- International Academy of Homotoxicology

Transcription

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Biomedical
Therapy
J o urnal o f
Volume 4, Number 1 ) 2010
Integrating Homeopathy
and Conventional Medicine
Pediatric
Diseases
• Imprinting in Early Life • ADHD in the Young Child
• Primary Ciliary Dyskinesia – a Case Report
Contents
I n Fo c u s
Imprinting in Early Life Predisposes to
Diseases in Adulthood. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
W h a t E l s e I s N e w ? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12
From the Practice
Use of Bioregulation Therapies for
a Severe Otorhinological Problem . . . . . . . . . . . . . . . . . . . . . . . 14
© iStockphoto.com/Rosemarie Gearhart
Meet the Expert
Dr. David Riley . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16
Around the Globe
Scientific Symposia in Belgium and the Netherlands:
The Extracellular Matrix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
Re f r e s h Yo u r H o m o t ox i c o l o g y
Attention-Deficit/Hyperactivity Disorder
in Infancy and in the Preschool-aged Child . . . . . . . . . . . . . .18
M a r ke t i n g Yo u r P r a c t i c e
Making Your Practice a Team . . . . . . . . . . . . . . . . . . . . . . . . . . .22
Re s e a r c h H i g h l i g h t s
New Approaches in the Treatment of
Respiratory Insufficiency in Neonates . . . . . . . . . . . . . . . . . . . 24
Making of ...
Production of Homeopathic Suppositories . . . . . . . . . . . . . . . 26
Cover photograph © FutureDigitalDesign/Fotolia.de
)2
Published by/Verlegt durch: International Academy for Homotoxicology GmbH, Bahnackerstraße 16,
76532 Baden-Baden, Germany, www.iah-online.com, e-mail: journal@iah-online.com
Editor in charge/verantwortlicher Redakteur: Dr. Alta A. Smit
Print/Druck: VVA Konkordia GmbH, Dr.-Rudolf-Eberle-Straße 15, 76534 Baden-Baden, Germany
© 2010 International Academy for Homotoxicology GmbH, Baden-Baden, Germany
© iStockphoto.com/Milena Lachowicz
)
)
Editorial
The Importance
of Early Intervention
Dr. Alta A. Smit
I
n bioregulatory medicine, treatment of pediatric patients poses
not only many opportunities but
also specific difficulties. Practice has
shown that children respond very
well to bioregulatory therapy, especially since the juvenile organism is
mostly still reactive and regulates
fairly easily. However, due to increases in environmental stressors
(such as toxins and psychological
factors) and in the use of suppressive
drugs, treating today’s children can
sometimes pose a challenge even for
integrative practitioners.
Postnatal development remains a
sensitive time, as many organ systems and autoregulatory systems
continue to mature after birth. Tissues that are still developing are especially vulnerable to environmental
imprints. The developing brain and
nervous tissue, in particular, are sensitive to the effects of environmental
toxins,1 as is the immune system.
Many diseases of adulthood result
from imprinting during the developmental period, and chronic pain
syndromes in particular can often be
traced back to events in childhood
(e.g., maternal separation).2 This
topic is discussed at length in our
focus article by Professor Marietta
Kaszkin-Bettag, who also suggests
some interventions to correct and
strengthen the bioregulatory apparatus. The issue of imprinting deserves to be taken seriously from the
scientific, health economics, and social perspectives, since early intervention may prevent illness in later
life.
The use of bioregulatory medicine
as adjuvant therapy in even moderate to severe illness is discussed in
two articles, the case study on ciliary
dyskinesia by neonatologist Dr. Sergio Vaisman and the summary of a
study by Professor Lidiya Ivanovna
Ilyenko et al. on respiratory distress
syndrome in neonates.
Dr. Leon Strauss tackles the difficult
subject of attention deficit/hyperactivity disorder in three articles, the
first of which, dealing with the
young child, appears in this issue.
The other two will follow in subsequent journals.
We also present our regular features:
Marc Deschler’s valuable marketing
column shows how your practice
staff will become an efficient team;
Dr. Cornelia Witt presents the manufacturing of bioregulatory suppositories in the Making of… series; and
Meet the Expert introduces Dr. David
Riley, the current president of the
International Society of Homotoxicology and Homeopathy.
Last but not least, Pascale Vlietinck
reports on a successful international
symposium in Belgium and the
Netherlands.
We are sorry to see the last of the
Making of … series in this issue but
pleased to announce that Dr. Robbert van Haselen has agreed to write
a column on research methodology
and the use of research data. We are
eagerly anticipating this new series
of articles, which will begin with
the next issue.
Dr. Alta A. Smit
References:
1. Harris JB, Blain PG. Neurotoxicology: what the neurologist needs to
know. J Neurol Neurosurg Psychiatry.
2004;75(suppl 3):iii29-iii34.
2. Clauw DJ. Fibromyalgia: an overview.
Am J Med. 2009;122(suppl 12):S3-S13.
Journal of Biomedical Therapy 2010 ) Vol. 4, No. 1
)3
) I n Fo c u s
Imprinting in Early Life Predisposes
to Diseases in Adulthood
By Marietta Kaszkin-Bettag, PhD
Professor of pharmacology, toxicology, and phytotherapy
Introduction
Prenatal development and early
childhood are influenced by endogenous and environmental factors
that act in concert by causing structural and functional changes that
may persist for the life span. This
phenomenon is termed “early-life
programming.”1 The concept of early-life physiological “programming”
or “imprinting” tries to explain the
associations among prenatal environmental events, altered fetal
growth and development, and the
occurrence of diseases in later life
(as previously reviewed).1 Such programming factors include nutrients
and endogenous hormones; they
may also involve environmental exposure to biological materials, chemicals, drugs, medical devices, and
physical factors.2
Early-life programming reflects the
action of certain factors on a specific
tissue during a sensitive developmental period or “window,” thereby
affecting its development, organization, and function. Different cells
and tissues are sensitive at different
times; therefore, the effects of environmental challenges will have distinct consequences, depending not
only on the challenge involved but
also on its timing.
)4
Developmental immunotoxicity
and health risks for adulthood
Developmental
immunotoxicity
(DIT) is an increasing health concern because DIT outcomes predispose children to certain diseases; the
diseases with increasing incidences
in recent decades include childhood
asthma, allergic diseases, autoimmune conditions, and childhood infections.3 The enhanced vulnerability of the developing immune system
for environmental influences is based
on unique immune maturation events
that occur during critical windows
in early life (e.g., negative selection
against autoreactive T cells in the
developing thymus).
Environmental influences on prenatal development and immunologic
responses
The in utero environment is thought
to play a major role in the risk of
later life disease. The semiallogeneic
pregnancy state is characterized by a
suppression of graft rejection because during the course of maturation, the potential for maternal-fetal
allogeneic reactions must be minimized. This situation is associated
with an impairment of the fetal and
neonatal immune system, which may
influence the specific nature of DIT
outcomes.4 The last-trimester fetus
and the neonate normally have decreased T-helper cell (Th) 1–dependent functions, and postnatal acquisition of necessary Th1 capacity is a
major concern with DIT.4 Evidence
for the reduced Th1 capacity of
newborns is reflected by the fact
that the production of interferon g
(the hallmark Th1 cytokine) is severely reduced in the neonate.
In utero exposure to pesticides, such
as polychlorinated biphenyls, or tobacco smoke is known to produce a
range of immunotoxic outcomes
(e.g., immunosuppression, autoimmunity, or misregulated tissue inflammation). Beyond T cells, dendritic cells and macrophages are
sensitive targets to chemicals, resulting in macrophage dysregulation,
changes in innate immunity, and inflammatory damage.
Immune response during early life
A cesarean delivery can affect neonatal immune responses and can increase the risk of atopy. Children
born by cesarean section have a
2-fold higher odds of atopy than
those born by vaginal delivery (odds
ratio, 2.1; 95% confidence interval,
1.1-3.9). In multivariate analyses,
birth by cesarean section was significantly associated with increased
odds of allergic rhinitis (odds ratio,
1.8; 95% confidence interval, 1.03.1), but not of asthma.5 This study
demonstrated that cesarean delivery
may be associated with allergic
rhinitis and atopy, particularly
among children with a parental history of allergies. This could be explained by lack of contact with the
Figure 1. Immune Dysregulation
in the Young: T-helper (Th) Cell 2
Predominance
A Th2 profile is associated with atopy.
maternal vaginal/fecal flora during
cesarean delivery.
During the neonatal period, the
mammalian host is exposed through
mucosal surfaces to a broad spectrum of environmental macromolecules and microbial agents. The neonatal mucosa has all major elements
of innate and adaptive immunologic
repertoire. The early neonatal period is also characterized by a relative deficiency in antigen-presenting
cell functions, altered cell-mediated
immune responses, and a relative in
crease in apoptosis and eosinophilic
responses.6 Recent investigations
have shown that the nature of mucosal microflora acquired in early
infancy determines the outcome of
mucosal inflammation and the subsequent development of mucosal
disease, autoimmunity, and allergic
disorders later in life. It seems that
altered mucosal microflora in early
childhood affect signaling reactions
that determine T-cell differentiation
and/or the induction of tolerance.
