Infectious Diseases - International Academy of Homotoxicology

d 2.00 • US $ 2.00 • CAN $ 3.00 

Journal of 

Biomedical 

Therapy 

Volume 2, Number 3 ) 2008 

Integrating Homeopathy 

and Conventional Medicine 

Infectious 

Diseases 

• The Immune System, Our Personal Bodyguard 

• Theories of Immunosenescence and Infection

) 

Contents 

In Focus 

The Immune System, Our Personal Bodyguard . . . . . . . . . . . . 4 

What Else Is New? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 

Fr o m t h e P ra c t i c e 

Acute Recurrent Otitis Media . . . . . . . . . . . . . . . . . . . . . . . . . . 12 

M a r ke t i n g Yo u r P ra c t i c e 

Managing Expenses and Prices in the Medical Practice . . . . 14 

Re f re s h Yo u r H o m o t ox i c o l o g y 

Theories of Immunosenescence and Infection: 

Cytomegalovirus, Inflammation, and Homotoxicology . . . . 16 

Around the Globe 

Advanced IAH Lecturer’s Trainings East and West . . . . . . . . . 19 

Practical Protocols 

Bioregulatory Treatment of Urinary Tract Infections . . . . . . 20 

Meet the Expert 

Dr. Ivo Bianchi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 

Research Highlights 

Engystol: A Homeopathic Medication 

for the Common Cold . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 

Making of ... 

From Plant to Bottle: The Production of 

Homeopathic Nasal Sprays . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 

Cover photograph © Sebastian Kaulitzki/Fotolia.de 

) 2 

Published by/Verlegt durch: International Academy for Homotoxicology GmbH, Bahnackerstraße 16, 

76532 Baden-Baden, Germany, e-mail: journal@iah-online.com 

Editor in charge/verantwortlicher Redakteur: Dr. Alta A. Smit 

Print/Druck: VVA Konkordia GmbH, Dr.-Rudolf-Eberle-Straße 15, 76534 Baden-Baden, Germany 

© 2008 International Academy for Homotoxicology GmbH, Baden-Baden, Germany

) 

Fighting Infections 

Dr. Alta A. Smit 

Only a very small number of all 

the millions of microbial species 

actually cause disease in humans. 

Antibiotic therapy, used appropriately, 

has saved humankind 

from the scourge of severe infection, 

but it has also been abused, resulting 

in contaminated ground water, resistant 

strains of microbes, and eradication 

of symbiotic bacteria that 

play a major role in our immune 

health. 

The early 21st century saw the 

emergence of the so-called hygiene 

hypothesis, as reported in this journal. 

According to this hypothesis, 

Th2 mediated diseases such as allergies 

and cancers are increasing due 

to systematic eradication (through 

hygiene and vaccination) of mild 

bacterial and viral infections that 

drive Th1 responses. However, the 

hygiene hypothesis has a number of 

flaws: it does not account for the rise 

in Th1 related diseases, and the exposure 

of children to dirt has not 

eradicated allergy. 1 

Meanwhile, it has become evident 

that we humans have an evolutionary 

pact with certain infectious 

agents that not only stimulate Th1 

or Th2, but also – yes, you guessed 

it! – increase T reg cells through bystander 

suppression to ensure optimal 

Th1/Th2 balance. These agents 

include helminths and certain mycobacteria 

as well as the symbiotic 

bacteria in our gut. It seems, therefore, 

that whenever we use antibiotics 

to eradicate infectious agents, we 

risk killing off some of these old 

friends that are vital to immune balance. 

Stimulating natural defenses against 

infection still seems to be the safest 

and most logical way to fight nonlife 

threatening infections. Several 

antihomotoxic medications have 

been shown to strengthen the immune 

system: Engystol increases interferon 

gamma in vitro, has been 

shown to increase phagocytosis and, 

along with others like Gripp-Heel 

and Euphorbium compositum, has 

proven itself effective against a variety 

of viruses. 2-6 

In this issue, you will also find a 

summary of a study by Volker 

Schmiedel et al. on the effectiveness 

of Engystol in treating the common 

cold. We asked two specialists in immunology 

and infectious diseases, 

Dr. Manfred Schmolz and Dr. Doris 

Ottendorfer, to write the focus article 

on the complex immunology of 

infectious disease. This focus article 

is complemented by a case study by 

Dr. Ivo Bianchi and examples of 

treatment protocols by Dr. Bert 

Hannosset, both practicing homotoxicologists. 

Dr. Jhann Arturo, a 

clinical and experimental immunologist, 

discusses the very interesting 

link between immunosenescence, 

chronic infection, and chronic inflammation 

in the elderly and offers 

comprehensive treatment protocols. 

Managing expenses in the medical 

practice is an important subject for 

all practitioners, and Marc Deschler, 

our marketing specialist, has useful 

tips for you. Our Making of … series 

describes how homeopathic nasal 

sprays are produced. And last but 

not least, our new column Meet the 

Expert presents a side of Dr. Ivo Bianchi 

that you probably haven’t seen 

before! 

Alta A. Smit, MD 

References: 

1. Rook GA, Brunet LR. Old friends for breakfast. 

Clin Exp Allergy. 2005;35(7):841-842. 

2. Enbergs H. Effects of the homeopathic preparation 

Engystol on interferon-gamma production 

by human T-lymphocytes. Immunol 

Invest. 2006;35(1):19-27. 

3. Wagner H, Jurcic K, Doenicke A, Rosenhuber 

E, Behrens N. Die Beeinflussung der Phagozytosefähigkeit 

von Granulozyten durch 

homöopathische Arzneipräparate: in vitro- 

Tests und kontrollierte Einfachblindstudien. 

Arzneim.-Forsch./Drug Res. 1986;36(9):1421- 

1425. 

4. Glatthaar-Saalmüller B. In vitro evaluation 

of the antiviral effects of the homeopathic 

preparation Gripp-Heel on selected 

respiratory viruses. Can J Physiol Pharmacol. 

2007;85(11):1084-1090. 

5. Glatthaar-Saalmüller B, Fallier-Becker P. Antiviral 

action of Euphorbium compositum 

and its components. Forsch Komplementärmed 

Klass Naturheilkd. 2001 Aug;8(4):207-212. 

6. Oberbaum M, Glatthaar-Saalmüller B, Stolt 

P, Weiser M. Antiviral activity of Engystol: 

an in vitro analysis. J Altern Complement Med. 

2005;11(5):855-862. 

) 3 

Journal of Biomedical Therapy 2008 ) Vol. 2, No. 3

) In Focus 

The Immune System, 

Our Personal Bodyguard 

By Manfred Schmolz, PhD, and Doris Ottendorfer, PhD 

) 4 

The central role of the 

human immune system 

The complexity of our immune system 

evolved over millions of years 

to minimize the threat by pathogens 

and neoplasms. Although we normally 

are not aware of its subtle 

functions as long as we enjoy our 

health, an early inflammatory reaction 

clearly denotes the beginning 

of the fight of our immune cells 

against invaders, such as viruses, 

bacteria, fungi, and even parasites. 

Close collaboration between innate 

and specific immunity ensures the 

elimination of the infectious agent 

by cellular and/or humoral immune 

responses. In some instances, longlived 

immunity is generated. The 

aim of the present article is to briefly 

outline important mechanisms of 

immune reactions against infectious 

microorganisms. The molecular details 

of these interactions are beyond 

the scope of this article, but they can 

easily be found in the reviews cited. 

Structural organization of the 

human immune system 

Whereas innate immune responses 

are immediately available on contact 

with pathogens, the activation of 

specific immunity takes longer. The 

T and B cells, with their highly diverse 

antigen receptors, play a central 

role in this activation. 

All immune cells originate from hematopoietic 

stem cells in the bone 

marrow. Under the influence of numerous 

cytokines and growth factors, 

the so-called pluripotent stem 

cells differentiate in a multistep process 

into several types of granulocytes 

(i.e., neutrophils, eosinophils, 

and basophils), each of which has 

specialized functions; monocytes 

(which differentiate to the tissue 

macrophages when settling in different 

organs); natural killer (NK) 

cells; and B and T cells. 

The lymph nodes are localized as a 

large network throughout the human 

body to sample antigens from 

the tissues via the lymph vessels. 

Lymph nodes are usually the site of 

sensitization of T cells by antigenpresenting 

cells (APCs). The mucosa-associated 

lymphoid tissue 

(MALT) includes the Peyer’s patches 

along the gastrointestinal tract, the 

tonsils, and the nasal- and bronchusassociated 

lymphoid tissue. All of 

these tissues form highly organized 

structures supporting the interaction 

of antigens with the few available 

antigen-specific lymphocytes circulating 

in the blood or the lymph. 

The MALT is essential as a protective 

barrier at the highly vulnerable 

mucosal surfaces. 1-3 

Innate immunity: 

a powerful first-line defense 

The first defense against infectious 

agents starts when the invader is recognized 

by phagocytes that nonspecifically 

engulf and digest pathogens. 

Even this most primitive 

defense function is a highly complex 

cellular process. 4,5 Two different 

types of phagocytosis exist: the 

removal of pathogens and the elimination 

of apoptotic tissue cells 

(apoptosis means programmed cell 

death). The former causes an inflammatory 

alarm response, whereas the 

latter (which is, for example, necessary 

during embyrogenesis) prevents 

inflammation. Moreover, phagocytosis 

bridges innate and adaptive 

immunity, through antigen presentation. 

The engulfment of pathogens by 

neutrophils and macrophages discriminates 

between diverse particles 

through an array of receptors expressed 

on their surface. Among 

these receptors are several for complement 

proteins, combinations of 

scavenger receptors, and numerous 

integrins, described extensively by 

Stuart and Ezekowitz in 2008. 5 

Most of these receptors are able to 

recognize both pathogens and altered-self 

ligands, such as apoptotic 

cells. 

After receptor ligation by the particle, 

a “phagosome” is formed within 

the phagocyte. This phagosome then 

fuses with a lysosome, generating 

the “phagolysosome.” In the latter, 

the final destruction of pathogens 

occurs by an arsenal of degrading 

enzymes, oxygen radicals, bactericides, 

etc. Proteomic analysis has revealed 

that phagosomes contain 

more than 600 different types of 


) In Focus 

proteins. A key role of phagolysosomes 

is to provide, by only partial 

degradation, the antigenic ligands 

for the stimulation of the T and B 

cells (which are further described 

later in the article). 

Role of toll-like receptors in 

antimicrobial immunity 

The family of receptors called tolllike 

receptors (TLRs) is essential for 

the discrimination between self and 

nonself structures, a central requirement 

for the immune system. This 

topic was extensively reviewed by 

Akira and Takeda 6 and Iwasaki and 

Medzhitov. 7 

The TLRs sense microbial infections 

as a “general danger” to the body, 

recognizing conserved molecular 

structures unique to the microbial 

world and widely invariant among 

the single classes of pathogens. Each 

of these pathogen-associated molecular 

patterns (PAMPs) is detected 

by a different TLR subtype (e.g., 

TLR4 recognizes lipopolysaccharides). 

The PAMPs are among the 

strongest stimuli for immune cells. 

The signal transduction pathways 

that TLRs activate in different immune 

cell subtypes result in a multitude 

of antimicrobial and inflammatory 

responses, which usually lead 

to the elimination of the pathogen. 

