Food allergy has been long recognized and well documented. Other adverse reactions to foods first referred to as “toxic idiopathies” by John Freeman, co inventor of immunotherapy, at the early part of the 1900s can be mediated by and have their impact on the nervous and endocrine systems. It can also be mediated by pharmacologic mechanisms and can also affect any part of the body. There’s a great clinical need to accurately identify triggers of adverse reactivity as they have now been linked with even the most serious of modern maladies and diseases. In fact, inflammation is the hallmark of metabolic syndrome. Given the multitude of pathogenic mechanisms underlying adverse reactions to foods and other environmental exposures it is necessary that a utilizable and cost effective technology be understood so that its application be utilized under the appropriate circumstances.
KEY LEARNING POINTS
• The natural ability of certain foods to initiate an inflammatory response and induce metabolic disruptions and counterbalancing mechanisms to prevent that
• How foods can trigger “danger signals” for the immune system
Pharmacologic vs. immunologic reactions to foods
• Is there a common final pathway of all these mechanisms that can reliably indicate triggers of clinical pathology?
• Cellular testing vs. serologic testing: The advantages of cellular testing
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Explore the cell's role in mediating adverse reactions
1. a scientific discussion on metabolic, immunologic
and pharmacologic mediators
Explore the cell’s role in mediating adverse reactions:
2. Roger Davis Deutsch is one of the
pioneers of food and chemical
sensitivities testing with
involvement in this field since 1986.
He has been responsible for the
commercialization of the Alcat Test
throughout the world. He is the co-
author of Your Hidden food
Allergies are Making You Fat. Roger
serves as the Founder and CEO of
Cell Science Systems.
About our Speakers
3. J Allergy Clin Immunol. 2001 Jan;107(1):129-34.
Distinct patterns of neonatal gut microflora in infants in whom
atopy was and was not developing.
Kalliomaki M, Kiriavainen P, Eerola E, Kero P, Salminen S, Isolauri E.
RESULTS:
• Atopic sensitization was observed in 22 (29%) of 76 children. At 3 weeks,
the bacterial cellular fatty acid profile in fecal samples differed
significantly between infants in whom atopy was and was not
developing (P =.005). By using fluorescence in situ hydridization, atopic
subjects had more clostridia (geometric mean [95% confidence
interval]: 9.3 x 10(7) [3.8-22.9 x 10(7)] vs 3.3 x 10(7) [1.8-6.1 x 10(7)], P
=.04) and tended to have fewer bifidobacteria (1.8 x 10(9) [0.4-7.6 x
10(9)] vs 6.1 x 10(9) [2.5-14.6 x 10(9)], P =.11) in their stools than
nonatopic subjects, resulting in a reduced ratio of bifidobacteria to
clostridia (P =.03).
CONCLUSION:
• Differences in the neonatal gut microflora precede the development of
atopy, suggesting a crucial role of the balance of indigenous intestinal
bacteria for the maturation of human immunity to a nonatopic mode.
4. Distinct Patterns of IgG and IgA against Food and Microbial
Antigens in Serum and Feces of Patients with Inflammatory
Bowel Disease
PLOS ONE Sept, 12, 2014 Lisa Freh, et. al.
• We therefore aimed at comprehensively
investigating local or systemic levels of anti-
microbial and anti-food Abs in IBD patients.
For this purpose, we analyzed in parallel
serum and fecal Abs specific for dietary and
microbial antigens in a cohort of IBD patients
and controls.
5. Figure 2.
Anti-food and anti-microbial
serum IgG and IgA levels in
CD patients with or without
stricturing/penetrating
disease and controls.
Frehn L, Jansen A, Bennek E, Mandic AD, Temizel I, et al. (2014)
Distinct Patterns of IgG and IgA against Food and Microbial
Antigens in Serum and Feces of Patients with Inflammatory Bowel
Diseases. PLoS ONE 9(9): e106750.
doi:10.1371/journal.pone.0106750
http://journals.plos.org/plosone/article?id=info:doi/10.1371/journal.
pone.0106750
6. Distinct Patterns of IgG and IgA against Food and
Microbial Antigens in Serum and Feces of Patients
with Inflammatory Bowel Disease
PLOS ONE Sept, 12, 2014 Lisa Freh, et. al. Department of Internal Medicine III, University Hospital Aachen, RWTH University, Aachen, Germany
Results
• Serum anti-Saccharomyces cerevisiae antibodies (ASCA) and anti-B.
fragilis IgG and IgA levels were increased in CD patients whereas
antibody (Ab) levels against E. coli and food antigens were not
significantly different within the patient groups and controls
7. • One important finding of our study is that we did not
find any correlation between food-specific Ab levels
and clinical symptoms. Our data does not support the
idea that measurements of anti-food specific IgG or
IgA is of any clinical relevance for patients suffering
from CD or UC. In particular, it does not predict the
presence of food intolerance.