Reduced Th1 and increased Th2
cytokine expression in the respiratory tract, associated with increased
allergic disease, has been correlated
with reduced exposure to microbial
agents associated with Th1 responses. These observations suggest that
the interaction between the external
environment and the mucosal tissues
in the early neonatal period and infancy may be critical in directing and
controlling the expression of diseasespecific responses in later life.
Abbreviation: Th, T-helper cell
Thus, early-life toxicologic exposure
to xenobiotic infectious agents or
stress may be pivotal in producing
the later-life onset of increased
childhood infections; neurologic
disorders; fatigue-related illnesses;
autoimmune diseases; allergic diseases, including asthma; food allergies; and even cancers (e.g., childhood leukemia).7
Childhood allergic diseases
The incidence of asthma in industrialized countries has increased dramatically in recent decades, with the
consequences of significant public
health cost. In 2002, there were already approximately 16 million adolescents with asthma.4 For childhood allergic asthma and rhinitis in
particular, various toxins, infectious
agents, airborne pollutants, and maternal smoking were identified as
significant risk factors.2 In addition,
the likelihood is discussed that fetalexpressed genes promoting Th2
may continue to be inappropriately
expressed in some neonates, thereby
increasing the risk of asthma.
In an 8-year prospective study of
308 children, younger than 7 years,
who had recurrent wheezing, a personal history of allergic disease, parental asthma, atopy, and late-onset
symptoms were identified as prognostic risk factors for asthma symptoms. The origin of this disease may
be traced to early childhood (i.e.,
the years before exposure to allergen).8
In summary, it was proposed that
managing the fetal and neonatal immune system to reduce the persistence of the fetal immune phenotype
and to promote rapid and effective
Th1 maturation has the potential to
significantly reduce the risk of asthma in childhood4 (Figure 1). Fur-
)5
) I n Fo c u s
Ad
g
re n a l l a n d
Tha
la m us & h
yp
th
o
a la
m us
Figure 2. Treatment of HypothalamicPituitary-Adrenal Axis Dysfunction
in Stressed Individuals and Patients
With Chronic Pain Syndromes:
Tonsilla compositum, Thalamus
Tonsilla compositum
M
compositum, and Spascupreel
at
Multi-target
regulation
rix
Thalamus compositum
Mu
sc
le
thermore, an increased risk for several childhood allergic diseases was
identified after maternal use of antibiotics during pregnancy.2
)6
Childhood neurologic disorders
Another example is chronic fatigue
syndrome (CFS) in children, for
which the causes are certainly earlylife events.9 Immune dysfunction is
recognized as part of the CFS phenotype but has received comparatively less attention than aberrant
neurologic or endocrine function.
However, recent research results
suggest that early-life immune insults, including DIT, which is induced by xenobiotics, may offer an
important clue to the origin of CFS.
Pediatric fibromyalgia seems to be
a variant of CFS, with a predominance of hypothalamic-pituitaryadrenal (HPA) dysfunction10 (Figure
2). Fibromyalgia is most common
in midlife, but may be seen at any
age. It is characterized by chronic
widespread pain.11 The syndrome
is associated with a constellation of
symptoms, including fatigue, nonrefreshing sleep, and irritable bowel.
Central nervous system sensitization
is a major pathophysiologic aspect
of fibromyalgia; in addition, various
external stimuli, such as trauma and
stress, may contribute to the development of the syndrome.
Many early postnatal neurologic lesions associated with postnatal neurobehavioral diseases are recognized
as being linked to a prenatal im-
Spascupreel
mune insult and inflammatory dysregulation (e.g., autism, autism spectrum disorders, and increased risk of
schizophrenia). Also, neurologic diseases of later life may be connected
to DIT because the gestational environment is thought to be important
in both Parkinson and Alzheimer
diseases.2,12
Cancer
Dysfunctional immune responses
may even lead to cancer, and childhood leukemia is thought to be directly linked with DIT.2,7 A key risk
factor seems to be an early-life dysfunctional immune response to common childhood infections.
Prenatal imprinting of
the metabolic syndrome
Prenatal glucocorticoid stress
Glucocorticoids are powerful mediators of early-life developmental
processes. Their potent effects on
tissue development (i.e., the accelerated maturation of organs, notably
the lung) underline their widespread
therapeutic use in obstetric and neonatal practice in threatened or actual
preterm delivery. In contrast, glucocorticoids are rarely used in the antenatal treatment of fetuses at risk of
congenital adrenal hyperplasia.1,13-14
However, glucocorticoid administration during pregnancy reduces offspring birth weight. It was hypothesized that prenatal stress derived
from DIT, as previously described,
or exposure to excess glucocorti
coids might represent a mechanism
linking fetal growth with adult
pathophysiology.15 Epidemiological
evidence suggests that particularly
low birth weight is associated with
an increased risk of cardiovascular,
metabolic, and neuroendocrine disorders in adult life.
Experimental studies in rats have
shown that the birth weight is reduced after prenatal exposure to the
synthetic steroid dexamethasone,
which readily crosses the placenta;
or to carbenoxolone, which inhibits
11b-hydroxysteroid dehydrogenase
type 2 (11b-HSD2), the physiological fetal-placental “barrier” to mater-
) I n Fo c u s
nal glucocorticoids. As adults, the
offspring exhibit permanent hypertension, hyperglycemia, increased
HPA axis activity, and behavior reminiscent of anxiety. Physiological
variations in placental 11b-HSD2
activity correlate directly with fetal
weight.
In humans, 11b-HSD2 gene mutations cause low birth weight. Moreover, low-birth-weight newborns
have higher plasma levels of corti
sol as a potential stress hormone
throughout adult life.1,13
In human pregnancy, severe maternal stress affects the offspring’s HPA
axis and is associated with neuro
psychiatric disorders; moreover, maternal glucocorticoid therapy may
alter offspring brain function.13
Low birth weight and
metabolic complications
Numerous studies have revealed an
association between lower birth
weight and the subsequent development of the common cardiovascular
and metabolic disorders of adult life
(i.e., hypertension, insulin resistance,
type 2 diabetes mellitus, and cardiovascular disease–related deaths).1
The early-life events described
above that alter birth weight are important predictors of adult morbidity.
In a study16 of 22,000 US men,
those who weighed less than 2.2 kg
at birth had relative risks of adult
hypertension of 1.26 and of type 2
diabetes of 1.75 compared with
those with an average birth weight.
Similar observations were made in
women.17 Moreover, the association
between birth weight and later cardiometabolic disease seems largely
independent of classic lifestyle risk
factors (e.g., smoking, adult weight,
social class, excess alcohol intake,
and sedentariness) that are additive
to the effect of birth weight.18
Prenatal origin of obesity,
cardiovascular disease, and insulin
resistance
The fetal origins of obesity, cardiovascular disease, and insulin resistance have been investigated in a
wide range of epidemiological and
animal studies, which revealed an
adaptation of the nutritionally manipulated fetus to maintain energy
homeostasis for ensuring survival.19
One consequence of such developmental plasticity may be a long-term
resetting of cellular energy homeostasis, most probably via epigenetic
modification of genes involved in a
number of key regulatory pathways.20 For example, reduced maternal-fetal nutrition during early to
mid gestation affects adipose tissue
development and adiposity of the
fetus by setting an increased number
of adipocyte precursor cells.21 More
important, clinically relevant adaptations to nutritional challenges in
utero may only manifest as primary
components of the metabolic syndrome if followed by a period of accelerated growth early in the postJournal of Biomedical Therapy 2010 ) Vol. 4, No. 1
natal period and/or if offspring
become obese. This suggests that
obesity is not simply the result of
lifestyle but has developmental determinants that are not of genetic
origin. Thus, an understanding of
the mechanisms that mediate the
epigenetic changes is crucial to determine dietary and pharmaceutical
approaches that can be applied in
the postnatal period.
Fetal undernutrition and hypoxia
are associated with an increased susceptibility to a number of adult-onset metabolic disorders. In addition
to obesity, these include cardiovascular disease and insulin resistance.
Interestingly, premature neonates
also have an increased cardiovascular risk in adult life.18 It was observed that different feeding regimens, particularly in human
premature neonates, have long-term
metabolic consequences.19 Some developmental responses may persist
through several generations. For example, the female reproductive tract
develops in the first half of human
fetal life. Girls who were growth retarded in utero have a reduced uterine size, and this reduction may lead
to impaired uterine-placental function when these women become
pregnant.
On the other hand, there is increasing evidence that maternal obesity is
linked to numerous metabolic complications, including subfertility,
gestational diabetes, hypertensive
disorders of pregnancy, and throm-
)7
) I n Fo c u s
yg
la n d
Placenta compositum
Fat
t
iss
Illustrations: Andrew Mingione
Pi t
ui
ue
r
ta
Figure 3. Treatment of Metabolic
Syndrome and the HypothalamicPituitary-Adrenal Axis in Children:
Placenta compositum, Lymphomyosot,
Hepar compositum, and Coenzyme
compositum
Liv
er
Multi-target
regulation
Lymphomyosot
M it
oc
on
h
)8
Mechanisms for the development
of metabolic syndrome in early life
The risks for obesity and insulin resistance may be programmed in utero as a result of decreased or increased birth weight because of the
reasons previously described.