The TLRs also do the following: 

1. help recruit cells to infected 

sites by triggering the release of 

chemotactic mediators (chemokines) 

2. help make functionally mature 

APCs 

3. contribute to antiviral immunity 

8 

Therefore, PAMPs very efficiently 

link innate and adaptive immune 

mechanisms, thus potentiating defense 

efficacy. 

The neutrophil: 

a prototypic cell type of antibacterial 

defense 

Neutrophil granulocytes are the 

most abundant cells of the immune 

system. Beyond being pure “eaters 

and killers,” they are recognized as 

major contributors to the overall 

regulation of immune responses. 

Neutrophils also contribute to the 

recruitment, activation, and programming 

of APCs by producing an 

array of cytokines, chemokines, lipid 

mediators, and, last but definitely 

not least, an arsenal of cytolytic 

agents for killing ingested pathogens, 

as described by Nathan. 9 

Among the latter are bactericidal 

peptides (defensins), oxygen radicals 

produced by myeloperoxidase, and 

others. Lactoferrin, or lipocalin, can 

slow down bacterial growth by depleting 

iron at the site of infection. 

In addition, neutrophils secrete factors 

that assist B-cell maturation and 

proliferation and can also function 

as prominent suppressors of T-cell 

function (e.g., by secreting prostaglandins). 

The role of complement 

proteins in immunity 

The complement system deserves attention 

in that this proteolytic machinery, 

resembling in its cascadelike 

mode of action the coagulation 

cascade, effectively interlinks innate 

and specific immune mechanisms. 

First described as a heat-sensitive 

factor in fresh serum that is able to 

“complement” the effects of specific 

antibodies in the lysis of bacteria, 

the complement system now represents 

a system of more than 30 serum 

proteins and cell surface receptors. 

An excellent review on 

complement concerning numerous 

immunoregulatory roles beyond the 

killing of bacteria has been published 

by Carroll. 10 

Messaging between cells of the 

innate immune system 

To accomplish the antibacterial defense 

during innate immune reactions, 

the phagocytosis of microbial 

pathogens is accompanied by the release 

of several messenger molecules, 

such as arachidonic acid metabolites 

(prostaglandins and leukotrienes), 

chemokines, cytokines, and proteases. 

Only a fine-tuned release of these 

hundreds of mediators coordinates 

the activities of different immune 

cells sufficiently to successfully clear 

the tissues of almost all infectious 

microorganisms before they can create 

problems. 

Initiation of an antigen-specific 

immune response against 

infection 

In many cases, the first line of defense 

established by the phagocytes 

is not enough, especially when microbial 

and viral pathogens evolved 

to exhibit sophisticated survival 

strategies. In such cases, antigenspecific 

immune responses are initiated. 

Even these begin with phagocytosis, 

although, as reviewed 

recently by Finlay and McFadden, 11 

some pathogens may resist phagocytosis 

and others interfere with antigen 

presentation. Those pathogens 

that resist digestion and multiply 

within the phagocytes constitute a 

tremendous threat to the body (e.g., 

mycobacteria and parasitic helminth 

worms). Despite their subversive activities, 

these pathogens can be destroyed 

by more specific cellular immune 

mechanisms. There is 

antibody-dependent cytotoxicity 

and enforced cellular immunity; the 

latter results in a profound activation 

of macrophages, boosting them 

to destroy even microorganisms as 

resistant as mycobacteria. Such reenforcement 

usually involves the 

cells from the antigen-specific part 

of the immune system, the T and B 

cells. 

) 5 


) In Focus 

Bacteria display a wide diversity of 

shapes and sizes. Here: Salmonella 

typhimurium (red) invading cultured 

human cells. 

Photo by Rocky Mountain Laboratories, NIAID, NIH, 

http://en.wikipedia.org/wiki/Image:SalmonellaNIAID.jpg 

) 6 

T and B lymphocytes are 

responsible for generating 

antigen-specific immune 

responses 

True antigen specificity resides in 

the T and B lymphocytes, which are 

able to recognize antigens through 

highly specific membrane-bound 

receptors. Each cell has peculiar receptors 

that recognize only one antigen. 

Yet, hypothetically, all B and 

T lymphocytes together are able to 

respond to virtually any antigen in 

the world. The antigen size may 

range from small chemical structures 

to highly complex molecules. The 

receptors of both cell types recognize 

only a small part of large antigens, 

referred to as the epitope. 

Complex antigens usually consist of 

more than one epitope. This tremendous 

variability in T- and B-cell 

specificities is achieved by DNA rearrangement. 

12,13 

Antigens are internalized and processed 

to smaller fragments, which 

are then presented at the surface of 

APCs to “naïve” T cells, teaching 

the latter about the current antigen 

load. Compared with T cells, B cells 

do respond to nondigested epitopes. 

The surface structures to which the 

antigens or the fragments are attached 

are the proteins of the major 

histocompatibility complex (MHC), 

of which 2 classes are highly important 

for immune and tissue cells: 

class I (MHC-I) and class II (MHC- 

II). 

Antigen presentation by MHCs 

Recognition of antigens in the binding 

grooves of MHC molecules by 

specific T-cell receptors (TCRs) is 

the central event to T-cell activation. 

MHC-I, found on all cells of the human 

body, was originally described 

as transplantation antigen(s), being 

the cause for organ rejection. The 

natural function of MHC-I is to 

sample antigens from within the 

cells (e.g., during infection [viruses 

or intracellular bacteria] or tumorigenesis). 

14 The recognition of antigens 

presented by MHC-I molecules 

leads to the activation of cytotoxic T 

cells (CTLs) bearing the CD8 surface 

marker (CD8+ CTLs). 

The MHC-II proteins are found exclusively 

on cells of the immune system 

(e.g., macrophages, B cells, and 

dendritic cells [DCs]). The DCs are 

recognized as the most efficient 

APCs to stimulate naïve T cells. The 

DCs seem to decide which type of 

T-cell response is induced by different 

antigens (Reis e Sousa 15 and 

Shortman and Naik 16 provide reviews). 

In contrast to MHC-I molecules, 

MHC-II molecules sample 

antigens from the extracellular space 

to activate CD4-positive (CD4+) T- 

helper (Th) cells. 

Effector/inflammatory CD4+ 

Th cells and cytotoxic CD8 T 

cells 

Viruses are crucial pathogens because 

they hide and multiply inside 

susceptible tissue cells. Antibodies 

neutralize viruses only outside cells 

(i.e., before they enter target cells or 

when they are released by these cells 

after replication). The elimination of 

virus-infected host cells is, therefore, 

a real challenge for the immune system. 

Evolution enabled infectious pathogens 

(i.e., viruses, bacteria, and parasites) 

to develop improved strategies 

to override the immune defense, 

which, in turn, improved its effector 

mechanisms to destroy even these 

pathogens. This is the reason why 

we have specialized populations of 

T cells, such as CTLs and various Th 

cells. 

Basically, CD4+ T-cell activation is 

initiated by the interaction of the 

antigen receptor (TCR) with antigen/MHC-II 

complexes on APC 

surfaces. Antigen/MHC-II complexes 

trigger a complex concert of 

intracellular signals, activating a 

whole series of genes that control 

the proliferation, differentiation, and 

effector functions of T cells. Antigen-specific 

T-cell activation is initiated 

only when these signals are 

strong enough. 17 When a T cell is 

activated, it proliferates to give a 

clone, with each clone cell having 

the same TCR specificity as the parent 

cell. Notably, proliferation needs 

several growth factors (e.g., the very 

well-known interleukin [IL] 2). IL-2 

is the prototype of a T-cell growth 

factor and acts to promote proliferation 

and differentiation of antigenactivated 

T cells. 18,19 


) In Focus 

A macrophage forming two processes 

to phagocytize two smaller particles. 

Photo by magnaram; licensed under the Creative Commons 

Attribution ShareAlike 2.0 (http://creativecommons. 

org/licenses/by-sa/2.0/), http://en.wikipedia.org/wiki/ 

Image:Macrophage.jpg 

CD4+ T cells activate cellular 

immunity 

A core function of CD4+ T cells in 

antibacterial defense is the re-enforcement 

of tissue macrophages to 

better kill intracellular parasites and 

bacteria that otherwise may survive 

phagocytosis and use these cells as 

incubators. Macrophage activation 

by T cells is essential to cellular immunity 

against pathogens, such as 

leishmania and mycobacteria. This 

activation of macrophages depends 

on cytokines from activated CD4 

Th cells, most importantly interferon 

(IFN) γ, which is also provided 

by NK cells. Other cytokines supporting 

cell-mediated immunity are 

mediators, such as IL-12 and IL-18, 

which are produced by activated 

APCs in a positive feedback loop. 

Macrophages activated in this manner 

express a higher ability to present 

antigens, provide stronger costimulation, 

and secrete more 

activating cytokines (e.g., IL-1, IL-6, 

and IL-10) or tumor necrosis factor 

a. Moreover, the CD4+ T lymphocytes 

are important helper cells for 

antiviral CTLs. CD4+ T cells are 

not only crucial for macrophage activation 

but also provide help to B 

cells by secreting growth factors favoring 

antibody production. 

Cytotoxic CD8+ T cells and Therefore, NK cells effectively limit 

NK cells kill virus-infected and the early spread of infection. 

tumor cells 

CD8+ CTLs recognize antigens by 

Virus-specific CD8+ CTLs are the their TCR in association with MHCmajor 

effector cells for eliminating I molecules. In addition, similar to 

established viral infections. NK cells CD4+ T cells, CD8+ T cells need 

also lyse virus-infected cells and tumor 

cells. Therefore, both cell types fector functions. 

clonal expansion to establish full ef- 

are often summarized as cytotoxic 

lymphocytes. It seems that both cell Role of IFN synthesis in 

types share common mechanisms antiviral immunity 

for antiviral and antitumor defense. 

20-22 For example, both cell dent killing mechanisms, soluble 

In addition to cell contact-depen- 

types secrete the cytotoxic protein mediators released during viral infection 

of cells directly stimulate the 

perforin, along with granzymes. Together, 

they kill infected cells and production of IFNs, of which type 1 

tumor cells on cell-to-cell contact. IFNs (α and β) possess the strongest 

This is a thoroughly controlled process 

to kill only the diseased target are produced by many cell types and 

direct antiviral activity. Type 1 IFNs 

cell (not healthy neighbor cells). cause an “antiviral state” in the infected 

cells; this state is character- 

The most important difference between 

the CTL and NK cells is that ized by inhibition of viral replication 

and cell proliferation. Type 1 

NK cells do not have a TCR; NK 

cells recognize virally infected cells IFNs also enhance NK cell activity 

by their ability to recognize and lyse to lyse target cells and improve antigen 

presentation in APCs. 

virally infected cells by other receptors 

showing a more general specificity 

for pathogen-induced changes Multiple ways to control T-cell 

in tissue cells (e.g., intracellular infection 

or neoplasia). Other NK cell T-cell responses do not only con- 

activation 

receptors possess inhibitory activity, sume lots of energy by clonal expansion 

but are also highly power- 

enabling a close control of cell killing. 

