journal of biomedical therapy infectious diseases

8/17/2019 Journal of Biomedical Therapy Infectious Diseases

1/28

Volume 2, Number 3 ) 2008

Therapy

Biomedical

Infectious

Diseases• The Immune System, Our Personal Bodyguard

• Theories of Immunosenescence and Infection

Integrating Homeopathyand Conventional Medicine

d 2.00 • US $ 2.00 • CAN $ 3.00

Journal of


2/28

In Focu s The Immune System, Our Personal Bodyguard . . . . . . . . . . . . 4

W hat E l s e I s N e w ? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

From t h e P rac t i c eAcute Recurrent Otitis Media . . . . . . . . . . . . . . . . . . . . . . . . . . 12

Mar ke t i ng Yo u r P ra c t i c eManaging Expenses and Prices in the Medical Practice . . . . 14

Ref r e sh Your Homotox ico logyTheories of Immunosenescence and Infection:

Cytomegalovirus, Inammation, and Homotoxicology . . . . 16

A round t h e Gl ob e Advanced IAH Lecturer’s Trainings East and West . . . . . . . . . 19

P r a c t i c a l P r o t o c o l s Bioregulatory Treatment of Urinary Tract Infections . . . . . . 20

Me e t t h e Exp e r t Dr. Ivo Bianchi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

Re s e a r ch High l i gh t s

Engystol: A Homeopathic Medicationfor the Common Cold . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

Mak in g o f . . .From Plant to Bottle: The Production of

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

)

) 2

Contents

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

76532 Baden-Baden, Germany, e-mail: [email protected]

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

Cover photograph © Sebastian Kaulitzki/Fotolia.de


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Fighting Infections

)

Only a very small number of allthe millions of microbial spe-cies actually cause disease in hu-

mans. Antibiotic therapy, used ap-

propriately, has saved humankindfrom the scourge of severe infection,

but it has also been abused, resulting

in contaminated ground water, resis-

tant strains of microbes, and eradi-

cation 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 jour-

nal. According to this hypothesis,Th2 mediated diseases such as aller-

gies 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 ex-

posure of children to dirt has not

eradicated allergy.1

Meanwhile, it has become evident

that we humans have an evolution-

ary pact with certain infectious

agents that not only stimulate Th1

or Th2, but also – yes, you guessed

it! – increase T reg cells through by-

stander suppression to ensure opti-

mal Th1/Th2 balance. These agents

include helminths and certain myco-

bacteria as well as the symbioticbacteria in our gut. It seems, there-

fore, that whenever we use antibiot-

ics to eradicate infectious agents, we

risk killing off some of these old

friends that are vital to immune bal-

ance.

Stimulating natural defenses against

infection still seems to be the safestand most logical way to fight non-

life threatening infections. Several

antihomotoxic medications have

been shown to strengthen the im-

mune system: Engystol increases in-

terferon 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 vari-

ety 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 im-

munology and infectious diseases,

Dr. Manfred Schmolz and Dr. Doris

Ottendorfer, to write the focus arti-

cle 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 homo-

toxicologists. Dr. Jhann Arturo, a

clinical and experimental immunol-

ogist, discusses the very interesting

link between immunosenescence,

chronic infection, and chronic in-

flammation 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 theExpert presents a side of Dr. Ivo Bi-

anchi that you probably haven’t seen

before!

Alta A. Smit, MD

Dr. Alta A. Smit

References:

1. Rook GA, Brunet LR. Old friends for break-

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

2. Enbergs H. Effects of the homeopathic prep-

aration Engystol on interferon-gamma pro-

duction by human T-lymphocytes. Immunol

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

3. Wagner H, Jurcic K, Doenicke A, RosenhuberE, Behrens N. Die Beeinflussung der Phago-

zytosefähigkeit 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 evalua-

tion of the antiviral effects of the homeo-

pathic preparation Gripp-Heel on selected

respiratory viruses. Can J Physiol Pharmacol.

2007;85(11):1084-1090.

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

tiviral 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


4/28Journal of Biomedical Therapy 2008 ) Vol. 2, No. 3

The Immune System,Our Personal Bodyguard

By Manfred Schmolz, PhD, and Doris Ottendorfer, PhD

The central role of the

human immune system

The complexity of our immune sys-

tem evolved over millions of years

to minimize the threat by pathogensand neoplasms. Although we nor-

mally are not aware of its subtle

functions as long as we enjoy our

health, an early inflammatory reac-

tion 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 agentby cellular and/or humoral immune

responses. In some instances, long-

lived immunity is generated. The

aim of the present article is to briefly

outline important mechanisms of

immune reactions against infectious

microorganisms. The molecular de-

tails 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 di-

verse antigen receptors, play a cen-

tral role in this activation.

All immune cells originate from he-matopoietic stem cells in the bone

marrow. Under the influence of nu-

merous cytokines and growth fac-

tors, the so-called pluripotent stem

cells differentiate in a multistep pro-

cess into several types of granulo-

cytes (i.e., neutrophils, eosinophils,and basophils), each of which has

specialized functions; monocytes

(which differentiate to the tissue

macrophages when settling in dif-

ferent organs); natural killer (NK)

cells; and B and T cells.

The lymph nodes are localized as a

large network throughout the hu-

man body to sample antigens from

the tissues via the lymph vessels.

