Transcript Dallas ACIM June 2013

Parasitic Microbial Influences in
Chronic Complex IllnessThe Scientific Basis
Jeff Wulfman, MD
Family Physician, Bristol, VT, Assistant Clinical
Professor Family Medicine Univ. of VT
Academy of Comprehensive Integrative Medicine
(ACIM) Conference: Integrative Lyme Solutions,
June 21-22, Ft. Worth, TX
Evidenced-based medicine, heterogeneity
of treatment effects, and the trouble with
averages.
Kravitz RL, et al Milbank Q 2004
• “The individual patient is not a
numeric average but, rather, falls
somewhere on the continuum of the
bell curve and, hence, requires
individualized care. Clinical guidelines should
not supplant the judgment of treating physicians.
Quality patient care requires the physician to
consider management decisions in light of the details
unique to each patient.”
We are not sterile, we are a “superorganism”, colonies of creatures.
• The Human Microbiome:
•
The microbiome is the full collection of microbes (bacteria, fungi, viruses, etc) that
naturally exist within the human body ... Our adult bodies harbor
10 times more microbial cells than human cells. (and 100x’s
more genes) Their genomes (the microbiome) endows us with physiological capacities
that we have not had to evolve on our own and thus are both a manifestation of who we
are genetically and metabolically and a reflection of our state of well being. (NIH)
•
Our human
body is an amalgam of human cells and
microbial cells, all must function in a healthy
synergistic way for our maximum health to be achieved. This is an expansion
in concept of who we are and what we are made of. This recognition of the importance
of the microbiome has led the NIH to the establishment of the Human Microbiome
Project with the goal of typing 100 organisms that are normal commensals of a health
human gut. Again, it will be an open process, cooperation- in-discovery, involving
scientists from all over the world.
Symbioses
• “Symbioses, prolonged associations between organisms often
widely separated phylogenetically, are more common in biology
than we once thought and have been neglected as a phenomenon
worthy of study on its own merits. Extending along a
dynamic continuum from antagonistic to
cooperative and often involving elements of both antagonism
and mutualism, symbioses involve pathogens, commensals, and
mutualists interacting in myriad ways over the evolutionary history
of the involved “partners.”…Symbioses can be:
– mutualistic (all partners benefiting),
– commensalistic (one benefiting and the others unharmed)
– parasitic (one benefiting and other harmed)
although many symbiotic associations are complex or
poorly understood and do not fit neatly into one category.
– Evolving Together: the biology of symbiosis, Gregory Dimijian, MD, Proc (Bayl
Univ Med Cent). 2000 July; 13(3): 217–226. PMCID: PMC1317043
Host-microbe: symbiotic dynamics:
Mutualistic
Commensalistic
Parasitic
“Emerging Infectious Determinants of
Chronic Diseases”
• CDC-Emerging Infectious Diseases •
www.cdc.gov/eid • Vol. 12, No. 7, July 2006 Siobhán
M. O’Connor,* Christopher E. Taylor,† and James M. Hughes‡
• “…noncommunicable chronic diseases can
stem from infectious agents. Furthermore, at
least 13 of 39 recently described infectious
agents (incl. Borrelia) induce chronic
syndromes …creating opportunities to reduce
the impact of chronic disease by preventing or
treating infection.”
Parasite Paradigm
•
“parasite”- from ancient Greek “parasitos” meaning “beside food”, initially
social description- mooching officials serving at temple feasts
– much later applied to biology:
– Parasitism is a type of symbiotic relationship between two
different organisms where one organism, the parasite, takes
favor from the host, sometimes for a prolonged time. In
general, parasites are much smaller than their hosts, show a
high degree of specialization for their mode of life, and
reproduce more quickly and in greater numbers than their
hosts. The harm and benefit in parasitic
interactions concern the biological fitness of the
organisms involved. Parasites reduce host fitness in
many ways, ranging from general or specialized pathology .
Parasites increase their fitness by exploiting
hosts for food, habitat and dispersal. …it is best
considered part of a continuum of types of interactions
between species,
-”parasite”- broad definition- persistent infection- bacterial, fungal,
viral, protozoal, etc…
“Parasites”
• Micro-parasites:
–
–
–
–
–
protozoa
Yeast/fungi
Bacteria
Viruses
prions
• Macro-parasites:
–
–
–
–
Worms- large and microfilaria
Mites
Larvae
Etc…??