23 

ful when it comes to destroying 

The major advantage that NK cells tissue cells. Taken together, the costs 

have over antigen-specific CD8+ T of false alarms are high; therefore, 

cells is that they kill target cells such a process needs to be controlled 

without the need for clonal expansion 

(i.e., without a “lag” phase). 

strictly. 

) 7 


) In Focus 

) In Focus 

The elimination of viruses is a real 

challenge for the immune system. 

© Sebastian Kaulitzki/Fotolia.de 

) 8 

The ability of T cells to become activated 

primarily depends on the 

signal strength received by the TCR; 

therefore, only those T cells showing 

the best binding fit to the antigen 

will become fully activated. Another 

potent means to effectively 

control T-cell activation is by “costimulation.” 

This is accomplished 

by a series of costimulating counterreceptors 

on the APC surface binding 

to ligands on T cells. These add 

positively and negatively to the regulation 

of the proliferation and differentiation 

of a given T-cell clone. 

One of the best characterized costimulation 

signals is induced by the 

CD28/CD80 receptor pair. 24 

Finally, much progress has been 

made to characterize the functional 

diversity of T cells, leading to the 

current description of subpopulations 

such as the Th cells (Th1, Th2, 

and Th3) and the regulatory T cells 

(which have been extensively reviewed 

by Kalinski and Moser 25 and 

Belkaid 26 ). Briefly, each of these 

subtypes of T cells expresses its own 

spectrum of activities and soluble 

mediators that it secretes. The Th1 

cells are involved in cell-mediated 

immunity, the Th2 cells support antibody 

production and participate in 

the induction of hypersensitivity, 

and the Th3 and Treg cells can generally 

be seen as the protectors 

(“down-regulators”) against reactions 

that are too strong, outdated, 

or undesired. Interestingly, the decision 

as to which type of T cell is 

generated is probably met largely by 

DCs, which are able to polarize 

nondifferentiated T cells toward 

these functional subtypes. This concept 

is a subject of continuing debate. 

25 

Humoral immunity: the generation 

of antibodies 

B cells are the only cells that produce 

antibodies (immunoglobulins). 

As with T cells, each B cell is specific 

for a particular epitope on an 

antigen (e.g., protein or carbohydrate). 

Antigens are specifically recognized 

by surface-anchored antibodies 

on these cells. By this B-cell 

receptor, antigens can be internalized. 

They are then broken down 

into fragments and displayed at the 

B-cell surface together with MHC- 

II to CD4+ Th cells, which subsequently 

trigger the activation of the 

presenting B cell. Activated B cells 

develop into plasma cells, producing 

huge amounts of antibodies of the 

same specificity as the B-cell receptor 

on their surface originally encoded. 

In the further course of the 

immune response, the interaction 

with T cells causes the B cells to 

switch their production from immunoglobulin 

M (IgM), which is always 

the first to be secreted, to the 

more versatile IgG. 

Effector functions of different 

antibody classes 

In humans, 5 different classes of immunoglobulins, 

called isotypes, are 

known (i.e., IgM, IgG, IgA, IgE, and 

IgD). These immunoglobulins all 

have different structures and activities. 

On primary activation, B cells 

first always synthesize IgM, peaking 

about 7 to 10 days after initial exposure. 

Because of its pentameric 

structure, representing 10 binding 

sites for antigen per IgM, IgM is 

particularly potent for agglutinating 

antigens, enhancing phagocytosis, 

and activating complement. 

At some point during B-cell activation, 

these lymphocytes can switch 

from IgM to a different class of antibodies. 

The most prominent of these 

antibodies is IgG. Its capacity to 

“coat” bacteria to improve phagocytosis 

is called opsonization. IgG also 

neutralizes microbial toxins, blocks 

viral adherence to target cells, activates 

complement, and is the main 

antibody found on repeated antigen 

contact. 

IgA, on the other hand, is the antibody 

found primarily in mucus, colostrum, 

and milk. It protects against 

respiratory and gastrointestinal tract 

infectious agents. 

Finally, IgE is produced in response 

to parasites and is also a characteristic 

mediator of type 1 allergy. In 

both of these instances, IgE collaborates 

closely with Th2 cells to shape 

this particular type of immune response. 

27 


) In Focus 

Antibodies usually neutralize viruses 

through binding to their surface, 

blocking the virus from entering the 

host cell. In addition, some viral infections 

lead to the expression of 

viral proteins on the surface of infected 

cells. These may bind virusspecific 

antibodies, leading to complement-mediated 

lysis, or activate a 

subset of NK cells to lyse infected 

cells through antibody-dependent 

cellular cytotoxicity. 

Immune cell memory 

Adaptive immune responses lead to 

a state of long-lived immunity, 

which is established by the generation 

of memory cells in the T- and 

B-cell lineage, exhibiting the same 

antigen specificity as their parent 

cells. By contrast, innate defense 

does not create memory. The advantage 

of memory cells is that they can 

be activated upon any repeated contact 

with their specific antigen much 

more rapidly than on first contact, 

which helps to keep reinfection 

down efficiently. 

Intercellular communication 

during infection 

The communication between different 

immune cells to establish a wellcoordinated 

response during antimicrobial 

defense, as previously 

described, would be impossible 

without the help of the vast array of 

soluble mediators that evolution 

elaborated to fine-tune immune responses. 

They comprise a large number 

of chemokines, cytokines, and 

growth factors; there are also whole 

series of lipid-derived mediators, 

proteases, antiproteases, coagulation 

cascade-derived mediators, kinins, 

and even neurotransmitters. All of 

these bind to receptors on the cells 

of the immune system and modify 

their reactions in a highly controlled 

manner. Most of these mediators 

form positive- and negative-feed- 

back signaling loops that timely adjust 

the general type and the extent 

of response to the current needs, 

which in fact differ substantially between 

the different types and phases 

of a defense reaction. 

Concluding remarks 

Immunological knowledge is growing 

fast. The recent discovery of the 

TLRs and their functions and of 

functionally different DC types, the 

ever-growing list of lymphocyte 

subpopulations displaying different 

functions, and the enormous amount 

of newly discovered mediators have 

contributed tremendously to our 

understanding of antimicrobial immunity. 

In addition, these discoveries 

are helping us understand the 

switch from well-regulated immune 

responses to detrimental conditions 

such as chronic inflammation. Readers 

are encouraged to consult one or 

more of the articles cited herein, 

which will provide a deeper guide 

into the complex and highly fascinating 

world of the immune system, 

our personal bodyguard.| 

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5. Stuart LM, Ezekowitz RA. Phagocytosis and 

comparative innate immunity: learning on the 

fly. Nat Rev Immunol. 2008;8(2):131-141. 

6. Akira S, Takeda K. Toll-like receptor signalling. 

Nat Rev Immunol. 2004;4(7):499-511. 

7. Iwasaki A, Medzhitov R. Toll-like receptor 

control of the adaptive immune responses. 

Nat Immunol. 2004;5(10):987-995. 

8. Kawai T, Akira S. Innate immune recognition 

of viral infection. Nat Immunol. 

2006;7(2):131-137. 

9. Nathan C. Neutrophils and immunity: challenges 

and opportunities. Nat Rev Immunol. 

2006;6(3):173-182. 

10. Carroll MC. The complement system in regulation 

of adaptive immunity. Nat Immunol. 

2004;5(10):981-986. 

11. Finlay BB, McFadden G. Anti-immunology: 

evasion of the host immune system 

by bacterial and viral pathogens. Cell. 

2006;124(4):767-782. 

12. Chaudhuri J, Alt FW. Class-switch recombination: 

interplay of transcription, DNA 

deamination and DNA repair. Nat Rev Immunol. 

2004;4(7):541-552. 

13. Schlissel MS. Regulating antigen-receptor 

gene assembly. Nat Rev Immunol. 

2003;3(11):890-899. 

14. Vyas JM, Van der Veen AG, Ploegh HL. 

The known unknowns of antigen processing 

and presentation. Nat Rev Immunol. 

2008;8(8):607-618. 

15. Reis e Sousa C. Dendritic cells in a mature 

age. Nat Rev Immunol. 2006;6(6):476-483. 

16. Shortman K, Naik SH. Steady-state and inflammatory 

dendritic-cell development. Nat 

Rev Immunol. 2007;7(1):19-30. 

17. Acuto O, Bartolo VD, Michel F. Tailoring 

T-cell receptor signals by proximal negative 

feedback mechanisms. Nat Rev Immunol. 

2008;8(9):699-712. 

18. Waldmann TA. The biology of interleukin-2 

and interleukin-15: implications for cancer 

therapy and vaccine design. Nat Rev Immunol. 

2006;6(8):595-601. 

19. Taniguchi T, Minami Y. The IL-2/IL-2 receptor 

system: a current overview. Cell. 

1993;73(1):5-8. 

20. Voskoboinik I, Smyth MJ, Trapani JA. 

Perforin-mediated target-cell death and 

immune homeostasis. Nat Rev Immunol. 

2006;6(12):940-952. 

21. Trapani JA, Smyth MF. Functional significance 

of the perforin/granzyme cell death 

pathway. Nat Rev Immunol. 2002;2(10):735- 

747. 

22. Orange JS. Formation and function of the 

lytic NK-cell immunological synapse. Nat Rev 

Immunol. 2008;8(9):713-725. 

23. Kumar V, McNerney ME. A new self: MHCclass-I-independent 

natural-killer-cell selftolerance. 

Nat Rev Immunol. 2005;5(5):363- 

374. 

24. Acuto O, Michel F. CD28-mediated co-stimulation: 

a quantitative support for TCR signalling. 

Nat Rev Immunol. 2003;3(12):939- 

951. 

25. Kalinski P, Moser M. Consensual immunity: 

success-driven development of T-helper-1 

and T-helper-2 responses. Nat Rev Immunol. 

2005;5(3):251-260. 

26. Belkaid Y. Regulatory T cells and infection: 

a dangerous necessity. Nat Rev Immunol. 

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) 9 


) What Else Is New? 

A recent study has shown that individuals 

with long arms have a lower risk of 

developing dementia than people with 

short extremities. 

Short arms, short memory? 

Alzheimer’s is more common in individuals 

with short arms and legs 

than in people with long extremities. 

At least, that’s the conclusion of 

a recent American study of approximately 

2,800 older subjects (average 

age = 72). 480 of the participants 

developed dementia during the fiveyear 

observation period. The risk of 

dementia was significantly higher 

among women with short arms and 

legs. In men, however, only arm 

length correlated with dementia 

risk. A possible explanation suggested 

by the researchers is that poor 

nutrition and lack of medical care in 

childhood might not only produce 

shorter limbs but also increase the 

risk of dementia in later life. 

Neurology. 2008;70(19):1818-1826 

No scientific proof of the 

health benefits of drinking 

more water 

How much water should you drink 

in a day? According to common recommendations, 

eight glasses, or 

approximately one and a half liters. 

It remains debatable, however, 

whether increased water consumption 

is necessary for health, aids in 

weight loss, or keeps skin firm. In an 

analysis of all available clinical studies 

on this topic, scientists from 

Philadelphia (USA) recently concluded 

that such claims don’t hold 

water. True, the kidneys get a good 

rinsing, but there was no evidence 

of clinical benefits to kidney or other 

organ functions. 