Lymph nodes are usually the site ofsensitization of T cells by antigen-

presenting cells (APCs). The muco-

sa-associated lymphoid tissue

(MALT) includes the Peyer’s patches

along the gastrointestinal tract, the

tonsils, and the nasal- and bronchus-

associated lymphoid tissue. All of

these tissues form highly organized

structures supporting the interaction

of antigens with the few available

antigen-specific lymphocytes circu-

lating in the blood or the lymph.

The MALT is essential as a protec-

tive 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 rec-

ognized by phagocytes that nonspe-cifically engulf and digest patho-

gens. Even this most primitive

defense function is a highly com-

plex cellular process.4,5 Two differ-

ent types of phagocytosis exist: the

removal of pathogens and the elimi-

nation of apoptotic tissue cells(apoptosis means programmed cell

death). The former causes an inflam-

matory alarm response, whereas the

latter (which is, for example, neces-

sary during embyrogenesis) prevents

inflammation. Moreover, phagocy-

tosis bridges innate and adaptive

immunity, through antigen presen-

tation.

The engulfment of pathogens by

neutrophils and macrophages dis-criminates between diverse particles

through an array of receptors ex-

pressed on their surface. Among

these receptors are several for com-

plement 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 al-

tered-self ligands, such as apoptotic

cells.

After receptor ligation by the parti-

cle, 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, bacteri-

cides, etc. Proteomic analysis has re-vealed that phagosomes contain

more than 600 different types of

)

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) 4



)

I n F o c u s

proteins. A key role of phagolyso-

somes 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 toll-

like receptors (TLRs) is essential for

the discrimination between self and

nonself structures, a central require-

ment for the immune system. This

topic was extensively reviewed by

Akira and Takeda6 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 mo-

lecular patterns (PAMPs) is detected

by a different TLR subtype (e.g.,

TLR4 recognizes lipopolysaccha-

rides). The PAMPs are among thestrongest stimuli for immune cells.

The signal transduction pathways

that TLRs activate in different im-

mune cell subtypes result in a multi-

tude of antimicrobial and inflamma-

tory 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 (chemo-

kines)

2. help make functionally mature

APCs

3. contribute to antiviral immu-

nity8

Therefore, PAMPs very efficiently

link innate and adaptive immune

mechanisms, thus potentiating de-

fense efficacy.

The neutrophil:

a prototypic cell type of anti-

bacterial 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 pro-

gramming 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 patho-

gens, 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 de-

pleting iron at the site of infection.

In addition, neutrophils secrete fac-

tors that assist B-cell maturation and

proliferation and can also function

as prominent suppressors of T-cell

function (e.g., by secreting prosta-glandins).

The role of complement

proteins in immunity

The complement system deserves at-

tention in that this proteolytic ma-

chinery, resembling in its cascade-

like 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 repre-

sents a system of more than 30 se-

rum proteins and cell surface recep-

tors. An excellent review on

complement concerning numerous

immunoregulatory roles beyond the

killing of bacteria has been pub-lished by Carroll.10

Messaging between cells of the

innate immune system

To accomplish the antibacterial de-

fense during innate immune reac-

tions, the phagocytosis of microbial

pathogens is accompanied by the re-

lease of several messenger molecules,

such as arachidonic acid metabolites

(prostaglandins and leukotrienes),

chemokines, cytokines, and proteas-

es. 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 cre-

ate problems.

Initiation of an antigen-specific

immune response against

infection

In many cases, the first line of de-

fense established by the phagocytes

is not enough, especially when mi-

crobial and viral pathogens evolved

to exhibit sophisticated survival

strategies. In such cases, antigen-

specific immune responses are initi-ated. Even these begin with phago-

cytosis, although, as reviewed

recently by Finlay and McFadden,11

some pathogens may resist phagocy-

tosis and others interfere with anti-

gen 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 ac-

tivities, these pathogens can be de-

stroyed by more specific cellular im-

mune mechanisms. There is

antibody-dependent cytotoxicity

and enforced cellular immunity; the

latter results in a profound activa-

tion of macrophages, boosting them

to destroy even microorganisms as

resistant as mycobacteria. Such re-

enforcement usually involves thecells from the antigen-specific part

of the immune system, the T and B

cells.

) 5



)

I n F o c u s

T and B lymphocytes are

responsible for generating

antigen-specific immune

responses

True antigen specificity resides inthe T and B lymphocytes, which are

able to recognize antigens through

highly specific membrane-bound

receptors. Each cell has peculiar re-

ceptors that recognize only one an-

tigen. 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. Thereceptors of both cell types recog-

nize only a small part of large anti-

gens, referred to as the epitope.

Complex antigens usually consist of

more than one epitope. This tremen-

dous variability in T- and B-cell

specificities is achieved by DNA re-

arrangement.12,13

Antigens are internalized and pro-

cessed 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 at-

tached are the proteins of the major

histocompatibility complex (MHC),

of which 2 classes are highly impor-

tant for immune and tissue cells:class I (MHC-I) and class II (MHC-

II).

Antigen presentation by MHCs

Recognition of antigens in the bind-

ing 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 hu-

man 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 tumori-

genesis).14 The recognition of anti-

gens presented by MHC-I molecules

leads to the activation of cytotoxic Tcells (CTLs) bearing the CD8 sur-

face marker (CD8+ CTLs).

The MHC-II proteins are found ex-

clusively on cells of the immune sys-

tem (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 differ-

ent antigens (Reis e Sousa15 and

Shortman and Naik16 provide re-

views). In contrast to MHC-I mole-

cules, 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

cellsViruses are crucial pathogens be-

cause 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 sys-

tem.