“Parasites”/chronic infection: survival
specialists
• Complex effects-interactions, variable
– Genetic manipulation- new genes/incorporation into host,
mutations, differential expression of existing genes
– Affect the other organisms already there, and vice-versa ,
Quorum-sensing, species interaction, gene exchange
– Defensive strategies: Biofilm formation, dormancy,
intracellular, cloaking, molecular mimicry
(“autoimmunity”), Polymorphism- multiple forms
(cyst/round-bodies, cell-wall deficient, granules, etc…)
A Theory of Chronic Illness (?and acute illness)-
IMMUNE
SYSTEM
MICROBES
HOST
A Chronic Illness Paradigm
Immune system
stressors
hormones
Emotions/spirituality
Immune system
Gut abnormalities
Nutrients:
MicrobesBacteria
Yeast
Virus
Protozoa
Worms
Etc…
Host
“genetic
Susceptibilities”
-deficiencies
-excesses
Etc…!
Metals
Toxins, Mold
Foundational Principles in the
chronically ill
• 1. Total Microbial Burden:
Chronic Parasitism
• 2. Immune Dysfunction:
Inflammation
– Increased activity “Inflammation”
– Reduced effectiveness a relative “immune deficiency”, Incomplete
clearance of microbes, etc…
“INFECTION”-chronic parasitism
“my body is on fire”
DIRECT TOXIC EFFECTS and
INFLAMMATION
Hyperinflammatory but poorly effective: cytokine smog
Downstream dysfunctions: evolve over time
HPA axis and hormonal disruption, altered detoxification,
Autoimmunity, multi-organ dysfunction, altered/compromised immunity,
behavioral changes, altered biologic terrain
Increased Total Microbial Burden:
-Acquire new infections
-Emerge out of dormancy
-Shift from commensal to parasitic
Microbes and…
– Alzheimers: 90% spirochetes, 80% chlamydophila,
HSV…
– Autism: 16X more likely –Borrelia, fungi, viruses,
mycoplasma, etc…
– Multiple Sclerosis: 90+%
Chlamydophila/mycoplasma/Borrelia
– Chronic Fatigue Syndrome: 18X more likely:
mycoplasma, borrelia, hhv-6, cmv, etc…
– Atherosclerosis/MI/stroke: increased w increase total
microbial load
– Premature labor: linear relationship btw. Total load of
microbes in amniotic fluid (>18species)
– Etc……!
G Nicolson, others
Alzheimer's disease - a neurospirochetosis. Analysis of the
evidence following Koch's and Hill's criteria. Journal of Neuroinflammation 2011,
8:90doi:10.1186/1742-2094-8-90 Judith Miklossy
BLOOD: A MICROBIAL ECOSYSTEM
“Although counter intuitive, it is increasingly obvious that
microorganisms, including Anaplasma, Babesia,
Bartonella, Borrelia, Chlamydia, Ehrlichia, Leishmania,
Mycoplasma species and retroviruses can persist in the
blood or other tissues of animals for protracted periods
of time (months to years).”
PERSISTENT BLOOD-BORNE INFECTIONS AND COMPLEX DISEASE EXPRESSION
Edward B. Breitschwerdt, DVM, DACVIM
Chief Scientific Officer, Galaxy Diagnostics, Inc.
Professor, Internal Medicine, NCSU, Raleigh, NC
Adjunct Professor of Medicine, Duke University Medical Center
http://www.galaxydx.com/web/wpcontent/uploads/2010/05/PersistentBloodBorneInfections.pdf
HHV-6 Reactivation
• 65% of pt’s admitted to ICU (medical/surgical/trauma) are
DNA+ for HHV-6 (active infection)
• 0% in healthy volunteers (silent carriers)
•
Reactivation of human b-herpesviruses (cytomegalovirus [CMV], human herpesvirus [HHV]–6, and HHV-7) in nonimmunocompromised hosts is rare.