Am Soc Nephrol. 2008;19(6): 

1041-1043 

Autohemotherapy helpful 

in heart failure 

In certain patients with chronic 

heart failure, autohemotherapy can 

reduce the risk of death or hospitalization, 

according to a study of 

2,426 patients with chronic heart 

failure. Over a period of 22 weeks, 

participants received at least eight 

intragluteal injections containing either 

their own blood or a placebo. 

Primary endpoints in the study were 

death or admission to a hospital. 

Autohemotherapy significantly delayed 

both endpoints in patients 

who had not yet suffered a heart attack 

and in patients with NYHA 

Stage II cardiac insufficiency. 

Lancet. 2008;371(9608):228-236 

) 10 

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products and/or ingredients (which may be different depending on the regulatory environment in your country), and is not intended to diagnose any illness, nor is it 

intended to replace competent medical advice and practice. IAH or anyone connected to, or participating in this publication does not accept nor will it be liable 

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articles in this journal. 

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The intent of the scientific information contained in this journal is not to “dispense recipes” but to provide practitioners with “practice information” for a better 

understanding of the possibilities and limits of complementary and integrative therapies. 

Some of the products referred to in articles may not be available in all countries in which the journal is made available, with the formulation described in any article or 

available for sale with the conditions of use and/or claims indicated in the articles. It is the practitioner’s responsibility to use this information as applicable 

and in a manner that is permitted in his or her respective jurisdiction based on the applicable regulatory environment. We encourage our readers to share 

their complementary therapies, as the purpose of the Journal of Biomedical Therapy is to join together like-minded practitioners from around the globe. 

Written permission is required to reproduce any of the enclosed material. The articles contained herein are not independently verified for accuracy or truth. They have 

been provided to the Journal of Biomedical Therapy by the author and represent the thoughts, views and opinions of the article’s author. 


) What Else Is New? 

Let’s have another cup … 

Regular coffee consumption protects 

the liver against cancer, and the effect 

increases with the amount of coffee 

consumed. 

The hormone ghrelin not only gives 

you a sensation of hunger – it also 

makes food look simply irresistible … 

Coffee for liver protection? 

Coffee protects the liver against cancer 

and the effect increases with the 

amount of coffee consumed, according 

to an Italian meta-analysis of 11 

original studies. The study’s findings 

are significant: Regular coffee 

consumption reduces the risk of liver 

cancer by almost 40 percent. The 

protective effect was evident even in 

subgroups of patients with pre-existing 

hepatitis or cirrhosis. 

This effect may be due to the presence 

of cafestol and kahweol diterpenes 

in coffee. In animal experiments, 

these compounds have been 

shown to modulate enzymes active 

in the detoxification of carcinogens. 

In vitro, caffeine also demonstrates 

antioxidant effects and inhibits lipid 

peroxidation. It has also been associated 

with improvement in liver 

transaminases. 

Hepatology. 2007;46(2):430-435 

Gastroenterologe. 2008;3(1):53-54 

“Spectator stress” can be 

dangerous! 

Half of Germany sat in front of the 

TV, on the edge of their seats as the 

German team competed in the title 

match of the European soccer championship. 

That’s not necessarily safe 

entertainment, according to a study 

conducted in Germany during the 

World Cup two years ago. Emergency 

physicians prospectively assessed 

cardiovascular events occurring in 

patients in the greater Munich area. 

They discovered that the statistical 

probability of suffering a cardiovascular 

event doubled when the German 

team was playing. Men were 

affected significantly more often 

than women, and the risk was especially 

high among those with preexisting 

coronary heart disease. So the 

physicians urged heart patients to 

take preventive measures, such as 

taking appropriate medication, before 

the German team’s games or 

similar important events. They also 

said that behavioral therapy to improve 

stress management could be 

helpful in the long term. 

N Engl J Med. 2008;358(5):475-483 

Hunger hormone makes 

foods look more appetizing 

The hunger hormone ghrelin 

(“growth hormone release inducing”) 

not only makes people feel 

hungry but also heightens responses 

to food stimuli, as Canadian scientists 

recently discovered. According 

to their study, the hormone (formed 

in the epithelium of the empty stomach) 

does more than simply encourage 

eating by causing sensations of 

hunger – it also makes specific brain 

regions more receptive to visual 

stimuli from food, which increases 

the urge to indulge in eating for 

pleasure. According to the study, 

ghrelin works on reward centers in 

the brain that are also affected by 

drug dependency, making what we 

call “hunger” nothing more than an 

eating addiction of sorts. The authors, 

however, warn against using 

ghrelin blocking medications as 

therapy for obesity, considering it 

too risky, since ghrelin affects brain 

regions where emotions and motivations 

arise. 

Cell Metabolism. 2008;7(5):400-409 

) 11 


) From the Practice 

Acute Recurrent Otitis Media 

By Ivo Bianchi, MD 

) 12 

Acute otitis media is a bacterial or viral infection of the 

middle ear. Pediatric cases are very common and usually 

recurrent. In children with a genetic-constitutional 

predisposition to this problem, every upper respiratory 

tract infection can be complicated by otitis media. 

Symptoms include otalgia that is 

often very acute, usually worsens 

at night, and is sometimes accompanied 

by nausea, vomiting, diarrhea, 

and fever. Although acute 

otitis media can occur at any age, it 

is most common between the ages 

of 3 months and 3 years, when the 

Eustachian tube is structurally and 

functionally immature and the 

mechanism that opens and drains 

the middle ear is less efficient. This 

condition is often stressful for the 

family and very painful for the child. 

According to recent surveys, antibiotics 

and decongestants have not 

been proven to be of value. In my 

experience, homotoxicology and 

homeopathy offer a valid method of 

treating this common condition. 

Clinical case 

A young mother brought her twoyear-old 

son to my office for recurrent 

acute episodes of otitis media. 

These episodes were extremely frequent, 

especially during the cold, 

damp season, and required frequent 

administration of antibiotics. In one 

episode, otitis media was complicated 

by acute mastoiditis, requiring 

hospitalization of the child. The 

situation had become almost chronic, 

and the child often seemed offbalance. 

The family medical history 

included the mother with frequent 

seasonal rhinopharingitis and a paternal 

uncle with allergic asthma. 

Upon examination, I found laterocervical 

microadenopathy, reddened 

pharynx, and hyperaemic tonsillar 

membranes. Thoracic and abdominal 

findings were normal. Generally, 

the child looked frail and thin but 

well-proportioned. He was gentle, 

shy, and timid. 

I asked the mother for additional 

clinical information, and she reported 

a normal childbirth with a birth 

weight of 3.5 kg. The child was 

breast-fed for 6 months. Ever since 

his first months, he has perspired 

profusely during sleep, especially in 

the occipital region, and tended to 

sleep without bedclothes. He used 

to gnash his teeth during the night. 

He has always had (and still has) a 

tendency toward diarrhea. 

At this point, I had sufficient information 

to develop a homeopathic 

and homotoxicological treatment 

strategy based not only on the 

child’s clinical history and symptoms 

but also on the homotoxicological 

constitution he presented. 

Therapy was based on the model of 

the three pillars of homotoxicology. 

1. Drainage: 

• Lymphomyosot: 8 drops 

morning and evening. 

2. Cellular activation and 

organ regulation: 

• Mucosa compositum: 

1 ampoule via the mucosa 

2 times a week for 3 months, 

increasing to once daily (in 

the evening) during upper 

respiratory infections (even 

in the early stage) to improve 

the structural condition of 

the upper respiratory tract. 

• Coenzyme compositum: 

½ ampoule orally 2-3 times 

a week for 6 months, 

according to appetite levels 

and general condition. 

• Belladonna-Homaccord: 

½ ampoule every 6-8 hours 

in acute ENT inflammatory 

conditions, especially if fever 

is present. 


) From the Practice 

Vestibular 

cochlear nerve 

Anatomy of the inner ear 

© OOZ/Fotolia.de 

Cochlea 

• Traumeel ampoules or Oteel: 

2 drops locally in the ear for 

inflammation and pain, every 

10-30 minutes during acute 

phases until improvement is 

noted. 

3. Immunomodulation: 

• Echinacea compositum forte: 

½ ampoule in the evening 

twice a week for 6 months, 

increasing to every 6 hours 

during acute upper respiratory 

infections until improvement 

is noted. This 

medication is our antibacterial 

support and immunomodulator. 

• Psorinoheel: ½ ampoule 

orally in the evening for 6 

months, to stimulate the 

immune system. 

• Calcium carbonicum-Injeel: 

1 ampoule orally in the 

morning once a week, to 

strengthen the constitutional 

response. 

• Osteoheel: 2 tablets daily (1 

each, morning and evening) 

during the winter to 

strengthen the reactivity of 

the osteocartilaginous tissue. 

This therapeutic protocol may seem 

complicated. Rather than just a simple 

therapy, it is a real strategic plan 

Eardrum 

to fight the disease and its symptoms, 

prevent complications, and 

stimulate general and local immune 

responses in order to prevent relapses. 

The mother was well-motivated 

and the whole therapy was administered 

correctly. After six months, the 

child had improved both in terms of 

localized symptoms and also more 

generally, in terms of appetite, 

strength, and mood. No other recurrences 

were reported, and I then recommended 

a simple maintenance 

therapy for the winter and early 

spring: 

Common factors related to 

acute otitis 

• Lymphomyosot: 

8 drops morning and evening. 

• Mucosa compositum: 

1 ampoule via the mucous 

membranes 2 times a week. 

• Echinacea compositum forte: 

½ ampoule in the evening twice 

a week. 

• Calcium carbonicum-Injeel: 

1 ampoule orally in the morning 

once a week. 

I continue to see the child every 

six months. Three years after the 

first consultation, he is in perfect 

shape physically and psychologically. 

| 

Viral infections 

Bacterial infections 

Genetic-constitutional 

factors 

Anatomical factors 

Exposure to smoke 

or pollution 

Eustachian tube 

Gastroesophageal reflux 

Factors related to otitis media 


) M a r k e t i n g Yo u r P r a c t i c e 

Managing Expenses and Prices 

in the Medical Practice 

By Marc Deschler 

Marketing specialist 

Have you ever asked yourself how much it costs to 

administer your practice? On average, administration 

costs can account for approximately ten percent of 

revenue. In this context, it is interesting to know which 

line items your national Bureau of Statistics includes 

under the heading “other costs.” Check to see whether 

you spot any potential for savings there. 

Office supplies and legal and accounting/tax 

preparation fees 

are often major entries. It can be 

well worth the effort to solicit competing 

bids and/or to renegotiate 

these costs. Be especially aware of 

how your spending on office supplies 

has changed over the last few 

years. You should also have logical 

explanations for any fluctuations in 

legal and accounting fees. To get an 

overview, I recommend making a 

list of costs accrued over a specific 

time period. Beyond your major expenses, 

don’t forget to add in what 

you spend on: 

• postage 

• telephone bills 

• office cleaning and disinfection 

• business entertainment 

• service contracts 

• purchases up to $50 

• uniforms and linens 

• waiting room reading material 

• gifts and office décor 

• incidental expenses and bank 

fees 

• other administrative expenses 

Your accountant should be able to 

provide a balance sheet showing 

this information. If there are any 

fluctuations you really cannot account 

for, discuss them with your 

accountant. 