Evolution enabled infectious patho-

gens (i.e., viruses, bacteria, and para-

sites) 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 Thcells.

Basically, CD4+ T-cell activation is

initiated by the interaction of the

antigen receptor (TCR) with anti-

gen/MHC-II complexes on APC

surfaces. Antigen/MHC-II com-

plexes trigger a complex concert of

intracellular signals, activating a

whole series of genes that control

the proliferation, differentiation, and

effector functions of T cells. Anti-

gen-specific T-cell activation is initi-

ated 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 par-

ent 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 growthfactor and acts to promote prolifera-

tion and differentiation of antigen-

activated T cells.18,19

) 6

Bacteria display a wide diversity of

shapes and sizes. Here: Salmonella

typhimurium (red) invading cultured

human cells.



)

I n F o c u s

CD4+ T cells activate cellular

immunity

A core function of CD4+ T cells in

antibacterial defense is the re-en-

forcement of tissue macrophages tobetter 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 im-

munity against pathogens, such as

leishmania and mycobacteria. This

activation of macrophages depends

on cytokines from activated CD4

Th cells, most importantly interfer-

on (IFN) γ, which is also providedby NK cells. Other cytokines sup-

porting 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 man-

ner express a higher ability to pres-

ent antigens, provide stronger co-

stimulation, and secrete more

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

and IL-10) or tumor necrosis factor

a. Moreover, the CD4+ T lympho-

cytes are important helper cells for

antiviral CTLs. CD4+ T cells are

not only crucial for macrophage ac-

tivation but also provide help to B

cells by secreting growth factors fa-

voring antibody production.

Cytotoxic CD8+ T cells and

NK cells kill virus-infected and

tumor cells

Virus-specific CD8+ CTLs are the

major effector cells for eliminatingestablished viral infections. NK cells

also lyse virus-infected cells and tu-

mor cells. Therefore, both cell types

are often summarized as cytotoxic

lymphocytes. It seems that both cell

types share common mechanisms

for antiviral and antitumor de-

fense.20-22 For example, both cell

types secrete the cytotoxic protein

perforin, along with granzymes. To-

gether, they kill infected cells andtumor cells on cell-to-cell contact.

This is a thoroughly controlled pro-

cess to kill only the diseased target

cell (not healthy neighbor cells).

The most important difference be-

tween the CTL and NK cells is that

NK cells do not have a TCR; NK

cells recognize virally infected cells

by their ability to recognize and lyse

virally infected cells by other recep-

tors showing a more general speci-

ficity for pathogen-induced changes

in tissue cells (e.g., intracellular in-

fection or neoplasia). Other NK cell

receptors possess inhibitory activity,

enabling a close control of cell kill-

ing.23

The major advantage that NK cells

have over antigen-specific CD8+ T

cells is that they kill target cells

without the need for clonal expan-sion (i.e., without a “lag” phase). ) 7

Therefore, NK cells effectively limit

the early spread of infection.

CD8+ CTLs recognize antigens by

their TCR in association with MHC-

I molecules. In addition, similar toCD4+ T cells, CD8+ T cells need

clonal expansion to establish full ef-

fector functions.

Role of IFN synthesis in

antiviral immunity

In addition to cell contact-depen-

dent killing mechanisms, soluble

mediators released during viral in-

fection of cells directly stimulate the

production of IFNs, of which type 1IFNs (a and β) possess the strongest

direct antiviral activity. Type 1 IFNs

are produced by many cell types and

cause an “antiviral state” in the in-

fected cells; this state is character-

ized by inhibition of viral replica-

tion and cell proliferation. Type 1

IFNs also enhance NK cell activity

to lyse target cells and improve anti-

gen presentation in APCs.

Multiple ways to control T-cell

activation

T-cell responses do not only con-

sume lots of energy by clonal ex-

pansion but are also highly power-

ful when it comes to destroying

tissue cells. Taken together, the costs

of false alarms are high; therefore,

such a process needs to be controlled

strictly.

A macrophage forming two processes

to phagocytize two smaller particles.



)

I n F o c u s

) 8

)

I n F o c u s

The ability of T cells to become ac-

tivated primarily depends on the

signal strength received by the TCR;

therefore, only those T cells show-

ing the best binding fit to the anti-gen will become fully activated. An-

other potent means to effectively

control T-cell activation is by “co-

stimulation.” This is accomplished

by a series of costimulating counter-

receptors on the APC surface bind-

ing to ligands on T cells. These add

positively and negatively to the reg-

ulation of the proliferation and dif-

ferentiation of a given T-cell clone.

One of the best characterized co-stimulation 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 subpopula-

tions such as the Th cells (Th1, Th2,

and Th3) and the regulatory T cells

(which have been extensively re-

viewed by Kalinski and Moser25 and

Belkaid26). 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 an-

tibody production and participate in

the induction of hypersensitivity,

and the Th3 and Treg cells can gen-

erally be seen as the protectors

(“down-regulators”) against reac-tions that are too strong, outdated,

or undesired. Interestingly, the deci-

sion 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 con-cept is a subject of continuing de-

bate.25

Humoral immunity: the genera-

tion of antibodies

B cells are the only cells that pro-

duce antibodies (immunoglobulins).

As with T cells, each B cell is spe-

cific for a particular epitope on an

antigen (e.g., protein or carbohy-

drate). Antigens are specifically rec-ognized by surface-anchored anti-

bodies on these cells. By this B-cell

receptor, antigens can be internal-

ized. They are then broken down

into fragments and displayed at the

B-cell surface together with MHC-

II to CD4+ Th cells, which subse-

quently 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 recep-

tor on their surface originally en-

coded. In the further course of the

immune response, the interaction

with T cells causes the B cells to

switch their production from immu-

noglobulin M (IgM), which is al-

ways the first to be secreted, to the

more versatile IgG.

