Dec_OI_2009

C • O • N • T • E • N • T • S

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

CLINT PUBLICATIONS

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

Original Internist T H E

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THE ORIGINAL INTERNIST

Research Editors

Debasis Bagchi, PhD, FACN Paul Basile, DC Scott Bautch, DC, SC, DACBOH Daniel Beeson, DC, DABCI Eleonore Blaurock-Busch, PhD Jerome Block, MD, FACP Harold M. Chalker, DC, DABCI Dallas Clouatre, PhD John W. Jones, MD, MPH, FAAO, HNS Shari Lieberman, PhD, CNS, FACN Charlyn Marcusen, PhD Duane Marquart, DC, DACBR Edward W. McDonagh, DO Terry Nelson, DC, DABCI Doran Nicholson, DC, DACBR Harry G. Preuss, MD, FACN, CNS Oscar Rasmussen, PhD Timothy Ray, DC, FACO, CCSP, CSCS Charles Rudolph, DO Sidney Stohs, PhD, FACN, FATS, FASAHP Edward C. Sullivan, DC, PhD, Dipl Ac (IAMA), BCIAC, DAPA Jon A. Sunderlage, DC, Dipl Ac (NCAOM) Sharon A. Vallone, DC, DICCP Steve Watterson, ATC Michael Whitehead, DC, DACBR David Wickes, DC, DABCI Jonathan V. Wright, MD

Editor-in-Chief

Jack Kessinger, DC, ND, DABCI Managing Editor Production Manager

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Jay Kessinger, DC, ND, DABCI Kimberly Foster

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DISCLAIMER The opinions expressed in The Original Internist are presented for the purpose of providing an open forum for unbiased case studies, contemporary ideas and discussion of matters relevant to natural health care. Its primary mission is to educate and inform those especially interested in promoting natural health care as a primary treatment. The opinions expressed in The Original Internist do not necessarily reflect the opinions and policies of Clint Publications or The Original Internist.

THE ORIGINAL INTERNIST DECEMBER 2009 177

CALENDAR OF EVENTS

THE ORIGINAL INTERNIST Spring 2006 05 178 THE ORIGINAL INTERNIST DECEMBER 2009

FOR ALL DABCI SEMINARS ….. VISIT OUR NEW WEBSITE www.DABCIdiplomate.com

For more information on our 2009-2011 seminars visit us online at

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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

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

From the Editor’s Desk by: Jack Kessinger, DC, ND, DABCI [email protected]

Dr. Jack Kessinger

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


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

(Continued on page 182)

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-

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

Functional Endocrinology Philosophy for the Practicing Internist by: Datis Kharrazian, DC, DHSc, MS, MNeuroSci, FAACP, DACBN, DIBAK, CNS


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.

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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.

• 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.


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.

The Legacy Continues


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,

Dr. Jay Kessinger by: A. Jay Kessinger IV, DC, ND, DABCI [email protected]

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(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

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

The Toxicity of Metals by: E. Blaurock-Busch, PhD


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


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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: [email protected] 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.


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 SEPTEMBER 2008 119

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

Immune Boosting Components to Arrest Colds and Flu by : Rachel Olivier, MS, ND, PhD Submitted by: Biotics Research Corporation

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



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

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.



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.



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:


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/

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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,

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 [email protected].

(Continued on next page) THE ORIGINAL INTERNIST DECEMBER 2009 193

Liver Flush: Help or Hoax? by: Dr. E. W. McDonagh, DO

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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. (Continued on next page)

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


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

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).

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.




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.

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).


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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)

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.


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


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




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:

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: 2X3=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-



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-

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

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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-

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.



References

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More photos are available at http://hcgobesity.org/hcg_obesity_photographs.htm

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.

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.

BLOOD TRANSFUSIONS ARE VERY DANGEROUS

by: Dr. James A. Howenstine


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

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



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.



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-


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.

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.


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

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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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 [email protected] 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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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?

• 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

Clinical Relevance of Neurotransmitter Testing by: Dr Scott Theirl Submitted by: NeuroScience, Inc.



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 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.

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.

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

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


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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

Abstracts of Interest


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-


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

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


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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

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




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

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.