Losses due to purchases 

Excessive expenses can occur in all 

aspects of a medical practice. Uneconomical 

behavior, for which 

there are many possible reasons, is 

often to blame. How purchases are 

made in your practice, for example, 

is a potential cause of losses. Use the 

following checklist to analyze purchasing 

behavior in your practice. 

1. Purchases are not planned. Supplies 

are often purchased only 

when they have already run out, 

when no one is likely to pay 

much attention to price and quality. 

) 14 

Have you ever analyzed the purchasing 

behavior in your practice? 

A few simple strategies can help you 

avoid unnecessary costs.

2. Work is delayed because supplies 

were not purchased in advance 

and are not available 

when needed. (E.g., emergency 

trips to the pharmacy for injectable 

medications.) 

3. Bulk purchases result in discounts 

but tie up too much 

capital for too long, or storage 

becomes a problem. 

4. Opportunities for discounts for 

cash payments are frequently 

overlooked. 

5. You always purchase from the 

same supplier as a matter of 

habit, without soliciting competing 

bids. 

6. It doesn’t occur to you to split 

bulk orders with other practices. 

Checking any of the above indicates 

weaknesses in the management 

of your practice that you 

should think about. But before you 

make changes in your purchasing 

behavior, categorize your expenses 

to identify where your efforts will 

pay off. So-called ABC analysis is a 

time-tested mechanism that helps 

you analyze and determine the relative 

budgetary impact of different 

items and suppliers. Here, as in 

many other areas, the 80/20 principle 

applies; that is, approximately 

20 percent of goods purchased account 

for 80 percent of spending 

(category A, in ABC analysis) and 

merits special attention. Make a list 

of all the supplies you purchase, 

along with the price for each item 

and how much you use in a year, 

and then calculate the cost of a 

year’s supply of each. Now list the 

items in order of percentage of total 

annual spending. The items that 

together account for 80 percent of 

your costs deserve a closer look. 

The others can be safely disregarded; 

they will take care of themselves 

in any subsequent reorganization. 

Discussing fees for services 

in your practice – what 

to do when patients are 

not accustomed to paying 

out-of-pocket? 

“Management,” “marketing,” and 

“sales” are words many physicians 

are not accustomed to using, but I’m 

convinced that medical practices today 

are medical “service providers” 

and need to function like the commercial 

enterprises they are. To ensure 

a reasonable income, a commercial 

venture must sell something and 

make its prices “palatable” to consumers. 

For this reason, talking 

about fees for your services should 

become a matter of course. Don’t be 

embarrassed to discuss the prices of 

additional services with your patients. 

Broach the subject and explain 

why there is an extra fee for a 

particular additional service that insurance 

may not cover. Health and 

beauty are very important in today’s 

society, so “selling” elective therapeutic 

services is not very difficult if 

you simply keep a few rules in mind. 

It’s important that you initiate the 

conversation. Don’t wait for the patient 

to bring up the subject of price, 

regardless of which one of you 

brought up the subject of treatment. 

Steps in the financial 

conversation: 

Step 1: Introduce the conversation 

by establishing a common basis. 

Make sure you both agree that the 

proposed treatment makes sense. 

Step 2: Make it clear that this service 

may not be covered by supplementary 

insurance. No big explanation 

is needed. 

Step 3: Next, present the advantages 

(some, not all of them!) of this 

course of treatment. At this stage, 

it’s especially important to remain 

calm and objective. Avoid giving the 

impression that you want to talk 

your patient into it. 

Step 4: Give the patient something 

to look at. You should have an information 

sheet at hand on each extra 

service you offer. 

Step 5: Now it’s time to discuss the 

fee. Never say, “The whole course of 

treatment will cost $400.” Of course 

your patient’s reaction will be, “I 

can’t afford that!” Think about how 

to break the fee down into small installments. 

For example, “I suggest 

starting with three sessions, each of 

which will cost $40. After that, we 

can see how you’re doing and decide 

whether or not to continue.” 

Your patient’s reaction? “$40 is reasonable, 

and I can always still change 

my mind.” 

Step 6: Now discuss additional advantages 

for the patient. 

Step 7: Suggest that the patient take 

the brochure home and think about 

it. Don’t press for an immediate decision. 

This gives your patient a way 

out if s/he can’t commit to the expense 

on the spot. 

Step 8: With your patient’s consent, 

say you’ll call to discuss how to proceed. 

There is no objectionable wheeling 

and dealing in any of these steps. 

They simply make it easier for you 

to offer valuable therapies to your 

patients. | 

) 15 


) Re f r e s h Yo u r H o m o t ox i c o l o g y 

Theories of Immunosenescence 

and Infection 

Cytomegalovirus, Inflammation, and Homotoxicology 

By Jhann Arturo, MD, MRes, MSc, PhD 

) 16 

Introduction 

Aging is generally a complex process 

which forms part of the cycle of 

physiological cell growth where living 

organisms going through one of 

the phases of tissue evolution undergo 

the hardest and most irreversible 

processes of tissue deterioration. 

This is based on cell wear and tear 

(increase in chromosomal and telomeric 

alterations) 1 and matrix wear 

and tear (protein and lymphatic deterioration), 

accelerated catabolism 

(increase in post-transductional protein 

changes and in oxidation with 

increased apoptosis), and loss of the 

regenerative capacity of tissues over 

time (loss of mitochondrial function 

and stem cell reparation). 

This progressive deterioration, considered 

to be physiological, affects 

not only the internal organs but also 

the skin, the central nervous system, 

and the immune system. The involvement 

of the immune system affects 

the ability to attack microbes, 

tumors, chemical or physical agents, 

or toxins (by slowing it down, diminishing 

it, down-regulating it, or 

preventing it altogether), compromising 

the organism’s general immunity. 

This immune aging is known 

as immunosenescence, and it is particularly 

important in current clinical 

practice, since an understanding 

of these subtle biological changes 

can provide us with the tools to carry 

out suitable immunotherapy in 

the clinical field. 

Changes in the immune system 

with aging 

The immune system consists of a 

complex network of cell subtypes, 

membrane receptors, chemical communication 

signals (cytokines and 

chemokines), and humoral defense 

elements (antibodies, complement, 

immune peptides) which together 

enable the defenses to work in harmony, 

and other tissues such as the 

extracellular matrix, and the lymphatic, 

neuroendrocrine, and metabolic 

systems to remain in homeostasis. 

The main features recognized 

to date in immunosenescence 2 are 

shown in Table 1. For example, it 

has been observed that young individuals 

have an adequate population 

of T lymphocytes producing interleukin 

(IL) 2, responsible for the 

clonal expansion of other T lymphocytes. 

However, elderly individuals 

have T cells with low IL-2 production 

and consequently far slower 

T cell clonal expansion which gives 

rise to incomplete or reduced immune 

responses. 3 These incomplete 

immune responses generally result 

in diseases: autoinflammation, autoimmunity, 

neoplastic processes (leukemias/lymphomas, 

cancer), or degenerative 

processes (Alzheimer’s 

disease). 

There are many factors which affect 

the TCD3+ cells in the elderly, but 

it is clear that one of the main types 

of damage to TCD3+ cells is caused 

by oxygen free radicals resulting 

from oxidative stress. It is important 

to mention that despite having high 

levels of free radicals, elderly individuals 

also appear to have high antioxidant 

levels in plasma. 4 Repeated 

accumulation and the increasingly 

chronic nature of the oxidative process 

therefore seem to cause the 

TCD3+ cells to become destabilized. 

Chronic inflammation and 

chronic infection in the elderly 

The most important impact of immune 

dysfunction in old age is, 

however, chronic inflammation (inflamm-aging). 

5 New theories and 

studies demonstrate how persistent, 

chronic inflammation throughout 

life (including that related to birth) 

is responsible for morbidity in old 

age. 6 The slow and on occasion imperceptible 

production of inflammatory 

mediators such as C-reactive 

protein, fibrinogen, amyloid protein, 

and cytokines such as platelet-derived 

growth factor, IL-6, IL-10, tumor 

necrosis factor (TNF) a, and 

transforming growth factor β alters 

the vascular epithelium and causes 

tissues to become chronically inflamed 

and to degenerate. The most 

important cause of this persistent inflammation 

is infectious diseases 

which contribute to a chronic state 

of immune activation and, over time, 

immunodeficiency. Some of the key 

microorganisms that produce chronic 

inflammation in humans are: 



Immune component 

Abnormality in immunosenescence 

Table 1: 

Main defects in immunosenescence 

Hematopoietic stem cells 

T lymphocytes 

B lymphocytes 

NK cells 

Increase in hematopoietic progenitor cell counts CD34+ 

Increase in circulating cytotoxic TCD8+/CD28+ lymphocytes 

Reduction in the quantity of naïve TCD3+/CD45RA+ cells 

Reduction in TCD3+/CD8+/CD45RO+ memory lymphocytes 

Reduction in CD4/CD8 ratio < 1.2 

Increase in B lymphocyte polyreactivity 

Reduction in specificity and quantity in antibody production 

Increase in the expression of receptor activators of 

NKCD16+/CD56+ and NKT CD16+/CD56+CD3 

• viruses: cytomegalovirus (CMV), 

hepatitis B virus, 7 hepatitis C virus, 

virus G, herpes virus type 6, 

-7, -8; 

• bacteria: Chlamydia, Toxoplasma, 

Helicobacter pylori, Mycobacteria, 

Mycoplasma, Listeria, Brucella, and 

Borrelia. 8 

Macrophages 

Lymph nodes 

Several recent studies have shown 

that populations of elderly patients 

have excess TCD8+ (cytotoxic) 

lymphocytes in their peripheral 

blood, compared to a healthy young 

or adult population, and these cell 

groups are linked by serological 

markers positive for CMV. 9 Although 

the risk of infection is higher 

than 70% according to study 

groups, this lentivirus has been 

shown to be capable of producing 

asymptomatic, persistent viral replications, 

causing chronic, undiagnosed, 

and untreated infections. 10 It 

is not known whether the loss of 

TCD3+/CD4+ lymphocytes in old 

age is caused directly by CMV (as 

has been seen in other diseases) or 

whether it is simply an opportunistic 

pathogen, but it is known that 

the reduction in the CD4/CD8 ratio, 

with increased cytotoxic TCD8+ 

expansion and being seropositive 

for CMV increases mortality in the 

first 4 years in more than 90%. 11 

The formulation of anti-CMV antiviral 

protocols should therefore be 

considered in patients with a suspected 

viral infection, and immunostimulant 

products specific to the 

cytotoxic functions of T cells should 

be considered in patients with a 

CD4/CD8 ratio below 1.2 (normal 

value 1.5 ± 0.3). CMV is thus directly 

concerned and is one of the 

main agents involved in immune deterioration, 

and from this point of 

view immunosenescence, with the 

loss of T cells, could be highly infectious 

in nature. 9 

Supportive therapy in 

immunosenescence 

Given these severe defects of immunity 

in the elderly and the important 

infectious link with CMV, it is 

essential to consider maintenance 

therapies adjusted to the individual’s 

condition, with low toxicity, 

good tolerance, and within reach of 

all. It is in this type of situation that 

homotoxicology has a vital role: in 

immunological regulation, inflammation 

regulation, detoxification 

and lymphatic, gastrohepatic, and 

renal drainage of toxins. Combination 

medications exist with proven 

antiviral activity and with the ability 

to increase IFN-γ levels (Engystol), 

or involved in cellular phagocyte 

recovery (Echinacea compositum), 

Reduction in lipopolysaccharide recognition and activity 

Reduction in the production of TNF-a 

Phagocyte deficiencies 

Reduction in the cellular and functional structure of lymph nodes 

which are undoubtedly an indisputable 

replacement therapy in immunosenescence. 