The development of metabolic syndrome, however, is the result of a
complex interaction of specific genes
and environmental influences.23 A
primary mechanism accounting for
perinatal adaptation is the epigenetic modification, via DNA methylation, that affects gene expression
permanently, with consequent endocrine and behavioral changes persisting into adulthood. In addition,
genetic polymorphisms in a regulatory pathway may accompany environmental factors acting on fetal
development and, thus, the origins
of many human diseases. Polymor-
a
Metabolic syndrome
in childhood
d ri
boembolism, with potential longterm health consequences for both
mother and child. Obesity and diabetes in women before pregnancy,
gestational diabetes, and glycosuria
(both diagnosed and ascertained
during pregnancy) result in a higher
mean birth weight and an increased
offspring obesity risk.22 Thus, maternal lifestyle should be altered as
possible to improve maternal and fetal outcomes.
Hepar compositum
phisms in the insulin promoter gene
and a parental background of metabolic syndrome predispose children
to be overweight and to have insulin
resistance (Figure 3).
In addition, an enhanced release
of inflammatory cytokines (tumor
necrosis factor a and interleukins 1
and 6) is correlated with the extent
of adiposity in adolescents. These
cytokines decrease insulin receptor
signaling, thereby contributing to
the insulin resistance state.
Childhood weight gain and obesity
have been shown to be linked to the
overall mortality risk in adulthood,
including the risk from cardiovascular disease. A recent update24 of the
worldwide prevalence of metabolic
syndrome in overweight children
and adolescents between the ages of
2 and 19 years indicated a rate of up
to 60%.
Nonalcoholic fatty liver disease
in children
Further metabolic consequences of
obesity include nonalcoholic fatty
Coenzyme compositum
liver infiltration, which is rapidly
emerging in the pediatric population.
Nonalcoholic fatty liver disease is
increasingly prevalent in pediatric
individuals, in parallel with increasing obesity, and can lead to liver inflammation, fibrosis, and even cirrhosis.25 Nonalcoholic fatty liver
disease is thought to occur as a consequence of an increase in free fatty
acid release into the portal circulation by abundant visceral adipocytes. This results in higher triglyceride levels and subsequent excessive
intrahepatic lipid storage. The prevalence of fatty infiltration of the liver
was recently estimated at 9.6% of
the US pediatric population. Fatty
liver prevalence differs significantly
by race and ethnicity (Asians, 10.2%;
blacks, 1.5%; Hispanics, 11.8%; and
whites, 8.6%). The highest rate of
fatty liver was seen in obese children
(38%).
Pediatric nonalcoholic fatty liver
disease may improve with lifestyle
therapy (maintaining weight and
) I n Fo c u s
regular exercise) and agents that
improve insulin sensitivity. Thus,
identifying effective strategies
for treating these obesity-related
comorbidities in children and adolescents is crucial to the prevention
of future cardiovascular disease and
poor health outcomes.
Metabolic risk factors for sexual
development of female adolescents
A risk factor for female sexual development of adolescents, connected
with type 2 diabetes mellitus and
cardiovascular disease, is polycystic
ovary syndrome (PCOS). Polycystic
ovary syndrome refers to hyperandrogenism, anovulatory menstrual
cycles or oligomenorrhea, hirsutism,
and the appearance of polycystic
ovaries on ultrasonography.26 Insulin
resistance and elevated serum
luteinizing hormone levels are also
common features of PCOS. Polycystic ovary syndrome is associated
with an increased risk of type 2 diabetes and cardiovascular events. Insulin resistance, in conjunction with
altered regulation of the HPA axis,
promotes a hyperandrogenic state at
the level of the ovary and adrenal
gland.23 Obese adolescents with
PCOS have an increased prevalence
of impaired glucose tolerance, insulin resistance, and atherogenic lipid
profiles compared with lean counterparts with PCOS.
Precocious puberty
Another factor of health and social
importance is precocious puberty
(i.e., early sexual maturation in female children). There is evidence
that girls are maturing at an earlier
age and that precocious puberty is
increasing.27
Precocious puberty affects 1 in
5,000 children and is 10 times more
common in girls. Statistics indicate
that girls in the United States are
maturing at an earlier age than they
did 30 years ago and that the number of girls with diagnosed precocious puberty (i.e., the appearance of
secondary sex characteristics before
the age of 8 years or the onset of
menarche before the age of 9 years)
is increasing. Early menarche has
been linked to a greater risk of
breast cancer as an adult. Therefore,
a precocious onset would seem to
increase that risk.
Responsible factors included genetic
and ethnic background, pediatric
obesity, and environmental variables
that disrupt endocrine function (i.e.,
chemicals, toxins, plasticizers, infant
feeding methods, skin and hair
products, and assisted reproductive
technologies), psychosocial stress,
and early exposure to a sexualized
society.27 The role of obesity is often
cited in association with the earlier
onset of puberty. The number of
overweight children aged 6 to 11
years has more than doubled in the
past 20 years (from 7.0% in 1980 to
18.8% in 2004), and the rate has
more than tripled among adolescents aged 12 to 19 years (from
5.0% in 1980 to 17.1% in 2004).
Conclusions
There is increasing evidence that genetic and epigenetic factors (i.e.,
early-life environmental influences)
can affect prenatal development and
cause structural and functional
changes that may be responsible for
the onset of diseases in childhood
and adulthood. This concept of early-life physiological programming
or imprinting1 has been examined
for prenatal and postnatal exposure
to endogenous factors (e.g., sex hormones) and exogenous agents (including toxins and drugs). Certain
windows of vulnerability are identified, in which different tissues, signaling pathways through the HPA
axis, and more important, the immune system, are sensitive to these
challenges. Many chronic diseases
with an increasing incidence (e.g.,
childhood asthma, allergies, neurologic syndromes, and metabolic syndrome) are triggered through earlylife environmental risk factors and
immune dysfunction. Therefore, the
identification of and protection
against risk factors for the developing immune system and resulting
immune dysfunction and tissue damage provide a major opportunity to
reduce health risks for the most
prominent chronic diseases of children and adults.|
)9
) I n Fo c u s
References:
) 10
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[published online ahead of print October
20, 2009]. Diabetologia. 2010;23(1):89-97.
doi:10.1007/s00125-009-1560-z.
23. Nathan BM, Moran A. Metabolic complications of obesity in childhood and adolescence: more than just diabetes. Curr Opin
Endocrinol Diabetes Obes. 2008;15(1):21-29.
24. Tailor AM, Peeters PH, Norat T, Vineis P,
Romaguera D. An update on the prevalence
of the metabolic syndrome in children and
adolescents [published online ahead of
print November 2, 2009]. Int J Pediatr Obes.
doi:10.3109/17477160903281079.
25. Sundaram SS, Zeitler P, Nadeau K. The
metabolic syndrome and nonalcoholic fatty
liver disease in children. Curr Opin Pediatr.
2009;21(4):529-535.
26. Rotterdam ESHRE/ASRM-Sponsored PCOS
Consensus Workshop Group. Revised 2003
consensus on diagnostic criteria and longterm health risks related to polycystic ovary
syndrome. Fertil Steril. 2004;81(1):19-25.
27. Cesario SK, Hughes LA. Precocious puberty:
a comprehensive review of literature. J Obstet Gynecol Neonatal Nurs. 2007;36(3):263274.
IAH Abbreviated
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from the International Academy for
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1 Access the IAH website at www.iah-online.com. Select your language.
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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
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) What Else Is New?
British researchers have found that
© iStockphoto.com/Shaun Lowe
compact fluorescent light bulbs emit
ultraviolet rays similar to the sun on a
summer day.
People living without a partner at
around age 50 have about twice the
risk of developing cognitive impairment
in later life compared with people living
in stable partnerships.
Sunburn from
energy-saving bulbs
Pain relief from swearing?
Marriage prevents
dementia
Saving energy is a good thing, but is
it totally safe? Researchers at the
British Health Protection Agency
have discovered that under normal
operating conditions, compact fluorescent lamps (CFLs) give off significant amounts of UV radiation. In
close proximity to the bulb, UV radiation easily reaches levels comparable to sun exposure on a summer
day. But don’t replace all your compact fluorescents with conventional
incandescents out of fear of sunburn.
At distances of as little as 30 centimeters (one foot), the intensity of
the radiation is reduced to levels safe
for people with normally sensitive
skin. And UV radiation is an issue
only with single-envelope CFLs. According to the study, double-walled
bulbs are perfectly safe.
Although swearing is a common response to pain, a recent British study
was the first to investigate the effects
of swearing on pain tolerance. The
64 participants were asked to immerse one hand in icy water until
they could no longer stand the pain.
The procedure was then repeated,
with participants either swearing
out loud or saying “neutral” words.
Pain intensity was assessed, along
with the length of time required for
the pain to become unbearable. The
findings indicate that swearing actually does increase pain tolerance and
decrease perceived pain. The painreducing effect was more pronounced in women than in men.
Being married or living with a partner at around age fifty is associated
with reduced risk of dementia in
comparison to those who live alone,
according to a recent Swedish-Fin
nish study that analyzed Finnish
WHO data from the 1970s and 80s.
The study found that men and women living in stable partnerships
around age 50 are significantly less
likely to develop dementia at ages
65 to 79 than are single, separated,
or widowed individuals. The greatest increased risk of Alzheimer’s was
found in widowed or divorced carriers of the apolipoprotein E e4 allele
who remained single during the follow-up period.