viruses are susceptible to reactivation by cytokines and
stress-related mechanisms, the incidence of their reactivation was investigated among 120 patients during stress
Because these
related to critical illness and compared with findings among 50 healthy volunteers. Human b-herpesvirus DNA was found in 65% of critically ill
patients (60% men; mean age, 63 years) who required admission to an intensive care unit for medical (40%) or surgical (53%) indications or trauma
(7%). HHV-6 reactivation was higher in critically ill patients than in healthy volunteers (54/101 vs. 0/50; P 1⁄4 .001). All patients except 1 were
confirmed as HHV-6 variant A (mean virus load, 5066 copies/106 peripheral blood leukocytes). The reactivation of HHV-6A did not affect disease
severity and outcome. No significant reactivation of HHV-7 or CMV was demonstrated among the critically ill patients. These findings contribute to
the less-defined epidemiology of HHV-6A infection.
–
Selective Reactivation of Human Herpesvirus 6 Variant A Occurs in Critically Ill Immunocompetent Hosts, Raymund R. Razonable, et al; The Journal of
Infectious Diseases2002;185:110–3
Multiple Microbial Effects:
• Gene alteration: Borreliaupregulates >300
genes in macrophage, Anaplasma
epigenetic silencing of multiple host cell
defense genes
• Inhibit Mitochondrial Metabolism (eg-Ehrlichia)
• Vascular Changes: e.g.- altered cerebral blood
flow and metabolism
•
Gautam A, et al, Infect Immun 2011 09 26; Jose C. Garcia-Garcia, PLoS Pathog 5(6): e1000488; Microbes
Infect. 2011 Mar;13(3):232-8. Epub 2010 Nov 9., Liu Y, et al; Arch Gen Psychiatry. 2009 May;66(5):554-63.
Lyme Disease (Borrelia burgdorferi)
2011 Case Definition
CSTE Position Statement Number: 10-ID-06,
www.cdc.gov/osels/ph_surveillance/nndss/casedef/lyme_disease_Current.htm
From the CDC:
"This surveillance case definition was developed
for national reporting of Lyme disease; it is not
intended to be used in clinical
diagnosis."
•
• From the FDA:
– “The tests should be used only to support a clinical diagnosis of Lyme
disease and should never be the primary basis for making diagnostic
or treatment decisions.” (FDA Medical Bulletin) Role of serology in the diagnosis of Lyme disease.
JAMA, 282(1): 62-65; 1999 Brown SL Hansen SL; Langone JJ.
Ratio of actual:reported- ~10:1 per CDC, ~40:1 per Martha’s Vineyard (25 vs. 1000 rx’s)
Definitions:
• Lyme Borreliosis = Lyme Disease
– Early Localized - skin only, no systemic symptoms
– Early Disseminated - early stages with systemic
symptoms (fatigue, myalgias, arthralgias, headache,
multiple skin lesions, fever, etc, etc….)
– Late Stage – prolonged evolving systemic
symptoms
– Neuroborreliosis- neurologic involvement
Borrelia bacteria have been found in:
•
•
•
•
•
•
•
•
•
•
•
Bladder
Blood
Bone
Brain
CSF
Eye
Heart- endo/myo/peri
Kidney
Ligaments
Liver
Lung
•
•
•
•
•
•
•
•
•
Lymph nodes
Muscle
Nerves
Skin
Spinal cord
Spleen
Synovial fluid
Synovial membranes
Intracellular: endothelium,
neurones, microglia,
fibroblasts…
• Biofilm: endocarditis, …
Local and generalized hyper-inflammatory response with
Elevated inflammatory cytokines (Tnf-a,,etc) in plasma, CSF, tissues, brain
LYME/Borrelia Labs
• Indirect tests: body’s response tosuggesting past exposure, not the
organism itself, there can be false negatives
and false positives.