Inflammation-regulating 

products (Traumeel) with the 

ability to inhibit proinflammatory 

cytokines (Il-1, IL-8, TNF-a) and 

therefore systemic chronic inflammation 

are essential as blockers of 

inflamm-aging. Tables 2 and 3 show 

several antihomotoxic measures useful 

in immunosenescence. According 

to the course, detoxification and 

drainage cycles may be repeated. If 

treatment starts with immunostimulation, 

the patient may experience 

changes counter to the therapeutic 

aims, owing to the high levels of 

inflammatory molecules. The nutritional 

status of the elderly patient 

must be improved at the same time 

as antihomotoxic medication is administered. 

In some cases, antioxidative 

supplementation (vitamin C, 

vitamin E, glutathione, N-acetylcysteine, 

and S-adenosyl methionine), 

which tends to improve phago 

cyte migration, phagocytosis, 

pro duction of TNF-α, and production 

of IL-1 and IL-2 in T lymphocytes, 

is also necessary. 

We can conclude from the above 

that the aging process has a major 

) 17 



DET-phase 

Impregnation, 

degeneration 

Basic and/or 

symptomatic 

• Ginseng 

compositum 

D&D 

IM 

Regulation therapy* 

• Advanced supportive 

detoxification and 

drainage 

• Traumeel 

Optional 

• Arnica-Heel 

(if the inflammation is 

more severe) 

inflammatory component, triggered 

by infectious activators (principally 

viral) which give rise to profound 

defects in the immunity of elderly 

individuals which must be corrected 

in a natural and biological manner. 

12 | 

OR 

• Coenzyme compositum 

• Ubichinon compositum 

• Tonsilla compositum 

) 18 

Notes: Advanced supportive detoxification and drainage consists of Hepar compositum (liver), Solidago 

compositum (kidneys), and Thyreoidea compositum (connective tissue). 

Dosages: Detoxification and drainage: 1 ampoule of each medication 3 times per week. Immunomodulation: 

Traumeel, 1 tablet 3 times per day for 6 weeks. Organ regulation: Coenzyme compositum, 

Ubichinon compositum, and Tonsilla compositum, 1 ampoule of each 3 times per week. 

Table 2: 

Immunosenescence: therapy scheme for weeks 1-5 

DET-phase 

Impregnation, 

degeneration 

Basic and/or 

symptomatic 

• Ginseng 

compositum 

D&D 

IM 

OR 


• Basic detoxification and 

drainage: Detox-Kit 

• Engystol 

• Pulsatilla compositum 

• Glyoxal compositum 

Optional 

• Echinacea compositum 

(if there is a suspicion 

of a bacterial infection) 

Notes: The Detox-Kit consists of Lymphomyosot, Nux vomica-Homaccord, and Berberis-Homaccord. 

Dosages: Detoxification and drainage: 30 drops of each medication in 1.5 l of water, drink over the 

day. Immunomodulation: Engystol, 1 tablet 3 times per day for 5 days, then break for 5, then take for 

5 days (continue in this fashion for 6 weeks). Organ regulation: Pulsatilla compositum, 1 ampoule 

3 times per week for 6 weeks; Glyoxal compositum, 1 ampoule only in the entire 6 weeks. 

Table 3: 

Immunosenescence: therapy schemes for weeks 6-12 

* Antihomotoxic regulation therapy consists of a three-pillar approach: 

– Detoxification & Drainage (D&D) 

– Immunomodulation (IM) 

– Organ regulation (OR) 

References 

1. Capri M, Salvioli S, Sevini F, et al. The genetics 

of human longevity. Ann NY Acad Sci. 

2006;1067:252-263. 

2. Pawelec G. Immunosenescence comes of age. 

Symposium on Aging Research in Immunology: 

The Impact of Genomics. EMBO reports. 

2007;8(3):220-223. 

3. Ginaldi L, De Martinis M, D’Ostilio A, et 

al. The immune system in the elderly: II. 

Specific cellular immunity. Immunol Res. 

1999;20(2):109-115. 

4. Hyland P, Duggan O, Turbitt J, et al. Nonagenarians 

from the Swedish NONA Immune 

Study have increased plasma antioxidant 

capacity and similar levels of DNA damage 

in peripheral blood mononuclear cells compared 

to younger control subjects. Exp Gerontol. 

2002,37(2-3):465-473. 

5. Franceschi C, Bonafè M, Valensin S. Inflamm-aging. 

An evolutionary perspective 

on immunosenescence. Ann N Y Acad Sci. 

2000;908:244-254. 

6. Barker DJ, Eriksson JG, Forsén T, Osmond 

C. Fetal origins of adult disease: strength of 

effects and biological basis. Int J Epidemiol. 

2002;31(6):1235-1239. 

7. Arturo JA, Avila GI, Tobar CI, Klinger JC. 

Inmunodesviación TH2 asociada a glomerulonefritis 

por HBV. Infectio. 2001;5(2):119- 

120. 

8. Nasralla M, Haier J, Nicolson GL. Multiple 

mycoplasmal infections detected in blood of 

patients with chronic fatigue syndrome and/ 

or fibromyalgia syndrome. Eur J Clin Microbiol 

Infect Dis. 1999;18(12):859-865. 

9. Pawelec G, Koch S, Franceschi C, Wikby 

A. Human immunosenescence: does it have 

an infectious component? Ann N Y Acad Sci. 

2006;1067:56-65. 

10. Schvoerer E, Henriot S, Zachary P, et al. 

Monitoring low cytomegalovirus viremia in 

transplanted patients by a real-time PCR on 

plasma. J Med Virol. 2005;76(1):76-81. 

11. Wikby A, Ferguson F, Forsey R, et al. An immune 

risk phenotype, cognitive impairment, 

and survival in very late life: impact of allostatic 

load in Swedish octogenarian and 

nonagenarian humans. J Gerontol A Biol Sci 

Med Sci. 2005;60(5):556-565. 

12. De la Fuente M. Effects of antioxidants 

on immune system ageing. Eur J Clin Nutr. 

2002;56(suppl3):S5-S8. 


) Around the Globe 

Advanced IAH Lecturer’s 

Trainings East and West 

By Bruno Van Brandt 

IAH Education Manager 

In addition to its much-visited e- 

learning program for medical 

doctors and licensed health care 

professionals worldwide, the International 

Academy for Homotoxicology 

also organized two international 

medical education seminars (“IAH 

Rollouts”) this year. In the spirit of 

“train the trainer,” these gatherings 

coached speakers on how to lecture 

on the IAH abbreviated course material 

in their countries. The goal is 

to have more medical students well 

prepared to take the IAH e-examination 

and obtain the IAH certificate 

in the future. Although tens of 

thousands of students have already 

visited the IAH e-learning program, 

the IAH sees live presentations of 

this material as an extra boost to its 

success in homotoxicology education. 

IAH Rollout East took place in 

Baden-Baden, Germany from May 

29-31, 2008, where 72 medical 

doctors and university professors 

from 11 different countries in Central 

and especially Eastern Europe 

came to be trained in the use of the 

IAH abbreviated course material. 

This initiative was followed by IAH 

Rollout West in Miami, Florida from 

July 10-12, 2008. The medical doctors 

from North and South America 

and Canada who studied the IAH 

educational material in depth 

brought the total of rollout participants 

to about 100 MDs. These advanced 

lecturers will soon be promoting 

the homotoxicological 

model in their home countries. 

Dr. Arturo O’Byrne from Colombia 

lecturing on immunomodulation 

at the IAH Rollout West in Miami, 

Florida 

The rollout training material (i.e., 

the IAH abbreviated course in applied 

homotoxicology) is available 

online to medical doctors and health 

care professionals worldwide at 

www.iah-online.com. Every student 

who successfully completes the e- 

examination is sent an IAH certificate. 

Since there is no charge either 

for registration or for the certificate, 

there are no costs involved in taking 

the course. Instructional materials 

are currently available in English, 

French, Spanish, Russian, and Polish, 

with German and Portuguese to 

follow in the next few months.| 

More than 70 medical doctors and 

university professors from Central and 

Eastern Europe participated in the IAH 

Rollout East in Baden-Baden, Germany. 

) 19 


) Practical Protocols 

Bioregulatory Treatment 

of Urinary Tract Infections 

By Bert Hannosset, MD 

) 20 

A urinary tract infection (UTI) is defined as an infection 

of any part of the urinary system: urethra, bladder, 

ureters, or kidneys. Lower UTIs are infections in the 

lower part of the urinary tract, which includes the bladder 

(cystitis) and urethra (urethritis). Upper UTIs are 

infections of the upper part of the urinary tract, which 

includes the kidneys (pyelonephritis) and the ureters. 

Upper UTIs are potentially more serious than lower 

UTIs because of the possibility of kidney damage. 

Recurrent UTIs will occur at least 

twice in six months or three 

times in one year (usually these are 

reinfections). Interstitial cystitis (IC) is 

a chronic disease of unknown origin 

that affects the urinary bladder. The 

symptoms of IC overlap with those 

of a wide range of other disorders, 

including UTIs. IC should be suspected 

when a patient complains of 

pressure or pain in the pelvis or reports 

bladder discomfort. The pain 

or discomfort typically increases as 

the bladder fills and decreases during 

voiding, is associated with urinary 

frequency or a persistent urge 

to void, and appears in the absence 

of infection or other pathology. 

Incidence and prevalence 

Approximately 8 to 10 million people 

in the United States develop a 

UTI each year. Women develop the 

condition much more often than 

men; the reasons are not fully 

known, although the much shorter 

female urethra is suspected. The 

condition is rare in boys and young 

men. 20 percent of women in the 

United States will develop a UTI 

during their lifetimes, and 20 percent 

of those will experience a recurrence. 

Symptoms 

The symptoms of a lower UTI can 

include: pain or burning sensation 

during or at the end of urination 

(dysuria); frequent (pollakisuria) or 

urgent (urgency) urination; need to 

urinate at night (nocturia); a sensation 

of being unable to urinate fully; 

cloudy, bloody or foul-smelling 

urine; and pain in the lower abdomen. 

Low-grade fever (37-38°C or 

98.6-101.0°F) may also be present. 

The symptoms of an upper UTI can 

include: any of the symptoms of a 

lower urinary tract infection, a high 

fever (over 38°C or 101.0°F), nausea 

or vomiting, shaking or chills, 

and pain in the lower back or side 

(renal angle pain), usually on one 

side only. 

Causes and risks factors 

Escherichia coli causes about 80 percent 

of UTIs in adults. These bacteria 

are normally present in the colon 

and may enter the urethral opening 

from the skin around the anus and 

genitals. Women may be more susceptible 

to UTIs because the female 

urethral opening is closer to the 

source of the bacteria (anus or vagina) 

and the urethra is shorter than in 

men, allowing bacteria easier access 

to the bladder. 