Dr. H.M. Chalker Meade, KS Dr. Dustin Cheney Phillipsburg, KS Dr. Rod Clements Eldorado, KS Dr. Paul Hughes Edgerton, KS Dr. Tobi Jeurink Gardner, KS Dr. Christena Nicholson Overland Park, KS Dr. Janie Pirner Wichita, KS Dr. Ron Young Salina, KS LOUISIANA Dr. Robert W. Smith Baton Rouge, LA MARYLAND Dr. Wayne Sodano Bel Air, MD MICHIGAN Dr. Daniel M. McGregor Prudenville, MI MINNESOTA Dr. Jeffrey Anderson Edina, MN Dr. Robert Bergan Minneapolis, MN Dr. Timothy Bertsch Champlin, MN Dr. Linda Bowers Bloomington, MN Dr. Russell DesMarais St. Paul, MN Dr. Joel Eichers Chanhassen, MN Dr. John Gerber Blaine, MN Dr. Timothy Gerhart Red Wing, MN Dr. Jedidiah Krauss St. Louis Park, MN Dr. Mac Beth Lindstrom Slayton, MN Dr. Todd McGillick Gaylord, MN

Dr. Frank Strehl Wheaton, IL Dr. Melanie Tiahrt* Alton, IL Dr. Steven Zaeske Orland Park, IL Dr. Alex Zevan,III Bloomingdale, IL INDIANA Dr. John Bernzott Connersville, IN Dr. Thomas Jansen Kendalville, IN Dr. William Lyden Mishawaka, IN Dr. Brian McGuckin Valparaiso, IN Dr. Robert Prather Indianapolis, IN IOWA Dr. Gary Bowden McGregor, IA Dr. Darlene Ehlers Tipton, IA Dr. Robert Friedrichs Mason City, IA Dr. Tracy A. Stomgren Glenwood, IA Dr. Lynn Theesfield Ames, IA Dr. Zach Watkins Johnston, IA Dr. Anita Wubenna Parkview, IA KANSAS Dr. Mark Albers Wichita, KS Dr. Lynn Betz Auburn, KS Dr. Ben Bowers Wichita, KS Dr. Richard Brown Olathe, KS Dr. Susan Buchanan-Cheney Phillipsburg, KS Dr. Ralph Cardin Overland Park, KS

IDAHO Dr. Uma Mulnick McCall, ID ILLINOIS Dr. Delilah Anderson Sandwich, IL Dr. Jeffrey Bergin Lindenhurst, IL Dr. Stephen Boudro Elmhurst, IL Dr. Sharon DeFrain Peotone, IL Dr. Mete Durum Arlington Heights, IL Dr. Raymond Ferre Decatur, IL Dr. Mark Fredrick Gurnee, IL Dr. David Hepler Lincoln, IL Dr. William Hogan Lombard, IL Dr. Lester Holze, Jr. Elgin, IL Dr. Cindy Howard Orland Park, IL Dr. Frederick Hult McHenry, IL Dr. Grant Iannelli Lombard, IL Dr. Harry Jensen Sterling, IL Dr. Thomas Jensen Sterling, IL Dr. Theodore Johnson Chicago, IL Dr. James McGinn, Jr. Crystal Lake, IL Dr. Anthony Pantanella Hoffman Estates, IL Dr. Michael Poierier Lombard, IL Dr. Robert Pyne, Jr. Palos Hills, IL Dr. William Shelton Lombard, IL Dr. Douglas Stam Bourbonnais, IL

Dr. Rita Cummings Denver, CO Dr. Paula Dechert Denver, CO Dr. Lewis Holm Littleton, CO Dr. William Kleber Berthoud, CO Dr. Reiner Kremer Franktown, CO Dr. Steven Lokken Colorado Springs, CO Dr. Duane Lowe Colorado Springs, CO Dr. David Paradiso Colorado Springs, CO Dr. Philip Pollock Sterling, CO Dr. Deborah Riekman Colorado Springs, CO Dr. Thomas Turner Boulder, CO Dr. Michael Vanaria Boulder, CO Dr. Brian Wilson Englewood, CO CONNECTICUT Dr. Paul DiDomizio Wolcott, CT FLORIDA Dr. John Findlay W. Palm Beach, FL Dr. David Frerking Tavares, FL Dr. Marguerite Gerger Clearwater, FL Dr. Janice Piro Palm Harbor, FL Dr. Susan Player Clearwater, FL Dr. John Podlaski Ocala, FL GEORGIA Dr. Larry Haberski Stone Mountain, GA Dr. Edward Kaszans Brunswick, GA