Effector functions of different

antibody classes

In humans, 5 different classes of im-

munoglobulins, called isotypes, are

known (i.e., IgM, IgG, IgA, IgE, andIgD). These immunoglobulins all

have different structures and activi-

ties. On primary activation, B cells

first always synthesize IgM, peaking

about 7 to 10 days after initial ex-

posure. 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 activa-

tion, these lymphocytes can switch

from IgM to a different class of anti-

bodies. The most prominent of these

antibodies is IgG. Its capacity to

“coat” bacteria to improve phagocy-

tosis is called opsonization. IgG also

neutralizes microbial toxins, blocks

viral adherence to target cells, acti-

vates complement, and is the main

antibody found on repeated antigen

contact.

IgA, on the other hand, is the anti-

body found primarily in mucus, co-

lostrum, and milk. It protects against

respiratory and gastrointestinal tract

infectious agents.

Finally, IgE is produced in response

to parasites and is also a characteris-

tic mediator of type 1 allergy. In

both of these instances, IgE collabo-rates closely with Th2 cells to shape

this particular type of immune re-

sponse.27

The elimination of viruses is a real

challenge for the immune system.

© S

e b a s t i a n K a

u l i t z k i / F o t o l i a . d e



)

I n F o c u s

8. Kawai T, Akira S. Innate immune rec-

ognition of viral infection. Nat Immunol.

2006;7(2):131-137.

9. Nathan C. Neutrophils and immunity: chal-

lenges and opportunities. Nat Rev Immunol.

2006;6(3):173-182.

10. Carroll MC. The complement system in reg-

ulation of adaptive immunity. Nat Immunol.

2004;5(10):981-986.11. Finlay BB, McFadden G. Anti-immunol-

ogy: evasion of the host immune system

by bacterial and viral pathogens. Cell.

2006;124(4):767-782.

12. Chaudhuri J, Alt FW. Class-switch recom-

bination: interplay of transcription, DNA

deamination and DNA repair. Nat Rev Immu-

nol. 2004;4(7):541-552.

13. Schlissel MS. Regulating antigen-re-

ceptor gene assembly. Nat Rev Immunol.

2003;3(11):890-899.

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

The known unknowns of antigen process-

ing 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 in-

flammatory 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 nega-

tive 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 re-

ceptor 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 signifi-

cance 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: MHC-

class-I-independent natural-killer-cell self-

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

374.

24. Acuto O, Michel F. CD28-mediated co-stim-

ulation: a quantitative support for TCR sig-

nalling. 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 infec-

tion: a dangerous necessity. Nat Rev Immunol.

2007;7(11):875-888.

27. Anthony RM, Rutitzky LI, Urban JF Jr, Sta-

decker MJ, Gause WC. Protective immune

mechanisms in helminth infection. Nat Rev

Immunol. 2007;7(12):975-987.

Antibodies usually neutralize viruses

through binding to their surface,

blocking the virus from entering the

host cell. In addition, some viral in-

fections lead to the expression of

viral proteins on the surface of in-

fected cells. These may bind virus-

specific antibodies, leading to com-

plement-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 genera-tion 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 advan-

tage of memory cells is that they can

be activated upon any repeated con-

tact 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 differ-

ent immune cells to establish a well-

coordinated response during antimi-

crobial defense, as previously

described, would be impossible

without the help of the vast array of

soluble mediators that evolution

elaborated to fine-tune immune re-

sponses. They comprise a large num-

ber 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 controlledmanner. Most of these mediators

form positive- and negative-feed- ) 9

back signaling loops that timely ad-

just the general type and the extent

of response to the current needs,

which in fact differ substantially be-

tween the different types and phases

of a defense reaction.

Concluding remarks

Immunological knowledge is grow-

ing 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 ourunderstanding of antimicrobial im-

munity. In addition, these discover-

ies are helping us understand the

switch from well-regulated immune

responses to detrimental conditions

such as chronic inflammation. Read-

ers are encouraged to consult one or

more of the articles cited herein,

which will provide a deeper guide

into the complex and highly fasci-

nating world of the immune system,our personal bodyguard.|

References

1. Coombes JL, Powrie F. Dendritic cells in in-

testinal immune regulation. Nat Rev Immunol .

2008;8(6):435-446.2. Sansonetti PJ. War and peace at mucosal

surfaces. Nat Rev Immunol. 2004;4(12):953-

964.

3. Holt PG, Strickland DH, Wikström ME,

Jahnsen FL. Regulation of immunological

homeostasis in the respiratory tract. Nat Rev

Immunol. 2008;8(2):142-152.

4. Stuart LM, Ezekowitz RA. Phagocytosis: el-

egant complexity. Immunity. 2005;22(5):539-

550.

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 signal-

ling. 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.


10/28

10


)

W h a t E l s e I s N e w ?

F O R P R O F E S S I O N A L U S E O N L Y

The information contained in this journal is meant for professional use only, is meant to convey general and/or specific worldwide scientific information relating to the

products or ingredients referred to for informational purposes only, is not intended to be a recommendation with respect to the use of or benefits derived from the

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

for any medical or legal responsibility for the reliance upon or the misinterpretation or misuse of the scientific, informational and educational content of the

articles in this journal.