Other bacteria that cause urinary 

tract infections include Staphylococcus 

saprophyticus (5 to 15 percent of 

cases), Chlamydia trachomatis, Mycoplasma 

hominis, Klebsiella and (more 

rarely) various species of Proteus and 

Pseudomonas. Chlamydia and Mycoplasma 

can be transmitted through 

sexual intercourse. 

For unknown reasons, sexual intercourse 

triggers UTIs in some women. 

Diaphragm users develop infections 

more often, and condoms with 

spermicidal foam may cause vaginal 

growth of E. coli, which can then 

enter the urethra. 



DET-phase 

Basic and/or 

symptomatic 


Optional 

Endodermal, 

urogenital 

• Berberis- 

Homaccord 

• Spascupreel 

D&D 

• Basic detoxification and 

drainage 


(for severe infection) 

Inflammation 

IM 

• Cantharis compositum 

OR 

• Solidago compositum 

Notes: In recurrent UTIs, Mucosa compositum and Solidago compositum are used (also as injection 

therapy; see Figure 1) for three months to strengthen the urinary tract. 

Urinary catheterization can also 

cause UTIs by introducing bacteria 

into the urinary tract. The risk of 

developing a UTI increases when 

long-term catheterization is required. 

In infants, bacteria from soiled diapers 

can enter the urethra and cause 

UTIs. E. coli may also enter the urethral 

opening when young girls do 

not wipe from front to back after a 

bowel movement. 

Other risk factors include: bladder 

outlet obstructions (e.g., bladder 

stones, benign prostatic hypertrophy), 

conditions that cause incomplete 

bladder emptying (e.g., spinal 

cord injury), congenital abnormalities 

of the urinary tract (e.g., vesical 

ureteral reflux), changes in the immune 

system (e.g., HIV and diabetes), 

and being uncircumcised. 

The causes of IC remain unknown 

and the underlying pathology has 

not yet been fully elucidated. Recent 

studies, however, have shown a possible 

relationship to production of 

autoantibodies to the muscarinic 

M3 receptor, located in the detrusor 

muscle cells of the bladder (which 

mediates cholinergic contraction of 

the urinary bladder). 

Diagnosis 

Differential diagnosis is made by 

laboratory analysis of a sample of 

mid-stream urine (the most reliable 

sample is obtained via suprapubic 

puncture), followed by a urine cul- 

Table 1: Treatment for lower UTIs 

DET-phase 

Mesodermal, 

nephrodermal 

Inflammation 

Basic and/or 

symptomatic 

• Berberis- 

Homaccord 

• Spascupreel 

D&D 

IM 

OR 

ture, if needed, to determine the 

specific bacteria and obtain an antibiogram. 

When leucocytes are elevated 

and the urine culture is negative, 

chlamydial urethritis, prostatitis, 

and IC are possibilities. In recurrent 

UTIs, ultrasound exams of the urinary 

tract and intravenous urography 

can be helpful diagnostic tools. 

A diagnosis of IC can be confirmed 

through cystoscopy with hydrodistention. 


• Advanced supportive 

detoxification and 

drainage 


• Cantharis compositum 

• Mucosa compositum 

Optional 

• Reneel 

• Belladonna-Homaccord 

(for high fever) 

• Mercurius-Heel (if there is 

frank pus in the urine) 

Notes: Mucosa compositum contains a Colibaccilinum nosode. Solidago compositum contains Equisetum, 

which strengthens the entire renal tract. Because upper UTIs affect a mesenchymal structure, treatment is 

deeper and includes more medications. 

Table 2: Treatment for upper UTIs 

* Antihomotoxic regulation therapy consists of a three-pillar approach: 

– Detoxification & Drainage (D&D) 

– Immunomodulation (IM) 

– Organ regulation (OR) 

Treatment 

In allopathic medicine, lower UTIs 

are most commonly treated with 

antibiotics (e.g., trimethoprim-sulfamethoxazole 

and amoxicillin), but 

bioregulatory therapy alone is also 

effective in treating this type of infection. 

According to homotoxicological 

guidelines, one or more basic 

symptomatic products should be 

added to the “three pillar approach” 

of drainage and detoxification 

(D&D), immunomodulation (IM), 

) 21 



Figure 1: 

Back shu points for the bladder 

and kidneys 

and, if necessary, cellular activation 

and organ regulation (OR). (See Table 

1.) 

In upper UTIs, antibiotics are unavoidable 

and antihomotoxic treatment 

should be seen as adjuvant 

therapy. The full range of antihomotoxic 

products should be used (see 

Table 2). 

BL 13 Lung 

BL 14 Circulation, sex 

) 22 

Injection therapy 

Injection therapy can be administered 

subcutaneously into the back 

shu points for the bladder and the 

kidney respectively (see Figure 1). 

This is useful either in acute treatment 

before a lower UTI patient is 

sent home with oral therapy or several 

times during the first week of 

an upper UTI. 

For IC and recurrent UTIs, once or 

twice weekly treatment over several 

weeks is helpful. In IC, however, 

due to the possibility of autoimmune 

disease, treatment should always include 

administration via the oral 

mucosa to induce oral tolerance to 

that tissue. Thus, small amounts of 

Mucosa compositum and Solidago 

compositum are injected into the AP 

point and the remainder is administered 

orally. | 

Solidago compositum 

Mucosa compositum 

Pulsatilla compositum 

Berberis-Homaccord 

Cantharis compositum 

Solidago compositum 

References 

1. van de Merwe JP. Interstitial cystitis and systemic 

autoimmune diseases. Nat Clin Pract 

Urol. 2007;4(9):484-491. 

2. Bergogne-Bérézin E. Lower urinary tract infections: 

bacterial epidemiology and recommendations 

[in French]. Prog Urol. 2008;18(1 

Suppl FMC):F11-14. 

3. Hooton TM. The current management 

strategies for community-acquired urinary 

tract infection. Infect Dis Clin North Am. 

2003;17(2):303-332. 

4. Talan DA, Krishnadasan A, Abrahamian FM, 

Stamm WE, Moran GJ; EMERGEncy ID 

NET Study Group. Prevalence and risk factor 

analysis of trimethoprim-sulfamethoxazoleand 

fluoroquinolone-resistant Escherichia 

coli infection among emergency department 

patients with pyelonephritis. Clin Infect Dis. 

2008;1;47(9):1150-1158. 

L2 

S2 

BL 15 Heart 

BL 16 Governing vessel 

BL 17 Conception vessel 

BL 18 Liver 

BL 19 Gall bladder 

BL 20 Spleen 

BL 21 Stomach 

BL 22 Triple heater 

BL 23 Kidney 

BL 25 Large intestine 

BL 27 Small intestine 

BL 28 Bladder 


) Meet the Expert 

Dr. Ivo Bianchi 

By Catherine E. Creeger 

Starting with this issue, our 

new column Meet the Expert 

will introduce physicians with 

a long-standing experience in 

homotoxicology. In addition 

to working with patients, many 

of them pass on their extensive 

knowledge as lecturers and authors 

of books and articles. 

However, this column will not 

strictly focus on medical careers, 

but aims to offer up a 

glimpse of the person behind 

the physician. As the first of 

our experts, please meet Dr. Ivo 

Bianchi. 

Ivo Bianchi grew up in the countryside 

around Verona, Italy, 

where he developed a love of nature 

at an early age. While studying medicine 

in Padua, he spent summers in 

Surrey, Great Britain, learning English, 

which he put to use doing research 

for his thesis project at University 

College in London. After 

completing his medical studies in 

1973, he worked at the University 

of Verona clinic, where he met a 

beautiful nurse 

named Marina, 

whom he soon 

married. They 

both wanted a 

big family and 

are now the 

parents of six 

grown children. 

In 1977, a chance encounter with 

Hahnemann’s Organon of Medicine 

“changed his life,” as he says, 

prompting him to think more deeply 

about medicine from both ethical 

and pragmatic perspectives. In 1979, 

while taking a course on acupuncture 

and homeopathy in Lausanne, 

Switzerland, he was introduced to 

homotoxicology. At the time, antihomotoxic 

products were unavailable 

in Italy, so he always returned 

home with a suitcase full of Zeel, 

Traumeel, etc., which he used in his 

practice with great success. His enthusiasm 

for homeopathy grew 

steadily and spilled over into his 

university lectures. As physician for 

the Verona soccer team, he was using 

injectable Traumeel and Zeel to 

treat the players, sometimes even 

during a match. (Perhaps coincidentally, 

the team won the first division 

cup that year!) This was all too much 

for the head of the university clinic, 

who forbade Dr. Bianchi to practice 

homeopathy or mention it in his 

lectures. Dr. Bianchi promptly quit 

his good university job to focus on 

his private practice, treating thousands 

of patients primarily with homotoxicology, 

homeopathy, and 

acupuncture, although he has never 

hesitated to prescribe conventional 

treatment when necessary. 

In the 1980s, Dr. Bianchi founded 

the Italian Medical Society for Homotoxicology 

in Milano and wrote 

several books on homotoxicology. 

Concerned about aligning his personal 

life with his values, he moved 

with his family to the country, 

where, supported by his children, he 

grew and collected plants and made 

medications from them. The Bianchi 

family also owned a lot of animals, 

including rabbits, chickens, goats, 

sheep, a donkey, and a horse. In the 

1990s, Dr. Bianchi travelled extensively 

to lecture on homotoxicology, 

while still practicing and teaching in 

Italy and authoring several more 

books. 

Now 60, he has recently made a renewed 

effort to balance work and 

travel with time spent relaxing with 

family at his country home, where 

he enjoys growing fruit trees and 

caring for his animals. | 

) 23 


) Research Highlights 

Engystol: A Homeopathic Medication 

for the Common Cold 

By Mary A. Kingzette 

) 24 

Introduction 

More and more complementary 

medications are being used in the 

United States and Europe. These 

complementary treatments are used 

for musculoskeletal complaints, vertigo, 

and mild viral infections, such 

as the common cold. 

Presently, no universal medication 

for the common cold exists. The antiviral 

agents available are not necessarily 

effective. Previous data have 

shown that alternative treatments 

may be as effective as conventional 

treatments for the symptoms of mild 

viral infections, such as the common 

cold. 

Engystol is a complex homeopathic 

medication (active ingredients, Vince 

toxicum hirundinaria [swallow wort] 

and sulfur) that has been used as a 

prophylaxis for influenza and the 

common cold. Recent reports suggest 

that it stimulates the phagocytic 

activity of granulocytes in vitro and 

may increase the percentage of 

interferon-γ-producing lymphocytes 

in vitro. 

In this pilot study, Engystol was 

compared with conventional treatments 

(e.g., antihistamines, antitussive 

medications, and nonsteroidal 

anti-inflammatory agents) for the 

common cold. The study was nonrandomized 

and observational, and 

the duration was 2 weeks or less. 

Because of this design, the patient 

groups were not comparable for all 

variables at baseline, confounding 

the analysis of results. Therefore, 

propensity score analysis was applied 

to the data. 