NeuroReport. 2009;20(12):
1056-1060. doi:10.1097/
WNR.0b013e32832e64b1
BMJ. 2009;339:b2462.
doi:10.1136/bmj.b2462
Radiat Prot Dosimetry.
2008;131(4):521-525
F O R P RO F E S S I ONA L U S E ON LY
) 12
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.
© iStockphoto.com/Sabrina dei Nobili
) What Else Is New?
For individuals with compromised
immune systems, pathogens contained
in the biofilms of showerheads may
pose a risk of infection.
A few extra pounds increase
life expectancy
Paradise for bacteria
Smart people live longer
“Being overweight is unhealthy.”
Without further qualification, however, this bit of conventional wisdom appears to be only partially
true. A Canadian study of the relationship between BMI and mortality
has concluded that average life expectancy is actually greater for individuals with only a little extra fat on
their ribs (BMI 25-30) than for people of normal weight. The study,
which analyzed data on 11,000 Canadian men and women aged 25
years or older, noted that both underweight (BMI < 18.5) and class II
obesity (BMI > 35) entailed a significantly increased risk of mortality
(1.73 and 1.36, respectively) in
comparison to normal weight,
whereas the relative mortality rate
among the slightly overweight (BMI
25-30) was significantly reduced at
0.83. Even for class I obesity (BMI
30-35), life expectancy was approximately the same as for normal
weight.
Especially for frail elders, taking a
nice, relaxing shower could be dangerous. Scientists at the University
of Colorado, USA discovered that
showering may entail a significant
risk of infection. The researchers
tested a total of 45 showerheads
taken from various locations around
the US for genetic traces of bacteria. The locations included major
cities such as New York and Denver. Almost one-third of the samples
contained significant quantities of
mycobacteria, which can cause pul
monary infections in individuals
with compromised immune systems.
Plastic showerheads were more
heavily contaminated than metal
ones.
In addition to mycobacteria, the
scientists discovered more than a
dozen other opportunistic pathogens that accumulate in varying
combinations in so-called biofilms
in showerheads. The concentration
of germs can be more than 100
times that of each city’s tap water
and is especially high when the
shower is first turned on, so the researchers advise not allowing the
first flow of water to strike the face.
Individuals of higher intelligence
have a greater chance of living to a
ripe old age than their less intelligent contemporaries. That’s the
greatly simplified conclusion of a
study of over 4,000 US veterans of
the Vietnam War. As always, the rea
lity is more complex.
David Batty of the University of
Glasgow (UK) was lead author of
the study, which analyzed data from
two intelligence tests as well as socioeconomic data and cardiovascular risk factors. As expected, higher
socioeconomic status was associated
with reduced cardiovascular and
overall mortality. Including the GIs’
IQs in the calculation, however, reduced the significance of social and
economic differences, indicating the
soldiers’ intelligence is an additional
significant factor in statistical life
expectancy. The question remains as
to how to interpret these findings.
One possible explanation is that individuals with higher IQs are more
aware of the importance of healthy
lifestyle choices.
Obesity. 2009.
doi:10.1038/oby.2009.191.
To download this issue,
visit our web site at
www.iah-online.com
Proc Natl Acad Sci U S A.
2009;106(38):16393-16399.
doi:10.1073/pnas.0908446106
Eur Heart J. 2009;30(15):
1903-1909.
) 13
) From the Practice
Use of Bioregulation Therapies for
a Severe Otorhinological Problem
By Sergio Vaisman Weinstein, MD
Pediatrician
A case of a patient with primary ciliary dyskinesia is presented. This condition resulted in difficult otorhinological
management, including several surgical interventions, the use
of multiple antibiotics, numerous radiological and immunological investigations, and prolonged conventional medical
treatments, without satisfactory clinical results. The incorporation of bioregulatory therapies into her treatment regimen
had a significant impact on her progress and quality of life.
) 14
Introduction
Primary ciliary dyskinesia is a congenital disorder affecting the structure of cilia and flagella. It is an autosomal recessive disease with a low
incidence (1 in 15,000 live births).1
Clinically, it manifests with various
signs and symptoms, such as recurrent obstructive bronchitis, repeated
pneumonia, recurrent sinusitis, recurrent acute otitis media, and bronchiectasis.
The ciliary ultrastructure defects include impairment of the dynein
arms, absent or changed radial proteins, and a switch in the number of
microtubules and/or their arrangement in the axoneme. Major defects
can be an absence of or changes in
the axoneme or plasma membrane
of the cilia and flagella. A definitive
diagnosis is made by using electron
microscopy to determine ciliary ultrastructure changes in transverse
sections of cilia.2
Clinical case
The case is that of a female patient
born at full term by spontaneous delivery, weighing 3450 g at birth.
The neonate was not breastfed, and
she had received replacement milk
products since birth. The newborn
also received the full program of
vaccinations, including pneumococcal polysaccharide vaccine.
Family medical history: The patient’s father experienced repeated
otitis, and her mother experienced
frequent pharyngotonsillitis. Her
paternal aunt experienced repeated
sinusitis.
Disease history: At the age of 1
month, the patient experienced viral
disease of the upper respiratory
tract. At the age of 4 months, she
was diagnosed as having obstructive
bronchial syndrome, which was
treated with amoxicillin and puffs of
a combination of salbutamol and
beclomethasone. This disease reJournal of Biomedical Therapy 2010 ) Vol. 4, No. 1
curred frequently, and at the age of
1 year 2 months, she was diagnosed
as having infantile asthma. She received multiple treatments, including puffs of salbutamol, fluticasone,
decongestants, antihistamines, mucolytics, and various antibiotics. Her
subsequent course indicates rhinitis,
rhinosinusitis, and otitis on repeated
occasions. At the age of 4 years, cystic fibrosis was excluded by a normal
sweat test result.
At the age of 4 years 7 months, in
view of the succession of episodes
of rhinosinusitis with simultaneous
otitis media with effusion and numerous attacks of acute otitis media,
an adenoidectomy was performed
and tympanostomy tubes were inserted. The anatomical pathology
report indicated adenoidal lymphoid
tissue with moderate follicular hyperplasia and an erosive acute and
chronic inflammatory process of the
surface lining epithelium.
At the age of 4 years 8 months, she
was examined by an immunologist.
At this time, she was diagnosed with
acute otitis media 8 times a year and
acute sinusitis 5 times a year. She
also experienced transient hypo
gammaglobulinemia; this condition
improved. The clinical investigations
included the following: IgE positive
to foods and certain foodstuffs (i.e.,
peanuts, eggs, and milk) and coloring agents; IgG1-IgG2-IgG3-IgG4,
normal result; response antibodies
to pneumococcal 23-valent vaccine,
normal result; and a minor change
) From the Practice
in chemotaxis. The treatment recommendation was as follows: desloratadine, puffs of intranasal mometasone, montelukast, and amoxicillin,
1 dose per day for 3 months.
At the age of 5 years, in view of the
persistent repeated rhinosinusitis,
endoscopic surgery of the paranasal
cavities was performed. The anatomical pathology report indicated
that the right maxillary sinus mucosa was affected by a marked acute
and chronic inflammatory process
and extensive erosion of the lining
epithelium, without specific effects.
The left maxillary sinus mucosa was
affected by a moderate acute and
chronic inflammatory process.
At the age of 5 years 4 months, a
biopsy specimen of the nasal respiratory mucosa was obtained. The
specimen showed preciliated cells,
caliciform cells, and ciliated cells
with mature stalks; these stalks
showed a 9×2 microtubular skeleton with no internal arm or with
both arms of dynein in approximately 50% of the cilia examined. A
number of preserved additional peripheral microtubules, basal bodies,
and radial spokes were also seen in
the specimen. These findings were
compatible with ciliary dyskinesia.
At the age of 7 years 8 months, the
patient was referred to me by the
otorhinolaryngologist because of
continued and repeated rhinosinusitis. She had received the following
medications during the previous 2
years: montelukast and cetirizine
constantly, puffs of intranasal mometasone as necessary, and frequent
administration of antibiotics. There
was a request for an integrated approach with biological medicine.
The following medications were
prescribed: Lymphomyosot, Trau
meel, Mucosa compositum, and
Euphorbium compositum. Montelukast and cetirizine were discontinued. In the first month of integrated
treatment, the patient experienced
a number of viral infections; these
were managed satisfactorily with
Gripp-Heel, Angin-Heel, and Husteel.
At the age of 7 years 10 months,
the patient was doing very well.
Treatment was continued with
Galium-Heel plus Histamin-Injeel,
Sinusitis-Nosode-Injeel, Coenzyme
compositum, Ubichinon compositum, and Grippe-Nosode-Injeel. The
treatment with Mucosa compositum
was maintained.
She was also doing well at the age
of 8 years 6 months. The patient led
a normal life, including swimming
in the pool and at the beach. In the
winter, Engystol was administered
prophylactically every other week
and Euphorbium compositum was
administered at the onset of any
rhinitis.
At the age of 8 years 10 months, she
experienced viral pharyngitis and
was given Angin-Heel, Engystol,
and Mucosa compositum. At the age
of 9 years, the patient experienced
viral tracheitis and was given Engystol and Husteel. At the age of 9 years
1 month, she was hospitalized because of acute gastroenteritis due
to a rotavirus. At the age of 9 years
10 months, the patient had influenza due to an AH1N1 virus. She was
treated with oseltamivir.
