibition of this pathway should increase life
expectancy in CA patients. Green tea polyphenols had
an inhibitory effect in the current trial.
Other markers of prostate CA status or progression
have also recently been found to either increase prolif-
eration of CA cells or interfere with apoptosis. The
authors of the current trial measured these newer
markers along with PSA scores in hopes that green tea
polyphenols would alter markers in directions compati-
ble with CA regression. It’s exciting to note that
THE ORIGINAL INTERNIST DECEMBER 2009
virtually all markers tracked by these researchers
moved in the direction of safety and most of these
changes attained statistical significance.
What are clinicians to do with these new findings? As
long as liver enzymes are monitored to insure the same
level of safety reported in the current trial (though not
in all previous reports), it may be time for healthcare
professionals to tell their prostate CA patients about
these new findings, which suggest the potential (though
not yet proof of) significant anti-cancer effects from
green tea extracts containing appropriate amounts of
polyphenols.‹
Nutrients for Migraine Prevention
by Alan R. Gaby, M.D.
More than 10% of Americans suffer from migraines.
Even the most effective medications prescribed for
migraine prophylaxis reduce migraine frequency by no
more than 50%, and many of these drugs are associated
with significant side effects. Safer and more effective
ways of preventing and treating migraines are therefore
needed.
Mitochondrial energy production appears to be im-
paired in people with recurrent migraines, and this im-
pairment might play a role in the pathogenesis of mi-
graines. Nutrients that are involved in energy produc-
tion might therefore be beneficial. Magnesium is a co-
factor for the synthesis of adenosine triphosphate
(ATP), the body's main storage form of energy.
Riboflavin (in the form of flavin adenine dinucleotide
[FAD]) and coenzyme Q10 are cofactors in the electron-
transport chain, a biochemical cascade that culminates
in ATP synthesis. Each of these three nutrients has
been shown in clinical trials to decrease the recurrence
rate of migraines.
Magnesium
Eighty-one migraine sufferers were randomly assigned
to receive, in double-blind fashion, 600 mg per day of
magnesium or placebo for 12 weeks. During the last
four weeks of the study, as compared with baseline, the
mean frequency of migraines was reduced by 42% in
the magnesium group and by 16% in the placebo group
(p < 0.04 for the difference in the change between
groups). Adverse effects of magnesium were diarrhea
in 18.6% of patients and gastric irritation in 4.7%.1 In
other research, effective migraine prophylaxis was
achieved with a magnesium dose of 360 mg per day,2
(Continued on next page)
225
which is less likely than the higher dose to produce
gastrointestinal side effects.
Riboflavin
Fifty-five migraine patients were randomly assigned to
receive, in double-blind fashion, 400 mg of riboflavin
once a day or placebo for three months. In intent-to-
treat analysis, riboflavin was superior to placebo in
reducing attack frequency (p = 0.005) and number of
headache days (p = 0.012). The proportion of patients
who experienced at least a 50% reduction in the
number of headache days was 59% for riboflavin and
15% for placebo (p = 0.002). Three minor adverse
events occurred, two in the riboflavin group (diarrhea
and polyuria) and one in the placebo group.3
The dose of riboflavin used in this study was about 400
times as much as the amount present in a typical diet.
Uncontrolled trials from the 1940s and 1950s suggest
that lower doses of riboflavin (such as 5-10 mg three
times per day) can also prevent migraine recurrences.
While high-dose riboflavin has not been associated
with significant toxicity in short-term studies, it has the
potential to act as a photo-sensitizer or to cause
imbalances of other nutrients. Therefore, it would seem
prudent to reserve high-dose riboflavin for patients who
do not respond to moderate doses.