The purpose of the Journal of Biomedical Therapy is to share worldwide scientific information about successful protocols from orthodox and complementary practi-

tioners. 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 sharetheir 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.

No scientific proof of the

health benefits of drinking

more water

How much water should you drinkin a day? According to common re-

commendations, eight glasses, or

approximately one and a half liters.

It remains debatable, however,

whether increased water consump-

tion is necessary for health, aids in

weight loss, or keeps skin firm. In an

analysis of all available clinical stud-

ies on this topic, scientists from

Philadelphia (USA) recently con-

cluded that such claims don’t holdwater. True, the kidneys get a good

rinsing, but there was no evidence

of clinical benefits to kidney or oth-

er organ functions.

Am Soc Nephrol. 2008;19(6):

1041-1043

Short arms, short memory?

Alzheimer’s is more common in in-

dividuals with short arms and legs

than in people with long extremi-ties. At least, that’s the conclusion of

a recent American study of approxi-

mately 2,800 older subjects (average

age = 72). 480 of the participants

developed dementia during the five-

year 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 suggest-ed 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

Autohemotherapy helpful

in heart failure

In certain patients with chronic

heart failure, autohemotherapy canreduce the risk of death or hospital-

ization, 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 ei-

ther their own blood or a placebo.

Primary endpoints in the study were

death or admission to a hospital.

Autohemotherapy significantly de-

layed both endpoints in patientswho had not yet suffered a heart at-

tack and in patients with NYHA

Stage II cardiac insufficiency.

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

A recent study has shown that individu-

als with long arms have a lower risk of

developing dementia than people with

short extremities.


11/28

) 11


)

W h a t E l s e I s N e w ?

Coffee for liver protection?

Coffee protects the liver against can-

cer and the effect increases with the

amount of coffee consumed, accord-ing to an Italian meta-analysis of 11

original studies. The study’s find-

ings are significant: Regular coffee

consumption reduces the risk of liv-

er cancer by almost 40 percent. The

protective effect was evident even in

subgroups of patients with pre-ex-

isting hepatitis or cirrhosis.

This effect may be due to the pres-

ence of cafestol and kahweol diter-penes in coffee. In animal experi-

ments, 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 asso-

ciated 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 theGerman team competed in the title

match of the European soccer cham-

pionship. That’s not necessarily safe

entertainment, according to a study

conducted in Germany during the

World Cup two years ago. Emergen-

cy physicians prospectively assessed

cardiovascular events occurring in

patients in the greater Munich area.

They discovered that the statistical

probability of suffering a cardiovas-cular event doubled when the Ger-

man team was playing. Men were

affected significantly more often

than women, and the risk was espe-

cially high among those with preex-

isting coronary heart disease. So the

physicians urged heart patients to

take preventive measures, such as

taking appropriate medication, be-

fore the German team’s games or

similar important events. They also

said that behavioral therapy to im-

prove 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 induc-ing”) not only makes people feel

hungry but also heightens responses

to food stimuli, as Canadian scien-

tists recently discovered. According

to their study, the hormone (formed

in the epithelium of the empty stom-

ach) does more than simply encour-

age eating by causing sensations of

hunger – it also makes specific brain

regions more receptive to visual

stimuli from food, which increasesthe 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 au-

thors, however, warn against using

ghrelin blocking medications as

therapy for obesity, considering it

too risky, since ghrelin affects brain

regions where emotions and motiva-

tions arise.

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

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 …


12/28

)

F r o m t h e P r a c t i c e

Acute Recurrent Otitis Media

By Ivo Bianchi, MD

) 12


Symptoms include otalgia that isoften very acute, usually wors-ens at night, and is sometimes ac-

companied by nausea, vomiting, di-

arrhea, and fever. Although acuteotitis 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, antibi-

otics 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 two-

year-old son to my office for recur-

rent acute episodes of otitis media.These episodes were extremely fre-

quent, especially during the cold,

damp season, and required frequent

administration of antibiotics. In one

episode, otitis media was compli-

cated by acute mastoiditis, requiring

hospitalization of the child. Thesituation had become almost chron-

ic, and the child often seemed off-

balance. The family medical history

included the mother with frequent

seasonal rhinopharingitis and a pa-

ternal uncle with allergic asthma.

Upon examination, I found latero-

cervical microadenopathy, reddened

pharynx, and hyperaemic tonsillar

membranes. Thoracic and abdomi-

nal 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 report-

ed 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 inthe 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 infor-

mation to develop a homeopathicand homotoxicological treatment

strategy based not only on the

child’s clinical history and symp-

toms but also on the homotoxico-

logical 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 feveris present.

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.



Factors related to otitis media

Anatomy of the inner ear

• Traumeel ampoules or Oteel:

2 drops locally in the ear for

inflammation and pain, every

10-30 minutes during acute

phases until improvement isnoted.

3. Immunomodulation:

• Echinacea compositum forte:

½ ampoule in the evening

twice a week for 6 months,

increasing to every 6 hours

during acute upper respira-

tory infections until im-

provement is noted. This

medication is our antibacte-rial support and immuno-

modulator.

• 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 sim-

ple therapy, it is a real strategic plan

to fight the disease and its symp-

toms, prevent complications, and

stimulate general and local immuneresponses in order to prevent relaps-

es. The mother was well-motivated

and the whole therapy was adminis-

tered 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 recur-

rences were reported, and I then rec-

ommended a simple maintenance

therapy for the winter and earlyspring:

• 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 morn-

ing once a week.