Methods 

This study was performed in 85 

German practices from November 1, 

2003, to February 29, 2004. Patients 

who had upper respiratory infection 

symptoms indicative of the 

common cold before enrolling in 

the study were included. Patients already 

receiving symptomatic cold 

treatment; those receiving antibiotic 

therapy for a secondary bacterial infection 

of the upper respiratory tract; 

patients with asthma, allergies, or 

chronic infections; and those recently 

receiving therapies that were similar 

to those in the present study 

were excluded. 

Patients in the homeopathic (alternative) 

group received Engystol. Patients 

in the conventional (control) 

group received over-the-counter 

cold treatments, including analgesics, 

nonsteroidal anti-inflammatory 

agents, and antipyretics. In both 

groups, the doses administered were 

decided on an individual basis. In 

the control group, there was no limit 

to the number of different therapies 

used. In the homeopathic group, 

patients could take other short-term 

medications but were not allowed 

long-term analgesics, antibiotics, or 

anti-inflammatory agents. 

The study variables were as follows: 

fatigue, sensation of illness, chill/ 

tremor, aching joints, overall severity 

of illness, sum of all clinical variables, 

and temperature. All of these 

variables measured the patients’ experiences 

of illness. 

The following symptoms were all 

evaluated on a scale from 0 to 3 

(where 0 indicates no symptoms; 1, 

mild symptoms; 2, moderate symptoms; 

and 3, severe symptoms): fatigue, 

sensation of illness, chill/ 

tremor, aching joints, and overall severity 

of illness. Temperature (measured 

in degrees Celsius) was also 

evaluated. For patients with rhinitis, 

pharyngitis, laryngitis, or bronchitis, 

changes in the symptoms associated 

with these conditions were also examined. 

Tolerability was monitored by a 

4-point scale based on adverse 

events (where 0 indicates excellent 

[no adverse effects]; 1, good [occasional 

adverse effects]; 2, moderate 

[frequent adverse effects]; and 3, 

poor [adverse effects noted with the 

administration of each study medication]). 

Results 

There were 397 patients in this 

study (175 in the Engystol group 

and 222 in the control group). Most 

of the baseline characteristics of the 

2 study groups did not differ, including 

age, sex, height, smoking 

status, temperature, and scores for 

sensation of illness, chill/tremor, 

aching joints, overall severity of illness, 

rhinitis, pharyngitis, laryngitis, 

and bronchitis. However, there were 

several significant (P < 0.05) differ- 


) Research Highlights 

ences between the 2 study groups. 

Patients in the Engystol group 

weighed less and had lower incidences 

of tracheitis and acute bronchitis 

than those in the control 

group, whereas patients in the control 

group had a slightly lower fatigue 

score than those in the Engystol 

group. However, once propensity 

score stratification was applied, these 

differences were no longer significant. 

The homeopathic study group received 

Engystol tablets, generally 3 

times a day. The dosage was not 

fixed, and 73.7% of the patients intermittently 

increased the dosage. 

The control group most commonly 

received paracetamol/acetaminophen, 

aspirin, metamizol, and ibuprofen. 

Additional therapies were allowed 

and used by both groups. In the 

Engystol group, the most common 

supplementary therapies included 

menthol- or chamomile-based inhalations, 

vitamins, sympathomimetic 

decongestants, and antipyretic/analgesic 

agents. In the control group, 

the most common supplementary 

therapies included cough remedies 

(antitussive agents/expectorants), 

menthol- or chamomile-based inhalations, 

vitamins, and decongestants. 

The results of the study showed no 

statistically significant difference between 

the 2 groups for 

fatigue, sensation of illness, chill/ 

tremor, aching joints, overall severity 

of illness, temperature, and sum 

of all clinical variables. 

However, the noninferiority analysis 

showed a trend toward Engystol 

treatment for overall severity of illness, 

aching joints, and temperature; 

there was a trend toward conventional 

treatment for fatigue only. For 

all other variables studied (sensation 

of illness, chill/tremor, and the sum 

of all clinical variables), the noninferiority 

analysis showed no trend toward 

either treatment group. 

One of the main findings of the 

present study was that significantly 

more patients using Engystol than 

those using conventional treatments 

displayed improvement in their cold 

symptoms within 3 days (77.1% vs 

61.7%; P < 0.05). 

When measuring satisfaction with 

treatment, 97.7% of the patients in 

the Engystol group were “very satisfied” 

or “satisfied” with their treatment 

(this was similar to the percentages 

in the conventional therapy 

group). 

“Excellent” overall tolerability was 

reported by more patients in the 

Engystol group than in the control 

group (89.2% vs 81.2%); this difference 

was statistically significant 

(P = 0.01) for unadjusted data. 

Finally, patients in the Engystol 

group showed mostly excellent 

(61.1%) and good (37.7%) compliance 

(this was similar to the percentages 

in the control group). 

Discussion 

Based on this exploratory, nonrandomized, 

observational study, 

Engystol treatment was not inferior 

to conventional treatments for the 

common cold. This conclusion is 

based on the analysis of their effects 

on 5 illness-related symptoms (fatigue, 

sensation of illness, chill/ 

tremor, aching joints, and temperature), 

on the summary score of all 

variables, and on overall assessment 

of illness severity. 

In previous studies, Engystol was 

used as a prophylactic agent for respiratory 

infections and as an ancillary 

treatment for viral infections. In 

vitro studies have shown that Engystol 

stimulates the immune system in 

terms of phagocytic activity, granulocyte 

function, and improved humoral 

response. However, the biochemical 

mechanism of Engystol 

remains largely unknown. 

According to the present study, 

Engystol treatment has several advantages 

when compared with conventional 

treatments for the common 

cold. First, the Engystol group 

experienced quicker first symptom 

improvement than the control group. 

This may be one of the most important 

factors for patients when evaluating 

the differences between therapies. 

Second, although both the 

Engystol and control groups had 

good tolerability profiles, the trend 

was toward a “very good” score in 

more Engystol-treated patients. 

Third, no adverse effects were reported 

for Engystol. 

In conclusion, Engystol seems to be 

as effective as any conventional 

therapy when treating the common 

cold. | 

Reference 

Schmiedel V, Klein P. A complex homeopathic 

preparation for the symptomatic treatment of 

upper respiratory infections associated with the 

common cold: An observational study. Explore 

(NY). 2006;2(2):109-114. 

Swallow wort (Vincetoxicum hirundinaria) 

is one of the active ingredients of Engystol. 

) 25 


) Making of … 

From Plant to Bottle: 

The Production of Homeopathic Nasal Sprays 

By Iris Woock 

Winter season is cold season. Sooner or later, it catches up 

with (almost) everyone: Your nose begins to itch, and you 

feel the beginnings of a cold. Now is the time for Euphorbium 

comp.-Nasal Spray,* a popular medication for 

cleansing, moistening, and soothing irritated mucous 

membranes. Thanks to its excellent tolerability, it is even 

suitable for pediatric use. 

To ensure the safety of homeopathic 

medications, the manufacturing 

process is very strictly 

regulated by law. In particular, producers 

must adhere to the following 

rules and standards: 

• the German Homeopathic 

Pharmacopoeia (HAB, Homöopathisches 

Arzneibuch), 

which contains detailed instructions 

for producing mother tinctures 

and potencies 

• the European Pharmacopoeia 

(Ph. Eur.), which describes the 

production of each dosage form 

and the physical and microbiological 

testing required 

• GMP Guidelines (Good Manufacturing 

Practice), which ensure 

the quality of pharmaceutical 

production processes and the 

production environment 

The manufacture of bottled Euphorbium 

comp.-Nasal Spray begins 

with written production instructions 

for implementing each process step. 

These instructions ensure that all 

process steps are reproducible and 

always completed in the same way. 

At a rate of 90 units per minute, the 

homeopathic nasal spray is filled into 

brown glass bottles. Filling, sealing, 

labeling, and packaging the bottles are 

fully automated processes. 

* Marketed as “Sinusin” in the US and Israel. 

Journal of

) Making of … 

All production steps are carefully 

monitored and documented in the 

production report. For safety reasons, 

a second person always double-checks 

all critical steps. 

All steps are very carefully monitored 

and documented in the production 

report according to the 

principle of dual control: for safety 

reasons, all critical steps are always 

checked and documented by a second 

person. 

On the basis of the production instructions, 

the first step is production 

of a mother tincture through 

extraction (plant materials) or solution 

or trituration (minerals). 

The mother tincture is then tested in 

the laboratory (for identity, relative 

density, dry residue, heavy metals, 

pesticides, microbial impurities, etc.) 

and must conform to test specifications 

before it is released for further 

processing. 

Mother tinctures are then potentized 

with an ethanol/water mixture in 

accordance with HAB regulations. 

The carrier for the last two potentizations 

is purified water because 

ethanol would irritate the nasal mucosa. 

Individual potencies are then 

blended, and the resulting potency 

mixture is combined with a base of 

isotonic salt solution to form the nasal 

spray mixture. Some formulas 

contain an additional preservative. 

Now the bulk product is finished. 

Filling is accomplished under a laminar 

flow hood, where a stream of 

ultra-clean air displaces any air that 

might contaminate the product with 

germs. But first the finished mixture 

is filtered and samples are drawn for 

testing in the quality control lab. 

Test parameters include Hazen color 

number, relative density, pH, osmolality, 

and microbiological purity. 

Once it has passed all of these tests, 

the nasal spray mixture is cleared for 

bottling. Six parallel nozzles pump 

the exact fill quantity (20 ml per 

bottle) into brown glass bottles. 

Tamper-proof seal 

Finally, to maximize ease of use for 

patients, spray heads with sealed 

patented caps are applied to the 

filled bottles. An unbroken seal ensures 

that the bottle has not been 

opened before the patient uses it for 

the first time. 

The optimum rate for filling and 

sealing is 90 bottles per minute. In 

the next step, each bottle receives an 

appropriate label with product data 

including the expiration date and 

batch number. Then the bottle, 

along with a product insert, goes 

into a folding box (so-called secondary 

packaging) and the batch 

number and “best before” date are 

printed on the top flap. 

The completed packages are weighed 

as a final check to ensure that none 

of the bottles are under-filled. They 

are then film-wrapped in batches of 

five for easier handling and packed 

into shipping cartons. 

Samples are drawn and tested 

throughout the entire filling process, 

and before the medication is released 

for sale, it is cleared one last 

time by the so-called Qualified Person 

in accordance with § 15 of the 

AMG (German Pharmaceuticals 

Act). Clearances are registered continually, 

so all steps of the production 

process as well as all tests are 

traceable. The product is then ready 

for shipping to wholesalers or pharmacies 

in Germany or anywhere else 

in the world. 

This is how approximately three 

million packages of Euphorbium 

comp.-Nasal Spray are produced 

each year.| 

The new patented seal immediately 

shows if the bottle has been opened 

before the patient uses it for the first 

time. 

) 27 


IAH Abbreviated 

Course 

An e-learning course leading to 

certification in homotoxicology 

from the International Academy for 

Homotoxicology in just 40 hours. 

1 Access the IAH website at www.iah-online.com. 

Select your language. 

2 Click on Login and register. 

3 Go to Education Program. 

4 Click on The IAH abbreviated course. 

5 When you have finished the course, click on Examination. 

After completing it successfully, you will receive your 

certificate by mail. 

For MDs and licensed healthcare practitioners only 

Free of charge 

www.iah-online.com

Infectious Diseases - International Academy of Homotoxicology

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