Coenzyme Q10
Forty-two migraine patients were randomly assigned to
receive, in double-blind fashion, 100 mg of coenzyme
Q10 three times per day or placebo for four months. The
proportion of patients who had a 50%-or-greater
reduction in attack frequency during the fourth month
compared with baseline was 48% in the coenzyme Q10
group and 14% in the placebo group (p = 0.02). The
mean reduction in attack frequency was 27% in the co-
enzyme Q10 group and 2% in the placebo group
(p < 0.05 for the difference in the change between
groups).4
B Vitamins, Homocysteine, and Migraines
Polymorphisms of the 5,10-methylenetetrahydrofolate
reductase gene (mainly homozygosity for 677C → T)
that are associated with reduced enzyme activity and
moderate hyperhomocysteinemia have been found to be
common in migraine patients. In one study, 16 of 22
children with recurrent migraines without aura had one
of these polymorphisms. In those children, supplemen-
tation with 5 mg per day of folic acid (which is known
THE ORIGINAL INTERNIST
226 Spring 2006
to lower homocysteine levels) resulted in a complete
cessation of migraine attacks in 10 of 16 children and
substantial improvement in each of the others. Plasma
homocysteine levels became normal in all 16 patients.5
While it was not clear whether elevated homocysteine
per se, was the cause of the migraines, another study
also found that treatment with homocysteine-lowering
nutrients (folic acid, vitamin B6, and vitamin B12)
markedly reduced headache frequency in patients with
elevated homocysteine levels. Based on these
observations, it would seem worthwhile to measure
plasma homocysteine levels in migraine patients and to
recommend B-vitamin supplementation for those with
elevated levels.
Other treatments
Other treatments that have been found to be effective
for preventing migraines include identification and
avoidance of allergenic foods, quitting smoking,
stopping the use of oral contraceptives, and administra-
tion of certain herbal remedies (i.e., feverfew and
butterbur).
References
1) Peikert A, Wilimzig C, Kohne-Volland R. Prophy-
laxis of migraine with oral magnesium: results
from a prospective, multi-center, placebo-
controlled and double-blind randomized study.
Cephalalgia 1996;16:257-263.
2) Facchinetti F, Sances G, Borella P, Gonazzani AR,
Nappi G. Magnesium prophylaxis of menstrual
migraine: effects on intracellular magnesium.
Headache 1991;31:298-304.
3) Schoenen J, Jacquy J, Lenaerts M. Effectiveness of
high-dose riboflavin in migraine prophylaxis. A
randomized controlled trial. Neurology
1998;50:466-470.
4) Sandor PS, Di Clemente L, Coppola G, Saenger U,
Fumal A, Magis D, et al. Efficacy of coenzyme
Q10 in migraine prophylaxis: a randomized con-
trolled trial. Neurology 2005;64:713-715.
5) Di Rosa G, Attina S, Spano M, Ingegneri G, Sgro
DL, Pustorino G, et al. Efficacy of folic acid in
children with migraine, hyperhomocysteinemia and
MTHFR polymorphisms. Headache 2007;47:1342-
1344.