I continue to see the child every

six months. Three years after the

first consultation, he is in perfectshape physically and psychological-

ly.|

Common factors related toacute otitis

Viral infections

Bacterial infections

Genetic-constitutionalfactors

Anatomical factors

Exposure to smokeor pollution

Gastroesophageal reux

)

F r o m t h e P r a c t i c e

Vestibular

cochlear nerve

Eardrum Eustachian tube

Cochlea

© O

O Z / F o t o l i a . d e


14/28

) 14

)

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

Managing Expenses and Pricesin the Medical Practice

By Marc Deschler Marketing specialist

Office supplies and legal and ac-

counting/tax preparation feesare often major entries. It can be

well worth the effort to solicit com-

peting bids and/or to renegotiate

these costs. Be especially aware of

how your spending on office sup-

plies 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 ex-

penses, don’t forget to add in what

you spend on:

• postage

• telephone bills• oce cleaning and disinfection

• business entertainment

• service contracts

• purchases up to $50

• uniforms and linens

• waiting room reading material

• gifts and oce 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 ac-

count for, discuss them with youraccountant.

Losses due to purchases

Excessive expenses can occur in all

aspects of a medical practice. Un-

economical 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 pur-chasing behavior in your practice.

1. Purchases are not planned. Sup-

plies are often purchased only

when they have already run out,

when no one is likely to pay

much attention to price and qual-

ity.

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.

Have you ever analyzed the purchasing

behavior in your practice?

A few simple strategies can help you

avoid unnecessary costs.


15/28

) 15

2. Work is delayed because sup-

plies were not purchased in ad-

vance and are not available

when needed. (E.g., emergency

trips to the pharmacy for in-

jectable medications.)

3. Bulk purchases result in dis-

counts 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 com-

peting bids.6. It doesn’t occur to you to split

bulk orders with other practic-

es.

Checking any of the above indi-

cates weaknesses in the manage-

ment 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 willpay off. So-called ABC analysis is a

time-tested mechanism that helps

you analyze and determine the rel-

ative budgetary impact of different

items and suppliers. Here, as in

many other areas, the 80/20 prin-

ciple applies; that is, approximately

20 percent of goods purchased ac-

count 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 to-

tal annual spending. The items that

together account for 80 percent of

your costs deserve a closer look.

The others can be safely disregard-ed; they will take care of them-

selves in any subsequent reorgani-

zation.

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 to-

day are medical “service providers”

and need to function like the com-

mercial enterprises they are. To en-

sure a reasonable income, a commer-cial venture must sell something and

make its prices “palatable” to con-

sumers. 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 pa-

tients. Broach the subject and ex-

plain why there is an extra fee for a

particular additional service that in-

surance may not cover. Health andbeauty are very important in today’s

society, so “selling” elective thera-

peutic 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 pa-

tient to bring up the subject of price,

regardless of which one of you

brought up the subject of treat-

ment.

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 ser-

vice may not be covered by supple-mentary insurance. No big explana-

tion is needed.

Step 3: Next, present the advantag-

es (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 infor-

mation 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, “Ican’t afford that!” Think about how

to break the fee down into small in-

stallments. For example, “I suggest

starting with three sessions, each of

which will cost $40. After that, we

can see how you’re doing and de-

cide whether or not to continue.”

Your patient’s reaction? “$40 is rea-

sonable, and I can always still change

my mind.”

Step 6: Now discuss additional ad-

vantages for the patient.

Step 7: Suggest that the patient take

the brochure home and think about

it. Don’t press for an immediate de-

cision. This gives your patient a way

out if s/he can’t commit to the ex-

pense on the spot.

Step 8: With your patient’s consent,

say you’ll call to discuss how to pro-

ceed.

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.|



16/28

Introduction

Aging is generally a complex pro-

cess which forms part of the cycle of

physiological cell growth where liv-

ing organisms going through one ofthe phases of tissue evolution un-

dergo the hardest and most irrevers-

ible processes of tissue deterioration.

This is based on cell wear and tear

(increase in chromosomal and telo-

meric alterations)1 and matrix wear

and tear (protein and lymphatic de-

terioration), accelerated catabolism

(increase in post-transductional pro-

tein changes and in oxidation with

increased apoptosis), and loss of theregenerative capacity of tissues over

time (loss of mitochondrial function

and stem cell reparation).

This progressive deterioration, con-

sidered to be physiological, affects

not only the internal organs but also

the skin, the central nervous system,

and the immune system. The in-

volvement of the immune system af-

fects the ability to attack microbes,

tumors, chemical or physical agents,

or toxins (by slowing it down, di-

minishing it, down-regulating it, or

preventing it altogether), compro-

mising the organism’s general im-

munity. This immune aging is known

as immunosenescence, and it is par-

ticularly important in current clini-

cal practice, since an understanding

of these subtle biological changes

can provide us with the tools to car-ry 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 com-munication signals (cytokines and

chemokines), and humoral defense

elements (antibodies, complement,

immune peptides) which together

enable the defenses to work in har-

mony, and other tissues such as the

extracellular matrix, and the lym-

phatic, neuroendrocrine, and meta-

bolic systems to remain in homeo-

stasis. The main features recognized

to date in immunosenescence2 areshown in Table 1. For example, it

has been observed that young indi-

viduals have an adequate population

of T lymphocytes producing inter-

leukin (IL) 2, responsible for the

clonal expansion of other T lym-

phocytes. However, elderly individ-

uals have T cells with low IL-2 pro-

duction and consequently far slower

T cell clonal expansion which gives

rise to incomplete or reduced im-

mune responses.3 These incomplete

immune responses generally result

in diseases: autoinflammation, auto-

immunity, neoplastic processes (leu-

kemias/lymphomas, cancer), or de-

generative 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 typesof 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 indi-

viduals also appear to have high an-

tioxidant levels in plasma.4

Repeatedaccumulation and the increasingly

chronic nature of the oxidative pro-

cess therefore seem to cause the

TCD3+ cells to become destabi-

lized.