Tier 1
Tier 2
• ELISA (“lyme Ab or
titer”)neg,equiv,pos
• Western blot- IgG, IgM - “positive
or negative” based off of number
of bands present (corresponding to Ag’s)
During the Acute Phase (<3mos)of
Lyme Disease:
• A single sample 2-tier testing scheme will be
NEGATIVE in >50% of patients (EM+)
– Sex Differences in the Clinical and Serologic Presentation of Early Lyme
Disease: Results From a Retrospective Review : Alison Schwarzwalder,
MPH, et al; Gender Medicine/Vol. 7, no. 4, 2010
– Aguero-Rosenfeld, ME, Nowakowski, J, McKenna, DF, Carbonaro, CA, and GP
Wormser. "Evolution of the serologic response to Borrelia burgdorferi in treated
patients with culture-confirmed erythema migrans." Journal of Clinical
Microbiology 34 (1996): 1-9
– Nowakowski, J.,et al, 2001. Laboratory diagnostic techniques for patients with
early Lyme disease associated with erythema migrans: a comparison of different
tech- niques. Clin. Infect. Dis. 33:2023–2027.
•
Two-tier serologic testing: Acute phase...40% Convalescent phase .....66%
“Course of Antibody Response in Lyme Borreliosis Patients
before and after Therapy”
Elisabeth Aberer and Gerold Schwantzer, Immunology 2012
IgG antibody response
Before (BT) and after(AT)
treatment
LYME/Borrelia Labs
• Direct tests:
– PCR- DNA identification, low yield, tissue better
than fluids
– Borrelia Culture- promising new technique developed- study:
96%sensitive, definitive if positive. Improved culture conditions for the
growth and detection of borrelia from human serum. Sapi E, Pabbati N, Datar
A, Davies EM, Rattelle A, Kuo BA. Int J Med Sci. 2013;10(4):362-76
– Biopsy (high yield in animal studies)- silver stain,
IHC
Multiple lesions=disseminated dz
Lyme Disease: a Neuropsychiatric
Illness
• “A broad range of psychiatric reactions have
been associated with Lyme disease including
paranoia, dementia, schizophrenia, bipolar
disorder, panic attacks, major depression,
anorexia nervosa, and obsessive compulsive
disorder.” Fallon BA, Nields JA. Columbia Univ.
American Journal of Psychiatry, 151(11):1571-83. 1994
Great resource:
www.lymeinfo.net  “literature summaries”
SPECT in Late Stage Neuroborreliosis
Control
Donta ST, Noto RB, Vento JA.
Clin Nucl Med. 2012 Sep;37(9):e219-22..
SPECT brain imaging in chronic Lyme disease- 75% w abnl SPECT scans,
70% improved w prolonged abx
Other issues
• Prior treatment with antibiotics:
– ***Can attenuate antibody response
• More likely to test negative, possibly forever.
• There is ***no “test for cure”
• Treatment Delayworse outcome
– If >60days from onset to treatment 6x more likely
to remain ill
– If ECM+  5x more likely cured w treatment
• Cameron D, 2006 Journal of Evaluation in Clinical Practice
Multiple Pathogens in ticks:
•
“PCR analysis of Ixodes scapularis ticks collected in New Jersey identified
infections with
– Borrelia burgdorferi (33.6%),
– Babesia microti (8.4%),
– Anaplasma phagocytophila [Ehrlichiosis] (1.9%),
– Bartonella spp. (34.5%).”
•
•
Adelson ME, et al, J Clin Microbiol 2004
.
Bartonella spp. bacteremia and rheumatic symptoms in patients
from Lyme disease-endemic region. Maggi RG, et al,Emerg Infect Dis. 2012 May;18(5):783-91
– 40% of patients PCR+ for Bartonella (Galaxy Diagnostics)
biofilm
“The influence of systemic inflammation on
inflammation in the brain: implications for chronic
neurodegenerative disease”
Perry H;Brain,Behavior, and Immunity 18(2004) 407-413
• “…systemic inflammation may impact on local
inflammation in the diseased brain leading to
exaggerated synthesis of inflammatory cytokines
and other mediators in the brain, which in turn
influence behavior. These interactions suggest
that systemic infections, or indeed any systemic
challenge that promotes a systemic
inflammatory response, may contribute to
the outcome or progression of chronic
neurodegenerative disease.”
Relationship of Inflammation and Autoimmunity to
Psychiatric Sequelae in Lyme Disease
Bransfield R, PSYCHIATRIC ANNALS 42:9 | SEPTEMBER 2012
• LATE-STAGE IMMUNE CNS EFFECTS: three
principal mechanisms leading to the injury of
neuronal cells are:
– 1) the secretion of cytotoxic substances by leucocytes
and glial cells
– 2) direct cytotoxicity
– 3) autoimmune-triggered processes via molecular
mimicry.