6) Lea R, Colson N, Quinlan S, Macmillan J, Griffiths
L. The effects of vitamin supplementation and
MTHFR (C677T) genotype on homocysteine-
lowering and migraine disability. Pharmacogenet
Genomics 2009;19:422-428.‹
THE ORIGINAL INTERNIST DECEMBER 2009
05
 DABCIs and Where They Are
ALABAMA Dr. Rita Cummings IDAHO Dr. Frank Strehl Dr. H.M. Chalker
Dr. Reginald Hug* Denver, CO Dr. Uma Mulnick Wheaton, IL Meade, KS
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FLORIDA Dr. Timothy Bertsch
Dr. John Findlay Dr. Harry Jensen Dr. Zach Watkins
Dr. Andrew Lucas Champlin, MN
W. Palm Beach, FL Sterling, IL Johnston, IA
Riverside, CA
Dr. Thomas Jensen Dr. Linda Bowers
Dr. Kathleen Power Dr. David Frerking Dr. Anita Wubenna Bloomington, MN
Tavares, FL Sterling, IL Parkview, IA
Pasadena, CA
Dr. Theodore Johnson Dr. Russell DesMarais
Dr. Rowen Richardson Dr. Marguerite Gerger KANSAS St. Paul, MN
Clearwater, FL Chicago, IL
Glendora, CA Dr. Mark Albers
Dr. James McGinn, Jr. Wichita, KS Dr. Joel Eichers
Dr. Scott Soluk Dr. Janice Piro Chanhassen, MN
Palm Harbor, FL Crystal Lake, IL
Los Angeles, CA Dr. Lynn Betz
Dr. Anthony Pantanella Auburn, KS Dr. John Gerber
Dr. Sylvie Wellhausen Dr. Susan Player Blaine, MN
Clearwater, FL Hoffman Estates, IL
Loma Linda, CA Dr. Ben Bowers
Wichita, KS Dr. Timothy Gerhart
Dr. Kelly Worth Dr. John Podlaski Dr. Michael Poierier
Red Wing, MN
Orange, CA Ocala, FL Lombard, IL
Dr. Richard Brown
Olathe, KS Dr. Jedidiah Krauss
COLORADO GEORGIA Dr. Robert Pyne, Jr.
St. Louis Park, MN
Dr. John Baer Dr. Larry Haberski Palos Hills, IL
Dr. Susan Buchanan-Cheney
Englewood, CO Stone Mountain, GA Phillipsburg, KS Dr. Mac Beth Lindstrom
Dr. William Shelton
Slayton, MN
Dr. Debra Carpenter Dr. Edward Kaszans Lombard, IL
Dr. Ralph Cardin
Pueblo West, CO Brunswick, GA Overland Park, KS Dr. Todd McGillick
Dr. Douglas Stam
Gaylord, MN
Dr. Terry Collinson Bourbonnais, IL
Colorado Springs, CO (Continued on next page)
* Retired DABCI Practitioner
THE ORIGINAL INTERNIST DECEMBER 2009 227
 DABCIs and Where They Are
Dr. Thomas Miller Dr. Robert Wiehe Dr. Mark Yeager Dr. Mark Homison Dr. Joe Lindley
Coon Rapids, MN West Plains, MO Charlotte, NC Cranberry Township, PA Houston, TX

Dr. Joseph Muldoon NEW JERSEY OHIO Dr. John LaHoda Dr. Tim McCullough
Slayton, MN Dr. Jon Mastrobattista Dr. Robert Gilbert Richboro, PA Houston, TX
Bernardville, NJ Mansfield, OH
Dr. Brenwyn Peddycoat Dr. Fredrick Osterberg Dr. Zachery McVey
White Bear Lake, MN Dr. Perry Ricci Dr. Mark McAdoo Red Lion, PA League City, TX
Egg Harbor City, NJ Athens, OH
Dr. Gregory Peterson SOUTH CAROLINA Dr. Gregory Mrozinski
Winona, MN NEW MEXICO Dr. Van Merkle Dr. Jon Bergrin Houston, TX
Dr. John Dalton Dayton, OH Florence, SC
Dr. Dane Roubos Roswell, NM Dr. Mike Prioux
Bloomington, MN OKLAHOMA Dr. Bruce Gwinnup Friendswood, TX
Dr. John H. Gelhot Dr. Stephanie Clay Charleston, SC