The girl is now aged 10 years 1
month and is doing very well. She
has not experienced further rhinosinusitis infections, and she has not
needed antibiotics in the last 2 years.
She leads a normal life.
Discussion
This patient presented with primary
ciliary dyskinesia that could not be
satisfactorily managed with what
conventional medicine has to offer.
After numerous treatments, several
surgical interventions, and continued and repeated rhinosinusitis, she
was referred to me to try supportive
treatment with antihomotoxic medications.
The patient’s condition was approached using the three therapeutic
pillars of homotoxicology: treatment
was started with the administration
of drainage products (Lymphomyosot), the modulation of the patient’s
chronic inflammatory state (Trau
meel), and the stimulation of the
body’s support for the recovery of
the diseased tissues (Mucosa compositum).
In a second stage of treatment, Galium-Heel was prescribed to stimulate
nonspecific defenses and as a detoxifying agent; and Coenzyme compositum and Ubichinon compositum
were added to stimulate blocked enzymatic processes.
The patient’s response has been very
good: she is no longer using antibiotics, she no longer has to miss
school, and she is starting to lead a
normal life for her age. This is an
important achievement given the
previous restrictions on her, something that is not often considered.3
Clearly, treatment with bioregulatory medications produced a notable
change in the course of this patient’s
disease. Their contribution in the integrated management of patients
with repeated rhinosinusitis and primary ciliary dyskinesia must be considered.|
References:
1. Chodhari R, Mitchison HM, Meeks M. Cilia,
primary ciliary dyskinesia and molecular genetics. Paediatr Respir Rev. 2004;5(1):69-76.
2. Iñiguez R, Fonseca X, Hernandez J,
González S, Sánchez I. Disquinesia ciliar:
diagnóstico ultraestructural, evolución clínica
y alternativas de tratamiento. Rev Méd Chile.
2007;135(9):1147-1152.
3. Whalley S, McManus IC. Living with primary ciliary dyskinesia: a prospective qualitative study of knowledge sharing, symptom
concealment, embarrassment, mistrust, and
stigma. BMC Pulm Med. 2006;6:25.
) 15
) Meet the Expert
Dr. David Riley
By Catherine E. Creeger
D
avid Riley was born in the
United States and moved to
Frankfurt, Germany as a boy. He
studied music and psychology at the
University of North Carolina in
Chapel Hill and graduated in 1976.
Prior to attending medical school,
he worked professionally as a musician and chef in Europe and the
United States.
After graduating from the University
of Utah medical school in 1983, he
completed a residency in internal
medicine. During his residency he
became interested in research and
conducted his first informal clinical
trial by doing pulmonary function
testing on advanced yoga teachers
attending a yoga workshop in San
Francisco in 1984. Since his residency, David Riley has studied many
integrative medical therapies, including yoga, homotoxicology, cranial osteopathy, nutrition, homeopathy, and herbal medicine.
He has been the editor-in-chief of
the leading indexed medical journal
in Integrative Medicine, Alternative
Therapies in Health and Medicine
(since 1995), has written chapters
for a variety of medical textbooks,
and is a clinical associate professor
at the University of New Mexico
medical school.
He currently practices integrative
medicine with Dr. Tieraona Low
Dog in Santa Fe, NM. Since 1992,
Dr. Riley has conducted or managed
more than 50 clinical trials ranging
from international practice-based
research networks to randomized
controlled clinical trials. In 1998,
Dr. Riley founded Southwest Health
Options, an independent practice
association managing the delivery
of complementary and alternative
medicine for insured patients. At
Southwest Health Options, he developed credentialing standards,
managed peer review, and coordinated service utilization. He has
been a member of the CONSORT
(CONsolidated Standards of Reporting Trials) group and worked
on the development of coding solutions for integrative medicine.
) 16
Dr. Riley is a board member of the
Homeopathic Pharmacopoeia Convention of the United States (a technical advisory body to the FDA) and
has consulted with other federal
agencies. Since 2008, he has been
the president of the International
Society of Homotoxicology and
Homeopathy. He currently lectures
and consults internationally on a
range of healthcare issues including
healthcare policy and regulation,
education and research, and issues
surrounding integrative medicine.
Dr. Riley enjoys traveling and has
visited North, Central and South
America, Europe, Africa, the Middle
East, and Asia. He is married and
lives in a country home just outside
of Santa Fe, New Mexico where he
likes to work in his garden and orchard.|
) Around the Globe
Scientific Symposia in Belgium and the Netherlands
The Extracellular Matrix
By Pascale Vlietinck
BVHAT Scientific Events Coordinator
The audience in Utrecht,
On the 16th and 17th of October, the Belgian Society for
Homotoxicology and Antihomotoxic Therapy (BVHAT)
the Netherlands listened carefully
to Dr. James Oschman’s lecture on
the extracellular matrix.
organized two sessions of the same symposium, one in
Brussels, Belgium, and one in Utrecht, the Netherlands,
on the importance of the extracellular matrix (ECM) in
preventive and curative medicine.
T
he symposium’s moderator,
Professor Eddie Wisse, professor emeritus of Cell Biology and
Histology at the College of Medicine and Pharmacy of the Free University of Brussels, opened each session by welcoming participants and
giving a brief summary of current
histological knowledge about the
ECM. He then presented the first
speaker, James Oschman, PhD from
the USA, the global leading expert
in bioregulatory matrix research. Dr.
Oschman gave a history of matrix
research and highlighted important
new discoveries, primarily in cellto-cell communication and molecule
receptor triggering.
The second speaker in both sessions
was cell biology expert Professor
Rolf Gebhardt, professor of biochemistry at the University of
Leipzig, Germany. His report on recent research illustrated the cell-protective effects of bioregulatory medications such as Lymphomyosot and
Hepeel. In his research, Professor
Gebhardt introduced toxins into
novel ECM through a transfilter well
system and studied the ability of
carefully selected Heel medications
to inhibit cell intoxication.
Last but not least, Bruno Van Brandt,
medical education manager of the
International Academy for Homotoxicology, presented the therapeutic possibilities and advantages of
bioregulatory medications. Starting
from the integrity of the ECM as absolute precondition for long-lasting
therapeutic effects in bioregulatory
medicine, he then went on to highlight immunomodulation and cell
and organ support as the two other
elements rounding out the comprehensive bioregulatory treatment of
chronic degenerative pathologies.
He described this entire approach as
the “three pillar” concept in antihomotoxic therapy.
In both locations, the members of
the audience were medical doctors
with considerable experience in bioregulatory medicine, which resulted
in interesting questions and discussions. Overall feedback on both sesJournal of Biomedical Therapy 2010 ) Vol. 4, No. 1
Professor Rolf Gebhardt’s research has
demonstrated the cell-protective effects
of selected bioregulatory medications
in vitro.
Bruno Van Brandt presented
the therapeutic possibilities of
bioregulatory medications.
sions was excellent, and attendees
expressed appreciation for the scientific content of the symposium.
With this symposium, the BVHAT
has once again proven itself to be an
active medical education institute
capable of organizing advanced scientific events in bioregulatory medicine.|
) 17
) Re f r e s h Yo u r H o m o t ox i c o l o g y
Attention-Deficit/Hyperactivity
Disorder
in Infancy and in the Preschool-aged Child
By Leon Strauss, MTechHom (TWR)
The diagnosis and treatment of attention-deficit/hyperactivity
disorder (ADHD) has been focused on school-aged children,
with recent attention drawn to adults with ADHD. Chronic
treatment programs from childhood through late adulthood
have become part of modern ADHD management programs,
identifying and treating key areas of need within each age
group.
A
) 18
ttention deficits are generally
thought to be mostly associated with children; however, it has
been recognized that attention problems not only continue into adulthood but also reveal themselves in
more adults as they get older.1 The
onset of ADHD typically occurs before the age of 3 years, with parents
of children with ADHD commonly
reporting excessive motor activity in
toddlers. Peak presentation to health
care professionals occurs between
the ages of 7 and 10 years.2
This article will concentrate on the
early identification and management
of ADHD in infants and preschoolaged children.* Early treatment of
ADHD can prepare children for the
academic years, as well as improve
relationships within the family,
which are often strained.3 Numerous
family studies have suggested a familial pattern to ADHD.4 These
studies suggest that there is a higher
prevalence of mood and anxiety,
learning, substance-related, and antisocial personality disorders in family members of individuals with
ADHD.5
The chemical messengers
Neurotransmitters include chemicals
classed as peptides, nitric oxides,
neurotrophic factors, and cytokines.
More than 300 substances that control our internal neural world and
directly influence our interaction
with others have been identified.
Catecholamines, such as dopamine,
and amines, such as serotonin, play
an important role in the evolution of
ADHD; these imbalances can be
identified in the preschool-aged
child with ADHD.6 Dopamine plays
a critical role in motivation, rewardseeking behavior, and attentional
processes.7 Imbalances of dopamine
in limbic regions have been linked
to ADHD,8 schizophrenia, and sub-
* Future articles will address ADHD and its management in school-aged children and hyperactivity in adults.
cortical neuropsychiatric disorders,
including Tourette syndrome and
possibly autism.9 Dopamine levels
are preferentially reduced in the
frontal brain regions of adult patients with ADHD. Furthermore, genetic abnormalities related to dopamine transporter proteins have
been reported in patients with
ADHD,10 supporting the concept
that ADHD has strong genetic ties
and is a disorder that begins early in
life and changes form through the
teenage years and adulthood.