Chronic inflammation and

chronic infection in the elderly

The most important impact of im-

mune dysfunction in old age is,

however, chronic inflammation (in-flamm-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 im-

perceptible production of inflamma-

tory mediators such as C-reactive

protein, fibrinogen, amyloid protein,

and cytokines such as platelet-de-

rived growth factor, IL-6, IL-10, tu-

mor necrosis factor (TNF) a, and

transforming growth factor β alters

the vascular epithelium and causes

tissues to become chronically in-

flamed and to degenerate. The most

important cause of this persistent in-

flammation is infectious diseases

which contribute to a chronic state

of immune activation and, over time,

immunodeficiency. Some of the keymicroorganisms that produce chron-

ic inflammation in humans are:

)

R e f r e s h Y o u r H o m o t o x i c o l o g y

16


Theories of Immunosenescenceand Infection

Cytomegalovirus, Inflammation, and Homotoxicology

By Jhann Arturo, MD, MRes, MSc, PhD


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• viruses: cytomegalovirus (CMV),

hepatitis B virus,7 hepatitis C vi-

rus, virus G, herpes virus type 6,

-7, -8;

• bacteria: Chlamydia, Toxoplasma,Helicobacter pylori, Mycobacteria,

Mycoplasma, Listeria, Brucella, and

Borrelia .8

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 serologicalmarkers positive for CMV.9 Al-

though the risk of infection is high-

er than 70% according to study

groups, this lentivirus has been

shown to be capable of producing

asymptomatic, persistent viral repli-

cations, causing chronic, undiag-

nosed, 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 opportunis-

tic pathogen, but it is known that

the reduction in the CD4/CD8 ra-

tio, 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 anti-

viral protocols should therefore beconsidered in patients with a sus-

pected viral infection, and immuno-

stimulant 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 di-

rectly concerned and is one of the

main agents involved in immune de-

terioration, and from this point of

view immunosenescence, with theloss of T cells, could be highly in-

fectious in nature.9

Supportive therapy in

immunosenescence

Given these severe defects of immu-

nity in the elderly and the impor-

tant infectious link with CMV, it is

essential to consider maintenance

therapies adjusted to the individ-

ual’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, inflam-

mation regulation, detoxification

and lymphatic, gastrohepatic, and

renal drainage of toxins. Combina-

tion medications exist with proven

antiviral activity and with the ability

to increase IFN-γ levels (Engystol),or involved in cellular phagocyte

recovery (Echinacea compositum),

which are undoubtedly an indisput-

able replacement therapy in immu-

nosenescence. Inflammation-regu-

lating products (Traumeel) with the

ability to inhibit proinflammatory

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

therefore systemic chronic inflam-

mation are essential as blockers of

inflamm-aging. Tables 2 and 3 showseveral antihomotoxic measures use-

ful in immunosenescence. Accord-

ing to the course, detoxification and

drainage cycles may be repeated. If

treatment starts with immunostimu-

lation, the patient may experience

changes counter to the therapeutic

aims, owing to the high levels of

inflammatory molecules. The nutri-

tional status of the elderly patient

must be improved at the same time

as antihomotoxic medication is ad-

ministered. In some cases, antioxi-

dative supplementation (vitamin C,

vitamin E, glutathione, N-acetyl-

cysteine, and S-adenosyl methion-

ine), which tends to improve pha-

gocyte migration, phagocytosis,

production of TNF-a, and produc-

tion of IL-1 and IL-2 in T lympho-

cytes, is also necessary.We can conclude from the above

that the aging process has a major ) 17


Immune component Abnormality in immunosenescence

Hematopoietic stem cells Increase in hematopoietic progenitor cell counts CD34+

T lymphocytes 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

B lymphocytes Increase in B lymphocyte polyreactivity

Reduction in specificity and quantity in antibody production

NK cells Increase in the expression of receptor activators of

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

Macrophages Reduction in lipopolysaccharide recognition and activity

Reduction in the production of TNF-a

Phagocyte deficiencies

Lymph nodes Reduction in the cellular and functional structure of lymph nodes

Table 1:

Main defects in immunosenescence


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)


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 man-

ner.12|

DET-phase Basic and/or

symptomatic

Regulation therapy* Optional

Impregnation,

degeneration

• Ginseng

compositum

D&D • Advanced supportive

detoxification and

drainage

• Arnica-Heel

(if the inflammation is

more severe)

IM • Traumeel

OR • Coenzyme compositum

• Ubichinon compositum

• Tonsilla compositum

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. Immuno-

modulation: 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


symptomatic


Impregnation,

degeneration

• Ginseng

compositum

D&D • Basic detoxication and

drainage: Detox-Kit

• Echinacea compositum

(if there is a suspicion

of a bacterial infection)IM • Engystol

OR • Pulsatilla compositum

• Glyoxal compositum

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 ge-

netics of human longevity. Ann NY Acad Sci.

2006;1067:252-263.2. Pawelec G. Immunosenescence comes of age.