Distinct Patterns of IgG and IgA against Food
and Microbial Antigens in Serum and Feces of
Patients with Inflammatory Bowel Disease
PLOS ONE Sept, 12, 2014 Lisa Freh, et. al.
8. Distinct Patterns of IgG and IgA against Food and
Microbial Antigens in Serum and Feces of Patients
with Inflammatory Bowel Disease
PLOS ONE Sept, 12, 2014 Lisa Freh, et. al.
• Acute exacerbation of disease does not correlate with
antibody levels, however enhanced ASCA and other
anti-microbial Ab levels correlate with more
complicated disease courses and anti-TNF-α therapy,
It has been shown that microbial-specific IgA
mediates gut homeostasis in animal models and
might therefore have anti-inflammatory functions in
IBD.
9. Distinct Patterns of IgG and IgA against Food and
Microbial Antigens in Serum and Feces of Patients
with Inflammatory Bowel Disease
PLOS ONE Sept, 12, 2014 Lisa Freh, et. al.
• In summary, our study reveals that CD, UC and AGE
patients as well as non-inflammatory controls have
distinct patterns of IgG and IgA against food and
microbial antigens in serum and feces suggesting
differentially regulated immune responses towards
intestinal antigens. However, food-specific Abs have
not yet been proven to be a valuable biomarker for
IBD or food intolerance.
10. RESEARCH ARTICLE
Gliadin Induces Neutrophil Migration via
Engagement of the Formyl Peptide Receptor,
FPR1.
Results
In vivo intestinal luminal injection of PT-gliadin induces an
immediate and substantial recruitment of neutrophils.
Increased intestinal permeability favors the access of gliadin and
other macromolecular antigens from the intestinal lumen into the
lamina propria where the host, by interpreting them as danger
signals, will respond with first-line defense mechanisms such as
neutrophil recruitment to the site of exposure.
11. Macrophage activity in semen is significantly
correlated with sperm quality in infertile men.
“The presence of leucocytes within semen has the potential to
impair sperm function. Neutrophils and macrophages make up
95% of seminal leucocytes, with both having the ability to damage
sperm via the generation of reactive oxygen species, proteases and
the induction of apoptosis…..We were able to confirm for the first
time that seminal plasma does indeed contain neopterin and that
the levels of this macrophage activity marker are threefold higher
in infertile than fertile men.”
Tremellen K, Tunc O. Research Centre for Reproductive Health, Discipline of Obstetrics and Gynaecology, School of
Paediatrics and Reproductive Health, University of Adelaide, Adelaide, SA, Australia. Int J Androl. 2010 Jan 28.
12. Neutrophils in local and systemic antibody-
dependent inflammatory and anaphylactic reactions
Friederike Jönsson,*,1,2 David A. Mancardi,*,1,2 Marcello Albanesi,*,† and Pierre Bruhns*
* Institut Pasteur, Département d’Immunologie, Laboratoire Anticorps en Thérapie et Pathologie, and INSERM, U760, Paris,
France and;† Université Pierre et Marie Curie, Paris, France
RECEIVED SEPTEMBER 28, 2012; REVISED MARCH 7, 2013; ACCEPTED MARCH 11, 2013. DOI: 10.1189/jlb.1212623
• It is, however, difficult to discriminate between the
consequences of the activation of resident macrophages and
the activation of infiltrating neutrophils: these two cell types
can secrete similar panels of molecules and antimicrobial
products. Nonetheless, the severity of IC induced
inflammation is closely linked to the extent of neutrophil
infiltration, suggesting that this cell type is responsible for
most of the observed symptoms.
13. alpha(4)-integrin mediates neutrophil-induced
free radical injury to cardiac myocytes
…circulating neutrophils adhere to cardiac myocytes and
cause cellular injury… emigrated PMNs have the capacity to
injure cardiac myocytes
Poon BY, Ward CA, Cooper CB, Giles WR, Burns AR, Kubes P.
Immunology Research Group, University of Calgary, Calgary, Alberta T2N 1N4, Canada. J Cell Biol. 2001 Mar 5;152(5):857-66.
14. Changes of neutrophil myeloperoxidase in
coronary circulation among patients with acute
coronary syndrome
“MPO is a better marker for inflammation of the local plaques. It
may be one of the mechanisms that MPO induces the
transforming from LDL to ox-LDL in plaques vulnerability.”