Dr. Sandra Spore Bartlesville, OK Dr. V.M. Thompsom
Albuquerque, NM
Stillwater, MN Dr. Peter Kfoury Arlington, TX
Dr. Shereen Jegtvig Dr. Gerry Langston Charleston, SC
Dr. Leslie Stewart UTAH
Albuquerque, NM Tulsa, OK
St. Paul, MN Dr. Morgan Kutzner Dr. Don Vradenburg
NEW YORK Dr. Richard Santelli Greenville, SC St. George, UT
Dr. Charles Strauman
Dr. Ronald Safko Bethany, OK
St. Louis Park, MN
New York City, NY Dr. Jacqueline McKool VIRGINIA
Dr. Michael Taylor Charleston, SC Dr. Robert Duca
Dr. Terese Tomanek
Dr. John Zilliox Tulsa, OK Dunn Loring, VA
Duluth, MN
Amherst, NY Dr. Robert Pascal
Dr. Timothy Whelan OREGON Charleston, SC Dr. Guntrang Khalsa
New Hope, MN NEVADA Dr. Daniel Beeson Herndon, VA
Dr. Howard Balduc Portland, OR Dr. Virginia Samuel
Dr. Jon Williams Las Vegas, NV Columbia, SC WASHINGTON
Bloomington, MN Dr. David Braman Dr. H. Earl Moore
Dr. Craig Roles Tuelatin, OR SOUTH DAKOTA Spokane, WA
MISSOURI Henderson, NV Dr. Roger Bommersbach
Dr. Kathleen M. Galligan Brookings, SD WISCONSIN
Dr. David Clark
NORTH CAROLINA Oregon City, OR Dr. Leslie Best
Oak Grove, MO
Dr. William R. Armstrong Dr. Roger Prill Madison, WI
Dr. Edward M. Geller Mitchell, SD
Dr. Charles Eckert Laurenburg, NC
Medford, OR Dr. Barbara Bradley
Raymore, MO
Dr. Phillip Arnone Dr. David Schwierert Wausau, WI
Dr. Usha Honeyman Rapid City, SD
Dr. Jack Kessinger Matthews, NC Corvallis, OR
Rolla, MO Dr. Kevin Branham
Dr. Stephen Button TENNESSEE Eagle River, WI
Dr. Steven Lumsden Dr. William Strauss
Dr. Jay Kessinger Mount Airy, NC Gresham, OR
Rolla, MO Lebanon, TN Dr. Bernie Finch
Dr. Karen Carrick Pepin, WI
Dr. Scott Northrup
Dr. Kelley Kirchner Raleigh, NC TEXAS
Brookings, OR Dr. Gwendolyn Gauerke
Kahoka, MO Dr. Edward Brown
Dr. Rick Davis Dallas, TX Iola, WI
Dr. Kristopher Peterson
Dr. Mable Leckrone Conover, NC Hermiston, OR
Dr. Ralph Burton Dr. Craig Gilbaugh
Liberty, MO
Dr. Nikolas R. Hedberg Kennedale, TX Ashland, WI
Dr. Thomas Richards
Dr. Duane Lowe Asheville, NC Beaverton, OR
Dr. Lance Carlton-Durrett Dr. Kathleen Maedke
Maplewood, MO
Dr. Dean Kenny The Woodlands, TX Milwaukee, WI
Dr. James Siegel
Dr. Terry Nelson High Point, NC Canyonville, OR
Dr. Janie Duke Dr. Cheryl Metzler
Independence, MO
Dr. Sandrine Martin Plano, TX Green Bay, WI
Dr. Mark Thomas
Dr. R Vincent Satterwhite Cornelius, NC Cottage Grove, OR
Dr. Steve Grimm Dr. Gina R. Schultz
Kansas City, MO
Dr. Barbara Saunders San Antonio, TX Blanchardville, WI
Dr. David Wickes
Dr. Jeremy Thornton Garner, NC Portland, OR
Dr. Doreen Lewis-Overstrom Dr. David A. Sommerfield
Stockton, MO Rice Lake, WI
Dr. Todd Smith San Antonio, TX
PENNSYLVANIA
Dr. Jeffrey S. Ware Winston-Salem, NC Dr. Bruce Fink Dr. Dean Willhite
Lake St. Louis, MO Coudersport, PA Manitowoc, WI

THE ORIGINAL INTERNIST

228 Spring 2006 THE ORIGINAL INTERNIST DECEMBER 2009
05
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