In Focus - International Academy of Homotoxicology

Transcrição

d 2.00 • US $ 2.00 • CAN $ 3.00
Biomedical
Therapy
J o urnal o f
Volume 2, Number 3 ) 2008
Integrating Homeopathy
and Conventional Medicine
Infectious
Diseases
• The Immune System, Our Personal Bodyguard
• Theories of Immunosenescence and Infection
)
Contents
I n Fo c u s
The Immune System, Our Personal Bodyguard . . . . . . . . . . . . 4
W h a t E l s e I s N e w ? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
From the Practice
Acute Recurrent Otitis Media . . . . . . . . . . . . . . . . . . . . . . . . . . 12
M a r ke t i n g Yo u r P r a c t i c e
Managing Expenses and Prices in the Medical Practice . . . .14
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 . . . . 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
Re s e a r c h H i g h l i g h t s
Engystol: A Homeopathic Medication
for the Common Cold . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
Making of ...
From Plant to Bottle: The Production of
Homeopathic Nasal Sprays . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
)2
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
)
Fighting Infections
Dr. Alta A. Smit
O
nly 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,
Journal of Biomedical Therapy 2008 ) Vol. 2, No. 3
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 Phagozytosef ähigkeit von Granulozyten durch
homöopathische Arzneipräparate: in vitroTests und kontrollierte Einfachblindstudien.
Arzneim.-Forsch./Drug Res. 1986;36(9):14211425.
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
) I n Fo c u s
The Immune System,
Our Personal Bodyguard
)4
By Manfred Schmolz, PhD, and Doris Ottendorfer, PhD
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.
merous 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
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 nu-
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
) I n Fo c u s
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 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 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 (chemo
kines)
2. help make functionally mature
APCs
3. contribute to antiviral immunity8
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
Photo by Rocky Mountain Laboratories, NIAID, NIH,
http://en.wikipedia.org/wiki/Image:SalmonellaNIAID.jpg
) I n Fo c u s
Bacteria display a wide diversity of
shapes and sizes. Here: Salmonella
typhimurium (red) invading cultured
human cells.
)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 (MHCII).
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 Sousa15 and
Shortman and Naik16 provide reviews). In contrast to MHC-I molecules, MHC-II molecules sample
antigens from the extracellular space
to activate CD4-positive (CD4+) Thelper (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
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
) I n Fo c u s
A macrophage forming two processes
to phagocytize two smaller particles.
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
NK cells kill virus-infected and
tumor cells
Virus-specific CD8+ CTLs are the
major effector cells for eliminating
established viral infections. NK cells
also lyse virus-infected cells and tumor cells. Therefore, both cell types
are often summarized as cytotoxic
lymphocytes. It seems that both cell
types share common mechanisms
for antiviral and antitumor defense.20-22 For example, both cell
types secrete the cytotoxic protein
perforin, along with granzymes. Together, they kill infected cells and
tumor cells on cell-to-cell contact.
This is a thoroughly controlled process to kill only the diseased target
cell (not healthy neighbor cells).
The most important difference between 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 receptors showing a more general specificity for pathogen-induced changes
in tissue cells (e.g., intracellular infection or neoplasia). Other NK cell
receptors possess inhibitory activity,
enabling a close control of cell killing.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 expansion (i.e., without a “lag” phase).
Therefore, NK cells effectively limit
the early spread of infection.
CD8+ CTLs recognize antigens by
their TCR in association with MHCI molecules. In addition, similar to
CD4+ T cells, CD8+ T cells need
clonal expansion to establish full effector functions.
Role of IFN synthesis in
antiviral immunity
In addition to cell contact-dependent killing mechanisms, soluble
mediators released during viral infection of cells directly stimulate the
production of IFNs, of which type 1
IFNs (α and β) possess the strongest
direct antiviral activity. Type 1 IFNs
are produced by many cell types and
cause an “antiviral state” in the infected cells; this state is characterized by inhibition of viral replication and cell proliferation. Type 1
IFNs also enhance NK cell activity
to lyse target cells and improve antigen presentation in APCs.
Multiple ways to control T-cell
activation
T-cell responses do not only consume lots of energy by clonal expansion but are also highly powerful 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.
)7
) I n Fo c u s
) I n Fo c u s
The elimination of viruses is a real
challenge for the immune system.
)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 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 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 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 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 MHCII 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
) I n Fo c u s
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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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):735747.
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):363374.
24. Acuto O, Michel F. CD28-mediated co-stimulation: a quantitative support for TCR signalling. Nat Rev Immunol. 2003;3(12):939951.
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.
2007;7(11):875-888.
27. Anthony RM, Rutitzky LI, Urban JF Jr, Stadecker MJ, Gause WC. Protective immune
mechanisms in helminth infection. Nat Rev
Immunol. 2007;7(12):975-987.
)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 re