ALABAMA Dr. Reginald Hug* Birmingham, AL ALASKA Dr. David Mulholland Anchorage, AK Dr. Stan Throckmorton Anchorage, AK ARIZONA Dr. R. Michael Cessna* Tucson, AZ Dr. Laura Frey Tucson, AZ Dr. Timothy Gerhart Glendale, AZ Dr. Kellie Gray Glendale, AZ Dr. Michael Stone Tucson, AZ ARKANSAS Dr. Lance Clouse Van Buren, AR Dr. Douglas Smiley* Siloam Springs, AR CALIFORNIA Dr. Jan Dooley Arcata, CA Dr. Jeffrey Greene Los Angeles, CA Dr. Jill Jordan Carlsbad, CA Dr. Andrew Lucas Riverside, CA Dr. Kathleen Power Pasadena, CA Dr. Rowen Richardson Glendora, CA Dr. Scott Soluk Los Angeles, CA Dr. Sylvie Wellhausen Loma Linda, CA Dr. Kelly Worth Orange, CA COLORADO Dr. John Baer Englewood, CO Dr. Debra Carpenter Pueblo West, CO Dr. Terry Collinson Colorado Springs, CO

DABCIs and Where They Are



* Retired DABCI Practitioner

DABCIs and Where They Are Dr. Mark Homison Cranberry Township, PA Dr. John LaHoda Richboro, PA Dr. Fredrick Osterberg Red Lion, PA SOUTH CAROLINA Dr. Jon Bergrin Florence, SC Dr. Bruce Gwinnup Charleston, SC Dr. Peter Kfoury Charleston, SC Dr. Morgan Kutzner Greenville, SC Dr. Jacqueline McKool Charleston, SC Dr. Robert Pascal Charleston, SC Dr. Virginia Samuel Columbia, SC SOUTH DAKOTA Dr. Roger Bommersbach Brookings, SD Dr. Roger Prill Mitchell, SD Dr. David Schwierert Rapid City, SD TENNESSEE Dr. William Strauss Lebanon, TN TEXAS Dr. Edward Brown Dallas, TX Dr. Ralph Burton Kennedale, TX Dr. Lance Carlton-Durrett The Woodlands, TX Dr. Janie Duke Plano, TX Dr. Steve Grimm San Antonio, TX Dr. Doreen Lewis-Overstrom San Antonio, TX

Dr. Mark Yeager Charlotte, NC OHIO Dr. Robert Gilbert Mansfield, OH Dr. Mark McAdoo Athens, OH Dr. Van Merkle Dayton, OH OKLAHOMA Dr. Stephanie Clay Bartlesville, OK Dr. Gerry Langston Tulsa, OK Dr. Richard Santelli Bethany, OK Dr. Michael Taylor Tulsa, OK OREGON Dr. Daniel Beeson Portland, OR Dr. David Braman Tuelatin, OR Dr. Kathleen M. Galligan Oregon City, OR Dr. Edward M. Geller Medford, OR Dr. Usha Honeyman Corvallis, OR Dr. Steven Lumsden Gresham, OR Dr. Scott Northrup Brookings, OR Dr. Kristopher Peterson Hermiston, OR Dr. Thomas Richards Beaverton, OR Dr. James Siegel Canyonville, OR Dr. Mark Thomas Cottage Grove, OR Dr. David Wickes Portland, OR PENNSYLVANIA Dr. Bruce Fink Coudersport, PA

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Dr. Joe Lindley Houston, TX Dr. Tim McCullough Houston, TX Dr. Zachery McVey League City, TX Dr. Gregory Mrozinski Houston, TX Dr. Mike Prioux Friendswood, TX Dr. V.M. Thompsom Arlington, TX UTAH Dr. Don Vradenburg St. George, UT VIRGINIA Dr. Robert Duca Dunn Loring, VA Dr. Guntrang Khalsa Herndon, VA WASHINGTON Dr. H. Earl Moore Spokane, WA WISCONSIN Dr. Leslie Best Madison, WI Dr. Barbara Bradley Wausau, WI Dr. Kevin Branham Eagle River, WI Dr. Bernie Finch Pepin, WI Dr. Gwendolyn Gauerke Iola, WI Dr. Craig Gilbaugh Ashland, WI Dr. Kathleen Maedke Milwaukee, WI Dr. Cheryl Metzler Green Bay, WI Dr. Gina R. Schultz Blanchardville, WI Dr. David A. Sommerfield Rice Lake, WI Dr. Dean Willhite Manitowoc, WI


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Ubiquinol-QH

raising the standard for optimal cardiovascular support.†

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† These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

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