Symposium on Aging Research in Immunol-

ogy: 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. Nona-

genarians from the Swedish NONA Immune

Study have increased plasma antioxidant

capacity and similar levels of DNA damage

in peripheral blood mononuclear cells com-

pared to younger control subjects. Exp Geron-

tol. 2002,37(2-3):465-473.5. Franceschi C, Bonafè M, Valensin S. In-

flamm-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 glomeru-

lonefritis 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 Micro-

biol 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 im-

mune risk phenotype, cognitive impairment,

and survival in very late life: impact of al-

lostatic 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.


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)

A r o u n d t h e G l o b e

Advanced IAH Lecturer’sTrainings East and West

By Bruno Van Brandt

IAH Education Manager

In addition to its much-visited e-learning program for medicaldoctors and licensed health care

professionals worldwide, the Inter-

national Academy for Homotoxicol-ogy 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 ma-

terial in their countries. The goal is

to have more medical students well

prepared to take the IAH e-exami-

nation and obtain the IAH certifi-

cate in the future. Although tens ofthousands 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 educa-

tion.

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 Cen-tral 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 doc-

tors from North and South America

and Canada who studied the IAH

educational material in depth

brought the total of rollout partici-

pants to about 100 MDs. These ad-vanced lecturers will soon be pro-

moting the homotoxicological

model in their home countries.

The rollout training material (i.e.,

the IAH abbreviated course in ap-

plied 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 certifi-

cate. Since there is no charge either

for registration or for the certificate,

there are no costs involved in takingthe course. Instructional materials

are currently available in English,

French, Spanish, Russian, and Pol-

ish, with German and Portuguese to

follow in the next few months.|

Dr. Arturo O’Byrne from Colombia

lecturing on immunomodulation

at the IAH Rollout West in Miami,

Florida

More than 70 medical doctors and

university professors from Central and

Eastern Europe participated in the IAH

Rollout East in Baden-Baden, Germany.


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Recurrent UTIs will occur at leasttwice in six months or threetimes 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 sus-

pected when a patient complains of

pressure or pain in the pelvis or re-

ports bladder discomfort. The pain

or discomfort typically increases as

the bladder fills and decreases dur-

ing voiding, is associated with uri-

nary 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 peo-ple 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 per-

cent of those will experience a re-

currence.

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 sensa-

tion of being unable to urinate fully;

cloudy, bloody or foul-smelling

urine; and pain in the lower abdo-men. 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), nau-

sea 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 per-

cent of UTIs in adults. These bacte-

ria are normally present in the colon

and may enter the urethral opening

from the skin around the anus and

genitals. Women may be more sus-ceptible to UTIs because the female

urethral opening is closer to the

source of the bacteria (anus or vagi-

na) and the urethra is shorter than in

men, allowing bacteria easier access

to the bladder.

Other bacteria that cause urinary

tract infections include Staphylococ-

cus saprophyticus (5 to 15 percent of

cases), Chlamydia trachomatis, Myco-

plasma hominis, Klebsiella and (more

rarely) various species of Proteus and

Pseudomonas . Chlamydia and Myco-

plasma can be transmitted through

sexual intercourse.

For unknown reasons, sexual inter-

course triggers UTIs in some wom-

en. Diaphragm users develop infec-

tions more often, and condoms with

spermicidal foam may cause vaginal

growth of E. coli , which can thenenter the urethra.

)

P r a c t i c a l P r o t o c o l s

Bioregulatory Treatmentof 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.


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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 re-quired.

In infants, bacteria from soiled dia-

pers can enter the urethra and cause

UTIs. E. coli may also enter the ure-

thral 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 hypertro-

phy), conditions that cause incom-plete bladder emptying (e.g., spinal

cord injury), congenital abnormali-

ties of the urinary tract (e.g., vesical

ureteral reflux), changes in the im-

mune system (e.g., HIV and diabe-

tes), 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 pos-

sible 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 reliablesample is obtained via suprapubic

puncture), followed by a urine cul-


)

P r a c t i c a l P r o t o c o l s

ture, if needed, to determine the

specific bacteria and obtain an anti-

biogram. When leucocytes are ele-

vated and the urine culture is nega-

tive, chlamydial urethritis, prostatitis,

and IC are possibilities. In recurrent

UTIs, ultrasound exams of the uri-

nary tract and intravenous urogra-

phy can be helpful diagnostic tools.

A diagnosis of IC can be confirmed

through cystoscopy with hydrodis-tention.

Treatment

In allopathic medicine, lower UTIs

are most commonly treated with

antibiotics (e.g., trimethoprim-sulfa-

methoxazole and amoxicillin), but

bioregulatory therapy alone is also

effective in treating this type of in-

fection. According to homotoxico-

logical guidelines, one or more basic

symptomatic products should be

added to the “three pillar approach”of drainage and detoxification

(D&D), immunomodulation (IM),


symptomatic


Endodermal,

urogenital

Inflammation

• Berberis-

Homaccord

• Spascupreel

D&D • Basic detoxication and

drainage

• Echinacea compositum

(for severe infection)

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.

Table 1: Treatment for lower UTIs


symptomatic


Mesodermal,

nephrodermal

Inflammation

• Berberis-

Homaccord

• Spascupreel

D&D • Advanced supportive

detoxification and

drainage

• Reneel

• Belladonna-Homaccord

(for high fever)

• Mercurius-Heel (if there is

frank pus in the urine)

IM • Echinacea compositum

• Cantharis compositum

OR • Mucosa compositum

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)


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and, if ne

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