– “No self-perpetuating immune process without
persistent infection has ever been scientifically
proven.”
Microglial priming:
(microgliaWBC’s of the brain)
• “Pre-existing microglial activation
greatly magnifies neurodegeneration
associated with subsequent episodes
of immune activation”
•
Blaylock RL, Strunecka A; Immune-Glutamatergic Dysfunction as a Central Mechanism of
the Autism Spectrum Disorders, Curr. Medicinal Chemistry, 2009,16,157-170.
• An inflammed brain(body) is highly
sensitive/vulnerable to further inflammatory insultmagnified response
• Bite of pizza
bite the teacher
Peripheral infection (?and any other peripheral immune
challenge?) can trigger CNS pathology
• Mice:
– Infected w CNS restricted Measles virus- no illness
– Infected w peripherally restricted (LCMV) virus- no illness
– Infected with both: ALL became diseased with 50%
mortality and most having seizures
• 12 fold increase activated Tcells in brain, inflammation/edema
• >35% where LCMV specific (despite NO LCMV in brain tissue)
• i.e.- CNS activator and recruiting signal + peripheral
immune response initiator= potentiated
neuroinflammation
• “CNS Recruitment of CD8+ T Lymphocytes Specific for a Peripheral
Virus Infection Triggers Neuropathogenesis during Polymicrobial
Challenge” Matullo CM, et al, 2011, PLoS Pathog 7(12)
PeripheralCNS cont’d
• “These results indicate that T cell trafficking can be
influenced by other ongoing immune challenges, and
that CD8 + T cell recruitment to the brain can trigger
CNS disease in the apparent absence of cognate
antigen.
• By extrapolation, human CNS diseases of unknown
etiology need not be associated with infection with any
particular agent; rather, a condition that compromises
and activates the blood-brain barrier and adjacent
brain parenchyma can render the CNS susceptible to
pathogen-independent immune attack.”
Matullo CM
Cytokine Associated Emotional and Cognitive Disturbances in Humans,
Arch Gen Psychiatry. 2001;58: 445-52, Reichenberg A, et al
• “Infectious, autoimmune and neurodegenerative
diseases are associated with profound psychological
disturbances.”
– Study: inject low-dose salmonella endotoxin (not
enough to give any subjective sense of illness, but enough to induce
transient inflammatory cytokine release) or placebo…tested
repeatedly over next 10hrs
• Within 1 hour: new onset of anxiety,
depression, reduced memory
• “…mild stimulation of primary host defense has negative effects on
emotional and memory functions.”
Infection and Autoimmunity“Infections and autoimmunity - friends or foes?”, Shaye Kivity, et al. Trends in Immunology 2009.
• “…not always a hit and run event, but rather
a cumulative process. The immune system is
affected by repeated infections from
childhood, and in immune sensitive
individuals, a breakthrough point might
occur when the infection burden crosses a
crucial level. This breakthrough point might
be reached when a specific pathogen load,
immune load or a unique combination of
pathogens is established.”
Synergy of Factors:
-Heavy metals and 1000’s of other toxins:
– “…profound and complex effects on the immune system…subtoxic doses of mercury
induces both the production of highly specific autoantibodies and a polyclonal
activation of the immune system” Mol Immunol. 2005 May;42(7):833-8
–
Mercury + PCB’s magnified neurobehavioral effects, Lead + Mercury 1+1= 50
-Massive nutritional shifts over time: refined
(carbs), toxic, nutrient devoid food
-energetic- EMF’s, societal, etc…
Nutritional immunology
“Minocycline, a microglial inhibitor, reduces
‘honey trap’ risk in human economic exchange”
•
•
“Males tend to cooperate with physically attractive females without careful
evaluation of their trustworthiness, resulting in betrayal by the female.
In this experiment, healthy male participants made risky choices (whether or not
to trust female partners, identified only by photograph, who had decided in
advance to exploit the male participants). The results show that trusting
behaviour in male participants significantly increased in relation to the perceived
attractiveness of the female partner, but that attractiveness did not impact
trusting behaviour in the minocycline group.