commendations, 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.
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
Am Soc Nephrol. 2008;19(6):
1041-1043
F O R P RO F E S S I ONA L U S E ON LY
) 10
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 practitioners. 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!
Hunger hormone makes
foods look more appetizing
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.
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
N Engl J Med. 2008;358(5):475-483
) 11
) From the Practice
Acute Recurrent Otitis Media
By Ivo Bianchi, MD
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.
S
ymptoms 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
) 12
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
Cochlea
Eardrum
• 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.
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:
Eustachian tube
• 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
Common factors related to
acute otitis
Anatomical factors
Exposure to smoke
or pollution
This therapeutic protocol may seem
complicated. Rather than just a simple therapy, it is a real strategic plan
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.
O
ffice 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:
Have you ever analyzed the purchasing
behavior in your practice?
A few simple strategies can help you
) 14
avoid unnecessary costs.
•
•
•
•
•
•
•
•
•
•
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.
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 immunosenescence2 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:
Table 1:
Main defects in immunosenescence
• 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
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 immuno-
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
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 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),
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-acetyl
cysteine, and S-adenosyl methion
ine), which tends to improve pha
gocyte migration, phagocytosis,
production 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
Basic and/or
symptomatic
Impregnation,
degeneration
• Ginseng
compositum
Regulation therapy*
Optional
D&D
• Advanced supportive
detoxification and
drainage
• Arnica-Heel
(if the inflammation is
more severe)
IM
• Traumeel
OR
• Coenzyme compositum
• Ubichinon compositum
• Tonsilla compositum
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|
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
Basic and/or
symptomatic
Impregnation,
degeneration
• Ginseng
compositum
Regulation therapy*
Optional
D&D
• Basic detoxification and
drainage: Detox-Kit
IM
• Engystol
• Echinacea compositum
(if there is a suspicion
of a bacterial infection)
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:
) 18
–
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, Bonaf è 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):119120.
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
I
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.
n addition to its much-visited elearning 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.
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 eexamination 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
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.
R
ecurrent 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.
) 20
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
Endodermal,
urogenital
• Berberis Homaccord
• Spascupreel
Inflammation
Regulation therapy*
Optional
D&D
• Basic detoxification and
drainage
(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
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-
DET-phase
Basic and/or
symptomatic
Mesodermal,
nephrodermal
• Berberis Homaccord
Inflammation
Regulation therapy*
Optional
• Advanced supportive
detoxification and
drainage
• Reneel
IM
• Cantharis compositum
• Mercurius-Heel (if there is
frank pus in the urine)
OR
• Mucosa compositum
D&D
• Spascupreel
• Belladonna-Homaccord
(for high fever)
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)
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.
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 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).
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. |
) 22
BL 13 Lung
BL 14 Circulation, sex
BL 15 Heart
BL 16 Governing vessel
BL 17 Conception vessel
BL 18 Liver
Solidago compositum
Mucosa compositum
Pulsatilla compositum
BL 19 Gall bladder
BL 20 Spleen
BL 21 Stomach
L2
BL 22 Triple heater
BL 23 Kidney
BL 25 Large intestine
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.
BL 27 Small intestine
S2
BL 28 Bladder
) Meet the Expert
Dr. Ivo Bianchi
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.
I
vo 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
By Catherine E. Creeger
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 hoJournal of Biomedical Therapy 2008 ) Vol. 2, No. 3
motoxicology, 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
) Re s e a r c h H i g h l i g h t s
Engystol: A Homeopathic Medication
for the Common Cold
) 24
By Mary A. Kingzette
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, Vin
cetoxicum 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 variJournal of Biomedical Therapy 2008 ) Vol. 2, No. 3
ables, 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-
) Re s e a r c h H i g h l i g h t s
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).
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. |
Discussion
Based on this exploratory, nonrandomized, observational study,
Engystol treatment was not inferior
to conventional treatments for the
Reference
Swallow wort (Vincetoxicum hirundinaria)
is one of the active ingredients of Engystol.
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.
) 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.
T
o 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, Ho
möopathisches
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
www.iah-online.com
Free of charge

In Focus - International Academy of Homotoxicology

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