Serotonin is essential in neurobehavioral processes, including mood
and anxiety.10 Serotonergic imbalances are related to mood disorders,
anxiety syndromes (including obsessive-compulsive disorder,11 posttraumatic stress disorder, and panic disorder), autism, and insomnia.9 Low
platelet serotonin concentrations
were identified in children with
ADHD more than 20 years ago; increasing serotonin levels to within
the normal range repeatedly lessens
ADHD symptoms in children with
low serotonin levels.5
Circulating serotonin and dopamine
levels and receptor site activity can
be adversely affected by genetic and
environmental factors.10 Functional
polymorphisms of the serotonin
transporter genes have been associated with depression and autism.12
Environmental toxins, such as
1-methyl-4-phenyl-1,2,3,6-tetrahy-
dropyridine (MPTP), can produce a
permanent hypodopaminergic state
indistinguishable from Parkinson
disease by killing neurons in the
substantia nigra of the brain.10 Toxins from the environment include
gases (e.g., carbon monoxide), metals (e.g., mercury), liquids (e.g., ethanol), and numerous solids. Prenatal
exposure to lead can result in mental
retardation and cerebral palsy. As
many as 1 in 10 women are at risk
of bearing children with learning
disabilities and other neurological
problems because of mercury exposure. Mercury affects both prenatal
and postnatal brain development; it
specifically damages or kills neurons
in utero. The consumption of fish is
the most common source of exposure, although airborne mercury
contamination is becoming more of
a concern. Exposure to neurotoxins
in pregnancy is associated with disordered cognitive development,
lowered IQ scores, impairments of
memory and attention, and coordination deficits.13
Identifying ADHD in
the preschool-aged child
In early childhood, it may be difficult to distinguish symptoms of
ADHD from age-appropriate behavior in active children. Family histories and environmental factors may
be more valuable in determining
whether treatment should be recommended in children with potential
ADHD.
Common symptoms in infancy include the following:
• excessive dribbling
• excessive motor activity
• increased thirst
• head banging
• fits
• tantrums
• screaming
• restlessness
• needing little sleep
• being difficult to feed
• inability to be pacified
• spurning affection and cuddles
Common symptoms in young children include the following:
• clumsiness
• impulsiveness
• being accident prone
• erratic disruptive behaviors
• compulsive touching
• constant motion
• nonstop and repetitive talking
• concentration deficits
• loud talking
• restless sleep
• nightmares
• being oversensitive to odors,
lights, sound, and cold
An early diagnosis of ADHD is difficult.
Symptoms in infants and toddlers
include restlessness, frequent crying
and fits of anger during which the child
© Oleg Kozlov/Fotolia.de
cannot be pacified.
) 19
Treatment
Prenatal neurotoxin exposure sets
the scene for neurochemical imbalances in the newborn and highlights
the need for drainage and detoxification, even in young children. Inherent tendencies to the development of illness may be genetic or
the result of environmental toxin exposure.
Young children will all benefit from
a two- to three-month course of
Lymphomyosot (2-5 drops of each
given 3 times daily). In more toxic
environments (because of environmental or medicinal exposure),
deeper detoxification protocols may
be necessary, with ampoule preparations such as Thyreoidea compositum and Pulsatilla compositum (1
dose biweekly). Prenatal or postnatal heavy metal exposure is an indication for the use of biocatalysts and
the corresponding low-dose metalcontaining product (i.e., bioregulatory products that contain mercurius, lead, and arsenic). Lead exposure
is an indication for Placenta compositum and Cerebrum compositum.
The use of Cerebrum compositum is
essential in all cases of potential
brain injury (traumatic or toxic) in
the young child.
Omega-3 fatty acids exert direct and
indirect influences on neurotransmission through modifications at
the postsynaptic receptor. They influence signal transduction by inhibiting the hydrolysis of inositol
triphosphate (IP3), an effect that
closely resembles the activity of lithium. Essential fatty acids also inhibit
membrane phospholipase activity14
and reduce arachidonic acid release
from neuronal cell membranes.15 A
deficiency of omega-3 fatty acids
has been linked to low dopamine
receptors in rats16; there is a direct
correlation between a low plasma or
membrane-bound essential fatty
Table: Specific Treatment Protocols for Children With ADHD.†
Presentation
Young Children With Low Serotonin Levels
Young Children With Low Dopamine Levels
• Sleep disturbances
• Listless behavior and possible delays in
reaching milestones
• Erratic and changing moods (often crying
with screaming and uncontrolled tantrums)
• Compulsive repetitive behaviors
• A history of depression is often seen in 1 or
both of the parents
• Low metabolic rates may be seen,
with a tendency toward constipation
• Children rock back and forth to music
(because they love rhythmic sounds),
with sensitivity to loud and unexpected sounds
• There may be a family history of addictive disorders
Treatment
) 20
• Nervoheel tablets (half a tablet 3 times daily)
• Neuro-Injeel ampoules (1 dose twice weekly)
• Ignatia-Homaccord drops (2-5 drops 3 times daily)
• Barijodeel tablets (half a tablet 3 times daily)
• Viburcol suppositories (to be used as needed for
tantrums and sleeplessness)
• Lymphomyosot drops (2-5 drops 3 times daily)
• Thalamus compositum ampoules (1 dose every
evening at sunset for 1 week for sleep disturbances)
• Calcoheel tablets (half a tablet 3 times daily)
• Bacillinum-Injeel (1 dose weekly if indicated
in unresponsive cases)
† The dosage of certain medications may vary depending on the age of the child. Please refer to the respective package insert.
© Sergey Chirkov/Fotolia.com
Young children with ADHD find it
hard to focus on one thing at a time.
Constantly in motion, they are
somewhat clumsy and tend to have
more accidents than their healthy age
peers.
acid level and depression.17 Modulation of sodium and calcium neuronal
channels and reduction of electrochemically excitable tissue are major
neuroprotective mechanisms of
omega-3 fatty acids. These fatty acids are essential for neural development in utero, and preschool-aged
children need omega-3 fatty acids
for all of the reasons specified. Children may show overt signs of fatty
acid deficiency, such as allergy development, indicating T-helper cell
type 2 dysregulation; and excessive
thirst levels and dryness of the mucous membranes, conjunctiva, and
skin as the result of cellular membrane phospholipid breakdown.
Concentrations of omega-3 fatty acids, particularly docosahexaenoic
acid (DHA), increase 3- to 5-fold
during the last 3 months of pregnancy and by the same amount during the first 3 months of life. The
accumulation of DHA in the brain
continues for at least the first 2 years
of postnatal life. The optimal recommended daily intake of omega-3
has not been established and may
vary from person to person.
Recommended daily intake:
• Children aged 2 to 4 years: 500
mg of omega-3, with a minimum of
125 mg of DHA and 30 mg of eicosapentaenoic acid (EPA)
• Children aged 4 years and older:
1000 mg of omega-3, with a minimum of 250 mg of DHA and 60 mg
EPA
As signs and symptoms progress and
differentiation between low serotonin and low dopamine levels in
infants and children become apparent, specific treatment protocols can
be approached (Table).
More specific protocols for the classic ADHD symptoms in school-aged
children and the difficulties they
face in learning will be addressed in
a future article.|
References:
1. Braverman ER. The Edge Effect. New York,
NY: Sterling Publishing Co; 2004:25.
2. Bakwin H, Bakwin RM. Behaviour Disorders
in Children. 4th ed. Philadelphia, PA: WB
Saunders Co; 1972:378-381.
3. Shaywitz SE, Shaywitz BA. Attention deficit
disorder: current perspectives. Pediatr Neurol.
1987;3(3):129-135.
4. Goodman R. Genetic factors in hyperactivity.
BMJ. 1989;298(6685):1407-1408.
5. American Psychiatric Association. Diagnostic
and Statistical Manual of Mental Disorders.
4th ed. Washington, DC: American Psychiatric Publishing Inc; 1994:78-85.
6. Lombard J. Neurotransmitters: a functional
medicine approach to neuropsychiatry. In:
Jones DS, Quinn S, eds. Textbook of Functional Medicine. Gig Harbor, WA: Institute for
Functional Medicine; 2005:638-639.
7. Luciana M, Collins PF, Depue RA. Opposing
roles for dopamine and serotonin in the modulation of human spatial working memory
functions. Cereb Cortex. 1998;8(3):218-226.
8. Russell VA, Sagvolden T, Johansen EB. Animal models of attention-deficit hyperactivity
disorder. Behav Brain Funct. 2005;1:9.
9. Lam KS, Aman MG, Arnold LE. Neurochemical correlates of autistic disorder: a
review of the literature. Res Dev Disabil.
2006;27(3):254-289.
10. Cleren C, Calingasan NY, Chen J, Beal MF.
Celastrol protects against MPTP- and 3-nitropropionic acid-induced neurotoxicity.
J Neurochem. 2005;94(4):995-1004.