•
Scientific Reports 3, Watabe et al, 18 April 2013
SYNERGY: mercury is in the
backgroundreduced ability to clear microbes
Dynamics in treating the chronically ill:
Strengthen,
Optimize Terrain
Reduce Parasitic
Microbial Burden
Anti-oxidant-
Pro-oxidant-
Symptoms… but ?
microbial clearance
Symptoms… but ?
microbial clearance
Stratifying Patients:
• Acutely ill- a “golden window”, especially with lyme
borreliosis to completely and definitively treat and
prevent chronic illness
– Treat the infection component early and completely
(adequate dosing and duration)
– Rapidly dividing infection(s)- more antibiotic responsive
– Patient usually doesn’t need much co-factor work (if preexisting health was high)
• Chronically ill– Sometimes may do better with “strengthening” and
addressing some co-factors first, before direct antimicrobials, but you may only get so far without going after
the “infection(s)”
Strengthen,Optimize Terrain
&/or Reduce Parasitic Microbial Burden
• Reduce Microbial Burden emphasis:
–
–
–
–
Severely ill and/or rapidly declining,
children
Acute decompensation
High level of prior health
• Terrain emphasis:
– Long-term ill, “stable”-chronic persistent state,
– adults,
– not rapidly declining
– (probiotics, remineralize, omega-3, B-12, micro/macro nutrients,
hormone balancing, diet, emotions…)
• Many concurrently
General Differences:
• Pediatric:
– **Respond better to
antibiotic therapy- more
likely to heal with this
single intervention.
– Harder to elicit symptoms
(and assess treatment
response)
– More gastrointestinal
symptoms, headache
– Relapses usually occur
rapidly
• Adults:
– More difficult to treat
– More co-factors
(dysfunction of immune/endocrine/
neurologic systems, additional
accumulated pathogens,
accumulated toxins)
– Relapses slower and less defined
Evaluation: most• Testing:
– CBC, Comp. Metabolic, B-12, ANA, RF, ESR
– IgG: gluten, casein (others- soy, corn, egg)
• And/or elimination trial even w NL labs
– GI- stool analysis w parasitology
– Thyroid eval- TSH, free T3, free T4, thyroid Ab’s
– Eval celiac- anti-transglutaminase, anti-gliadin
IgA, total IgA
– Toxin- urinary porphyrin &/or dmsa provoked
urine and/or MELISA
– Mold- ERMI test on home
– Electrodiagnostics, ZYTO, ART, others
– TGF-Beta1, C4a ?
– Etc…
Specifics- infection evaluation
• Borrelia (“lyme”)- western blot- with complete band analysis,
sometimes treat first then test/re-test, PCR(tissue>fluids), new
culture test (Advanced Laboratories), with biopsy- do pcr, silver stain and IHC
• Usually:
– Babesia- titers, also FISH (Igenex) , and Duncani/WA-1, (Immunosciences)
– Bartonella-titers, pcr (enriched culture pcr- Galaxy); with biopsy- do: PCR, IHC and silver
stain
– Ehrlichia and Anaplasma titers
• Occasional:
– Mycoplasma- PCR (tissue, blood, urine; MDL, Clongen), Mycoplasma
Pneumonia Ab, others
– Fry labs blood smear- ?organism?
– Others…chlamydia Ab, viral titers, etc…
• Avoid Tunnel Vision- check other non-infectious possibilities-
Total microbial load
– Treatment sequence: start with large organisms
and move toward small
Big
• Worms
• Yeast
• Protozoa
• Bacteria
Small
• viruses
(Synergists: licorice, ginger, blk pepper(piperine)
Herbal: black walnut, garlic, etc…
Pharma: Alinia, albendazole, biltricide
Herbal: probiotics, caprylic acid, garlic,
Oregano, etc…
Pharm: fluconazole, itraconazole….
Herbal: Mora, Cryptolepis, Sida acuta…
Pharm: Mepron/zithr, ?Alinia….
Herbal: multitude
Pharma: multitude
Often pushed into dormancy
once above addressed, Olive leaf extr.,
mult combo’s
Pharm- ?valtrex, etc..