Li L, Zhang Y, Chen YG, Li GS, Wang Y, Ma X, Li JF, Zhong M, Zhang W. Key Laboratory of Cardiovascular Remodeling and Function Research,
Chinese Ministry of Education and Public Health, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China.
15. Chronic activation of the innate immune
system may underlie the metabolic syndrome
Most importantly, activation of this system leads to
fundamental changes in body metabolism. In this regard, it is
notable that pro-inflammatory cytokines are major stimulants
of the hypothalamic-pituitary-adrenal axis, leading to
increased cortisol secretion and inhibition of sex hormone
production.
Sao Paulo Med. J. Vol. 119 no.3 Sao Paulo May 2001
Social Medicine Department, School of Medicine, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil
16. Increase in fragmented phosphatidylcholine
in blood plasma by oxidative stress.
Oxidatively modified phospholipids have attracted much
interest because of their pro-inflammatory activity and their
potential involvement in atherosclerosis…The increase
coincided with a surge of circulating neutrophils.
Frey B, Haupt R, Alms S, Holzmann G, Konig T, Kern H, Kox W, Rustow B, Schlame M. Department of Anesthesiology and
Intensive Care Medicine, University Hospital Charite, Humboldt University, Berlin, Germany. J Lipid Res. 2000 Jul;41(7):1145-53
17. Adaptive Metabolic Leukocyte
Activation
“Careful study of diet-induced obesity has identified chronic
leukocyte-mediated low grade inflammation within
professional metabolic tissues as the characteristic
pathophysiology of metabolic syndrome.”
J. Olefsky, C. Glass, Macrophages, inflammation, and insulin resistance. Annu. Rev. Physiol. 72,219 (2010). 10.1146/annurev-physiol-021909
A. Chawla, K. D. Nguyen, Y. P. Goh, Macrophage-mediated inflammation in metabolic disease. Nat. Rev. Immunol. 11, 738 (2011).
18. Amy Pieczarka, RD is a
dietitian/nutritionist, in practice for
over 26 years. She is delighted to be
a part of the PreviMedica team of
exceptional professionals, dedicated
to promoting optimal health through
customized nutrition. Amy received
her Bachelor of Science degree in
Nutrition and Medical Dietetics from
the Pennsylvania State University.
Currently, Amy serves as the creator
and manager of PreviMedica
Nutrition Services.
About our Speakers
19. -Philip Regal, Biologist
“Plants are little biochemical factories that produce scores of bioactive
compounds in order to mess up the metabolism of a great variety of
predators and pathogens. That’s why all the first drugs were discovered in
plants. Even in small amounts some plant chemicals are good for us and
some are dangerous, so ethnobotanists seek knowledge from local tribal
people about which are which.”
20. • Tryptamine
• Gluten
• Lectin
• Aflatoxin
• Lactose
• Chlorogenic Acid
• Solanine
“Pilot study into the Effect of Naturally
Occurring Pharmacoactive Agents on the
Alcat Test” - P.J. Fell, MD
• Dopamine
• Histamine
• Lactoglobulin
• Octopamine
• Phenylethylamine
• Serotonin
21. • The white cell can act as a model of activity by either
a toxic or pharmacological effect. This effect
produces a change in size of parts of the white cell
population which the Alcat Test can detect.
22. About our Speakers
Craig Koniver, MD is a Board Certified
Family Medicine Physician who has
extensive experience and interest in
the field of natural and organic
medicine. Dr. Koniver completed his
undergraduate degree at Brown
University and received his Medical
Doctorate from Jefferson Medical
College. He opened Primary Plus
Organic Medicine, LLC in Charleston,
South Carolina in 2006 and has been
utilizing the Alcat Test since.
23. The Alcat Test
• NOT just for GI issues
• Symptomatic vs. Preventive (Optimizing Health)
• Everything we interact with in life, affects our biochemistry
33. Chemical Sensitivity
• JS, 53 y/o female presented with c/o mouth sores, joint pain
• Ran full Alcat Test Panel
34.
35. GI Issues
• TS is a 43 y/o male with no significant medical problems
• 9 month h/o gas, bloating, constipation, rash on LE,
difficulty gaining weight, fatigue
• Ran 200 Food Panel
• After 1 month of being very strict with both elimination
and rotational diet, he reported that his symptoms were
90% better
36.
37.
38. Metabolic Issues
• CB, 56 y/o female with c/o fatigue, inability to lose
weight, diabetes, on multiple medications
• Ran 200 Food Panel
• After just three weeks of changing her diet, she reported
that her normal fasting AM glucose level was 86.
Followed by several in the 90’s and then several in the
80’s (her norm was 120’s).