11. Simpson HB, Fallon BA. Obsessive-compulsive disorder: an overview. J Psychiatr Pract.
2000;6(1):3-17.
12. Gondo Y, Hirose N, Arai Y, et al. Contribution of an affect-associated gene to human
longevity: prevalence of the long-allele genotype of the serotonin transporter-linked gene
in Japanese centenarians. Mech Ageing Dev.
2005;126(11):1178-1184.
13. Du Nann Winter D, Koger SM. The Psychology of Environmental Problems. 2nd ed. Mahwah, NJ: Lawrence Erlbaum; 2004:129.
14. Stoll AL, Severus WE. Mood stabilizers:
shared mechanisms of action at postsynaptic
signal-transduction and kindling processes.
Harv Rev Psychiatry. 1996;4(2):77-89.
15. Strokin M, Sergeeva M, Reiser G. Role
of Ca2+-independent phospholipase A2
and n-3 polyunsaturated fatty acid docosahexaenoic acid in prostanoid production in brain: perspectives for protection
in neuroinflammation. Int J Dev Neurosci.
2004;22(7):551-557.
16. Delion S, Chalon S, Guilloteau D, Besnard
JC, Durand G. a-Linolenic acid dietary deficiency alters age-related changes of dopaminergic and serotoninergic neurotransmission in the rat frontal cortex. J Neurochem.
1996;66(4):1582-1591.
17. Peet M, Murphy B, Shay J, Horrobin D.
Depletion of omega-3 fatty acid levels in red
blood cell membranes of depressive patients.
Biol Psychiatry. 1998;43(5):315-319.
) 21
) M a r k e t i n g Yo u r P r a c t i c e
Making Your Practice a Team
By Marc Deschler
Marketing specialist
How important is your assistants’ self-esteem? What
motivates employees? How important is continuing
education for the team as a whole? These are questions I
hear frequently, and I’d like to address them in this issue.
P
) 22
atients have significantly more
confidence in a medical practice
when they know who they’re dealing with. That’s why, for example,
when I consult with physicians, I
recommend name tags for assistants
in the practice. The idea gets rejected for the strangest reasons, such as
“The pins mess up our nice T-shirts.”
Many office assistants don’t even
have the self-confidence to give
their names when answering the
phone, let alone wear a name tag.
The real reason, however, is usually
that identifying yourself by name
means you’re no longer able to hide
behind anonymity. You’re afraid of
making a mistake the boss will find
out about. This is an expression of
inadequate self-confidence.
You as a practitioner, however, must
make it your explicit goal to have a
strong team whose members radiate
competence through their self-confident, professional manner. That’s a
good reason for patients to stay with
your practice and recommend it to
others. Self-confidence doesn’t always come naturally to employees,
however, so you, as the ultimate
“manager” of your own practice,
may have to actively promote it.
Here are some rules to follow in order to build up your assistants’ selfconfidence and reap the benefits:
1. Show your assistants that their
work is important to you. Don’t
accept their good work as a matter of course and register only
their mistakes. Offer praise –
even in front of patients.
2. Help your assistants learn from
their mistakes. Individuals with
low self-esteem tend to doubt
their own ability after making
mistakes. Help them come up
with ways to avoid repeating the
same mistake. If you must criticize, do it in private, and never
in front of patients.
3. Praise or criticize only what your
employees do, not the individuals themselves. Personal criticism
of an employee is strictly taboo;
it can make that person start to
disengage inwardly.
4. Assign tasks in a way that showcases your associates’ abilities. If
one assistant is especially good
at taking blood samples, make
that one of his or her permanent
assignments. You will save time
because the work gets done more
efficiently and the working environment improves because employees are content.
5. Delegate increasingly demanding jobs. Letting go of some
things can be difficult, but in
most cases you’ll soon get used
to it, and you’ll gain time that
you can devote to managing your
practice, for example. Giving
your employees more individual
responsibility enhances both
their commitment and their productivity.
6. Communicate with your employees in ways they understand, and
find out what they expect from
you. Surveys have shown that
most employees who do unsatisfactory work simply don’t know
what the boss actually wants.
At the moment, many of your colleagues are complaining about cost
pressure, shortage of time, etc. and
are looking for new services to offer
or sources of income. In my opinion, however, the competitiveness of
a practice depends not only on implementing new methods or technology but also to a great extent on
“human capital.” Personal commitment, competence, and the results of
creativity and energy – not just
yours, but also your employees’ –
are important resources available to
you at no extra cost, so to speak.
Improving employee skills and delegat-
© Auremar/Fotolia.de
ing more demanding tasks will increase
your staff’s self-esteem and make your
practice more efficient.
What motivates assistants
in your practice?
More money, a more secure job, and
the opportunity to make a career for
oneself are the old standard motivating factors in workplaces. These
resources are very limited, however,
and not just in healthcare practices.
The result is decreasing interest in
work, accompanied by more frequent mistakes. How can you counteract this problem before it’s too
late? Here are some simple, no-cost
ways to motivate your team:
1. Wherever possible, give your
employees free rein. Set a goal,
but leave it up to them how to
accomplish it.
2. Broaden your assistants’ perspective by including them in decision-making.
3. Explain why specific work needs
to be done.
4. Sharing important information,
including bad news, shows that
you appreciate and value your
associates.
5. Support your employees’ individual development. For example, cover part of the cost of
a continuing education seminar.
Or for a no-cost variation, look
for opportunities to invite them
to accompany you to industrysponsored educational events.
Ultimately, you will be the one
to benefit.
6. In a team, everyone has to compromise sometime. Whenever
possible, take your employees’
personal needs into account.
Show your employees that you value
them not only as workers but also as
individuals. These motivating factors can ensure that working in your
practice remains fun in the long run.
And there’s no limit on the availability of any of these resources.
Continuing education for
your team
“If you don’t keep up with the times,
you get left behind” is the motto of
one licensed healthcare practitioner
in Munich, Germany, meaning that
his practice wouldn’t function as
well without constant further education. In our fast-paced modern lives,
it’s not so easy to find time to keep
your knowledge and skills up-todate, but to remain successful you
must have a well-conceived plan for
continuing education in your practice. The daily flood of information
you’re subjected to can make this
difficult. Always ask these three
questions:
1. What matters most for my practice?
2. What are the options?
3. Is it realistic for us to implement
what we would learn?
To answer the first question,
• set goals for the practice, your
employees, and yourself
• plan in enough time
• establish a budget for individual
continuing education programs
With regard to the second question,
consider all the opportunities and
evaluate which ones to take advantage of:
• newspapers and professional
journals
• reference books
• seminars and workshops
• trade fairs and exhibitions
• exchanging information with
other practices
• electronic options (web sites,
mailing lists, and newsletters)
The third question is especially
important, because education –
whether for yourself or for your
associates – is not a good investment
if you can’t apply it. Here’s what
to consider:
• Have I processed the information?
• Have I effectively introduced the
information into my practice?
• Have I informed all my employees about what I learned?
• Are my employees all enthusiastic about implementing it?
• Have I established regular times
for sharing information and experiences within the practice?
• Have I set criteria for and monitored the positive impact of
newly acquired knowledge and
skills?
When thinking about continuing
education, don’t limit yourself to
professional content. Continuing
education in organization and management is equally important.|
) 23
) Re s e a r c h H i g h l i g h t s
New Approaches in the Treatment of
Respiratory Insufficiency in Neonates
By Professor Lidiya Ivanovna Ilyenko, DrMedSci, and
Nataliya Aleksandrovna Suvalskaya, CandMedSci*
Abstract
In this study, 67 newborns receiving
artificial respiration, who were diagnosed as having respiratory distress
syndrome, were divided into 2
groups, were examined, and were
treated. The first group (n = 33) received standard treatment plus Mucosa compositum sublingually, and
the second group (n = 34) received
only standard therapy. With the
therapy provided, there was a 1.3fold decrease in the duration of artificial respiration in the neonates in
the Mucosa compositum group.
Keywords: neonates, respiratory insufficiency, respiratory distress syndrome,
artificial respiration
Mucosa compositum (Heel, BadenBaden, Germany) was applied in the
treatment of RDS. The literature describes the use of this medication in
neonates with dysbiotic disorders;
in infants and in older children, as
an efficacious antitussive agent; and
in combination therapy for bronchial asthma.† The interest in this bioregulatory combination medication
arises from its composition, which is
based on a porcine mucosa extract,
catalysts, and substances of vegetable and mineral origin. All components of the formulation are represented at high levels of dilution and
do not possess any potential toxic or
allergic effect.
In terms of its action, the product is
postulated to have anti-inflammatory, spasmolytic, reparative, vascular,
and immunomodulating effects. Mucosa compositum is thought to assist
the passage of mucus and has a
drainage effect, reduces dyspnea and
cyanosis and normalizes the respiration rhythm, reduces the number of
attacks of coughs and of coughing
instances in a single attack, prevents
the process of respiratory distress
from becoming chronic, and acts on
the entire respiratory tract (upper,
middle, and lower).
The objective of the present study
was to evaluate the efficacy of Mu-
Introduction
The successes that have been
achieved in delivering resuscitation
aid to neonates who are in critical
states have mainly been brought
about by the introduction of protocols and standards and by a comprehensive approach to therapy. However, intensive therapy for respiratory
disorders remains a difficult problem, especially for neonates with respiratory distress syndrome (RDS).