Microbial
reduction/suppression/balancing:
• Pharmaceutical antibiotics
– Variable responses- life-saving in some, not in others
– May induce reactive pleomorphism, dormancy and yeast dominance
• Botanical:
– slower, more subtle…requires patience, sometimes 2-3+mos. to start
seeing improvement
– 6-8 different ones I use (japanese knotweed Resveratrol- inhibits
TNF-alpha and downregulates NF kappa B),, cumanda, banderol,
smilax, artemesia, red root, samento, stephania, sida, etc…)
– Alone or in combinations
– Constant and/or rotational- cycling- 6-8wks on- 2wk off then change,
12 day on/2off,
– Watch Liver enzymes if given with ABX
“Lyme Tea”
Lyme tea table
(optional)
Combine herbs and water in a large stockpot. Stir, cover and bring to a boil, then lower heat and simmer for 2 hours.
Strain (use a mesh strainer covered with cheese cloth ) and pour into a clean canning jar, wine bottle, glass bottle
or use an iced tea jug w/spigot. Store in the fridge. Compost herb
. General dosage guideline: about 3-4 ounces 3 times a day, adjust dose base on tolerance; reduce dose in children
(use only under supervision of physician/herbalist,etc)
Anti-microbials/microbial balancers:
• Pharmaceutical
– Most effective/useful:
• rapidly dividing/escalating
illness
• Heavy neurologic
involvement
• Early acute illness
• Children
• Elderly
• Fewer co-factors
• Good pre-existing vitality
• Botanical:
– Most effective/useful:
• Slow smoldering illness
• Prior heavy anti-biotic use
and have stopped
responding, relapsing
• Prolonged illness
• Adults
• Many co-factors
• Weak/depleted vitality
Antimicrobial techniques:
• Dealing with “Adaptation”: (if happens, generally see in the 26mos time-frame with both herbal/pharma)
– “cycling”- 6-8wks with a given therapy, stop for 3-4wks or
until highly symptomatic, then go to next therapy
• *however, if getting progressive continued slope of improvement,
may be best to hold the current course
– Proteolytic enzymes- lumbrokinase, serrapeptase,
nattokinase- most effective if give after been on
antimicrobials for several weeks
– “cyst” busting anti-microbials AFTER on others and give
course every 2-4wks (flagyl/tindamax, GSE, plaquenil…)
– Poly-pharmacy: poly-botanical, poly-pharmaceutical,
botanical-pharmaceutical
– “pulsing”- on and off, same therapy- eg 3 days in row/wk.
Finding blocks and rate-limiting-steps
• Some common obstacles:
– Food sensitivities: Gluten>Casein>soy>corn
• IgG reactions….add fuel to the fire
– Untreated intestinal parasites
– Untreated/imbalanced systemic parasites
(bacteria/yeast/protozoa/viral)
– Inflammatory nutritional excesses- ex: refined
carbohydrates
– Emotional/relational/spiritual discord
– Ongoing Mold exposure (in a sensitive pt.)
– Unmediated/ongoing toxin exposures
– Sleep and rest
– Keep: looking, reassessing, therapeutic trials
– Some may not be destined for healing
Cases:
Being Healthy Is a Revolutionary Act: A
Manifesto for Thriving in a Mixed-Up World
• By Pilar Gerasimo, www.RevolutionaryAct.com
• “In case you haven’t noticed, we live in a society where the
idea of health and fitness is wildly popular, but where
actually becoming a truly healthy person can be mighty
tough to pull off.
• There’s a reason so many of us are sick, overweight,
depressed and stressed out: We’re living in a society that is
wired up to make us sick, overweight, depressed and
stressed out.
• We can change this mixed-up reality. We can reclaim our
well-being and create a better, more blissful world. But it’s
going to take some revolutionary moxie to make it happen.”
Empowerment and
Transformation…vs. fear and anger
• Re-claim responsibility for healing your life
• Relentlessly forces one to face the realities of one’s
life: priorities, choices, knowledge of what
strengthens you and what weakens you
• -become exquisitely sensitive to one’s internal and
external world…sound, touch, food,
relationships…insight and spiritual experience.
•The healing journey…can be a journey of selfexploration, heightened awareness,
empowerment and transformation
End- Thank You