One new approach for solving this
problem is the use of bioregulatory
combination medications. In this
study, the antihomotoxic medication
) 24
*
cosa compositum in the combination treatment of respiratory disorders.
Patients and methods
This study included 67 neonates under observation. All patients were
similar in terms of sex, age, and
week of gestation; they received
standard treatment for RDS (i.e.,
correction of hemodynamic parameters and administration of surfactant, antibiotics, and infusion therapy). Thirty-three were included in
the treatment group (i.e., newborns
who received standard treatment
plus Mucosa compositum for respiratory disorders), and 34 were included in the control group (i.e.,
newborns who received only standard treatment for respiratory disorders).
The inclusion criteria included premature infants in the first 24 hours
of life, a gestational age of 36 weeks
or younger, a body mass of 900 g or
greater, and a clinical and/or X-ray
diagnosis of RDS. The exclusion criteria included congenital developmental defects, periventricular hemorrhaging at level 2 or greater, and
clear symptoms of intrauterine infection.
In the antihomotoxic treatment
group, Mucosa compositum was ta
Hospital Pediatric Department, Moscow Branch, Advanced Medical Training Faculty, State Educational Institution for Higher Occupational Education,
Russian State Medical University, Federal Agency for Healthcare and Social Development (Roszdrav), Moscow, Russia.
† References available on request.
© iStockphoto.com/Chris Williams
) Re s e a r c h H i g h l i g h t s
Premature newborn in an incubator
ken sublingually at a dose of 0.5 mL
every 6 hours for 5 to 7 days.
The evaluation criteria included
clinical, functional, and laboratory
variables.
The clinical parameters were as follows: altered chest excursion, auscultation sounds in the lung, skin
color, increase in feed volume, body
mass, and diuresis dynamics.
The functional variables included altered artificial respiration (AR) parameters (i.e., fraction of inspired
oxygen, peak inspiratory pressure,
and ventilation rate), respiration mechanics (aerodynamic resistance and
distension), heart rate monitoring
results, respiratory frequency, blood
pressure, and arterial oxygen saturation.
The laboratory parameters were as
follows: general blood analysis,
blood gas measurement, and acidalkali status.
To exclude congenital developmental defects and to evaluate cerebral
blood flow, the neonates underwent
neurosonography and echocardiography.
Results
Within several minutes of product
administration, the results showed
that there was an improvement in
chest excursion (i.e., a diminution in
contraction of yielding places in the
chest, a “swing” symptom, and an
improvement in respiration rhythm
and amplitude), respiration conducted in the lungs, a diminution in the
number of rales, and an improvement in skin color.
In control group patients, a tendency for general edema syndrome (i.e.,
soft tissue swelling) was noted. By
day 3, with the treatment being administered, the incidence of this set
of symptoms was almost 3 times
lower in the antihomotoxic treatment group versus the control group
(6.1% versus 17.0%).
The subsequent comparative analysis showed that in the Mucosa compositum treatment group, a quicker
reduction in the oxygen concentration in the respiratory mixture with
AR was achieved: a fraction of inspired oxygen of greater than 0.3
was recorded for a mean ± SD of
50.28 ± 9.34 hours (versus 77.65 ±
10.68 hours for the control group;
P < 0.05). There was also an earlier
transfer of the neonates to independent respiration (overall duration of
AR in the control group versus the
antihomotoxic group, 116.15 ±
10.38 versus 87.63 ± 9.34 hours;
P < 0.05).
Discussion and conclusion
The data obtained reflect the efficacy of Mucosa compositum in combination treatment for respiratory insufficiency. The product slows the
rate of development of broncho
spasm by 5 times (P < 0.01), has an
established broncholytic effect, and
reduces lethality (as shown in this
experiment).
When this product is used, the
course of the clinical picture of RDS
in neonates is ameliorated and the
incidence of development of general
edema syndrome is lowered by 3
times versus the control group. The
use of this product shortens the time
for which AR is required by 1.3
times (P < 0.05) and the time spent
by newborns in the intensive care
unit.|
) 25
) Making of ...
Production of Homeopathic
Suppositories
By Cornelia Witt, PhD
Many bioregulatory medications are produced in the form
of suppositories, the preferred method of administration
for infants and children who have difficulty swallowing or
patients who are vomiting due to their illness. Pharmaceutical
manufacturers confront special challenges in the production
of suppositories, which must maintain their shape at room
temperature but melt at body temperature once administered.
I
n Viburcol, Spascupreel, or Vomitusheel suppositories, the base
material is hard fat with a melting
point of 35°C/95°F, i.e., slightly
below body temperature. Hard fat is
derived from vegetable oils and consists of a mixture of tri-, di-, and
monoglycerides. As a natural emulsifier, it aids in uniform distribution of
the liquid homeopathic active ingredients in the base.
Pharmaceutical production must pay
special attention to ensuring both
uniformly high product quality and
good consumer safety. The production instruction document for each
medication describes all manufacturing steps in detail. These instruction documents also serve as records
of the production process, since all
successfully completed production
steps (such as initial weighing of ingredients or machinery settings) are
confirmed and can be monitored by
a second person. Thus each production batch has its own record in
which all of the individual steps can
be retraced.
The fluid suppository base is pumped
out of the melting vessel into sealable
forms in a continuous strip of foil.
Uniform pumping pressure ensures
)
that each mold is filled with the same
amount of material.
26
) Making of ...
Hard fat, the base material of bioregulatory suppositories, has to be melted
before the liquid active ingredients can
be added.
During the entire production process,
samples are taken at regular intervals
and tested for a variety of parameters.
Suppository production takes place
in several different phases. First the
liquid ingredients are prepared. The
required mother tinctures are made
from the appropriate plant parts and
from mineral components. After the
mother tinctures have been tested in
the lab to ensure they meet all specifications, they are released to be
processed into specific homeopathic
potencies, which are then ready to
be used in making the suppositories.
Meanwhile, the appropriate quantity
of hard fat is weighed out, placed in
a temperature-controlled vessel, and
melted overnight. The active ingredients are added just before further
processing begins. The suppository
base is then poured into sealable
forms in a continuous strip of foil.
During pouring, the melting vessel
is held at a temperature of 37°C and
the base is stirred constantly so the
entire batch maintains a constant
temperature and the active ingredients remain homogeneously distributed. The fluid mass is then pumped
out of the melting vessel through
tubes into the molds. Uniform
pumping pressure ensures that the
same amount of material is placed in
each mold. The pour rate must be
rapid enough so the suppository
base does not begin to solidify before the mold is completely filled.
Next, the filled foil molds (still open)
are run through a cooling tunnel
where they are gradually cooled to
room temperature. Controlled cooling and hardening of the suppositories is important because overly
rapid cooling results in a brittle,
breakable final product. Conversely,
if the hardening process takes too
long, some of the incorporated mixture of liquid active ingredients may
separate from the base.
After the strips of suppositories leave
the cooling tunnel, they are sealed
and simultaneously imprinted with
their batch number and expiration
date. These “batch data” ensure
traceability of individual production
batches as required by Good Manufacturing Practice standards. The
continuous strip of individual suppositories is then cut into sheets of
six suppositories each, and a production worker packs them into cartons for storage until further packaging.
In-process monitoring takes place at
regular intervals throughout the entire production process, which continues uninterrupted as samples are
taken and tested for a variety of parameters. First, the seals and batch
data printing are checked. Then
sample suppositories are removed
from the foil and weighed, and another test confirms that the foil
forms are completely filled. These
tests are conducted on whole suppositories as well as some that are
cut open. Additional samples taken
at various times in the process are
submitted to the Quality Control
department, together with the production report, when the production
run is completed. In Quality Control, the finished suppositories and
their documentation are checked
again. Earlier in-process monitoring
is now supplemented by more timeconsuming testing of parameters
such as melting time and tensile
strength. These procedures ensure
that the very exacting pouring process actually produces uniformly
high-quality suppositories.
After the sheets of suppositories are
released by Quality Control, they
are packed together with an instruction insert into a folded box that is
again imprinted with the batch data.
In one final test, all packages are
weighed again and checked for
completeness. Any packages that deviate from the predetermined target
weight are sorted out and discarded.
Individual boxes of the final product
are then packed into shipping cartons.
In the final step, the completed
production documentation and individual samples of finished suppositories are again tested by Quality
Control before they are released
for sale.|
) 27
C a s e St u dy
Co m p e t i t i o n
Submit your case study on bioregulatory treatment for presentation at
a scientific symposium in Baden-Baden, Germany!
Authors of the two best case studies received by the International
Academy for Homotoxicology (IAH):
q will present their findings in person at the scientific symposium
of the International Society of Homotoxicology and Homeopathy
(ISOHH) during Medical Week in late October 2010 in Baden-Baden,
Germany;
q will have their studies published in a subsequent issue of the wellknown “Journal of Biomedical Therapy;”
q will receive free travel and accommodations courtesy of the IAH.
For criteria and conditions of entry, along with guidelines for writing up
your research, visit the IAH website at www.iah-online.com and click on
“Case study competition.”
Let the world know about your expertise in bioregulatory medicine!
www.iah-online.com

- International Academy of Homotoxicology

Transcription

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