Optimizing GI Function and Heavy Metal Burden in Lyme Disease - PowerPoint PPT Presentation

About This Presentation
Title:

Optimizing GI Function and Heavy Metal Burden in Lyme Disease

Description:

Optimizing GI Function and Heavy Metal Burden in Lyme Disease Raj Patel, MD Medical Options for Wellness Los Altos, CA 650-964-6700 www.DrRajPatel.net – PowerPoint PPT presentation

Number of Views:141
Avg rating:3.0/5.0
Slides: 32
Provided by: drrajpatel
Category:

less

Transcript and Presenter's Notes

Title: Optimizing GI Function and Heavy Metal Burden in Lyme Disease


1
Optimizing GI Function and Heavy Metal Burden in
Lyme Disease

Raj Patel, MD Medical Options for Wellness Los
Altos, CA 650-964-6700 www.DrRajPatel.net
2
Overview
  • Optimize GI Function
  • Antibiotic induced diarrhea
  • Intestinal dysbiosis (definition, causes,
    treatment)
  • Liver/GB Support
  • B. Heavy Metals
  • Prevalence
  • Signs symptoms
  • Testing
  • Treatment options
  • Methylation in non-responders
  • C. Conclusion


3
A. Optimize GI Function
  • 1. Antibiotic Induced Diarrhea (AID)
  • Common complication from extended antibiotic
    use
  • Probability increases with use of gt2
    antibiotics
  • Doxy Flagyl for 10 d
    caused a significant increase
  • in GI and vaginal candida
    counts than either alone.
  • Maraki S. J
    Chemother. 2003 Aug15(4)369-73.
  • Certain antibiotics more commonly associated
    with
  • AID (Cephalosporins and
    Penicillins)
  • Clostridium difficile induced enterocolitis
  • Symptoms diarrhea, abdominal
    pain, fevers
  • Incidence only accounts for
    10-20 of all AID cases
  • E. Bergogne-Bérézin Int
    J Antimicrob Agents. 2000 Dec16(4)521-6


4
  • Non-Clostridium AID
  • Common pathogens include
    Clostridium perfringens,
  • Staphylococcus aureus, Klebsiella
    oxytoca, Candida species,
  • and Salmonella species.
  • Accounts for 80-90 of all AID cases
  • Clin Infect Dis. 1998
    Oct27(4)702-10
  • AID Treatment Options
  • Mild Symptoms Saccharomyces
    boulardii

  • Probiotics
  • Bland
    diet
  • Drug
    holiday/Change antibiotics
  • Elmer GW. et al JAMA.
    1996 Jul 3 276(1)29-30 Biotherapeutic agents. A
    neglected
  • modality for the
    treatment and prevention of selected intestinal
    and vaginal infections.
  • Severe Symptoms Metronidazole


5
  • 2. Intestinal Dysbiosis
  • a. Definition
  • Term originally coined by Metchnikoff to
    describe altered pathogenic
  • bacteria in gut. Today, abnormal
    milieu due to bacterial and fugal
  • imbalance.
  • These abnormal bacteria have been shown to
    produce
  • toxic products- endotoxins,
    phenols, ammonia, indoles
  • Macfarlane C et al. Proteolysis
    and amino acid fermentation. In Gibson GR,
    Macfarlane GT, eds.
  • Human Colonic Bacteria
    Role in Nutrition, Physiology, and Pathology.
    Boca Raton, FL
  • CRC Press 199575-100.
  • Chronic degenerative diseases - inflammatory
    bowel disease,

  • ankylosing spondylitis, RA
  • Peltonen R, Nenonen M, Helve T,
    et al. Br J Rheumatol 19973664-68.
  • Brandtzaeg P. Review
    article Aliment Pharmacol Ther 19971124-37.


6
  • Intestinal Dysbiosis (cont)
  • b. Functions of the microflora
  • Immune stimulation
  • Vitamin synthesis (B group K)
  • Enhancement of gut motility, digestion
    nutrient absorption
  • Improve epithelial function via increased SCFA
    production,
  • decreased apoptosis, increased barrier
    integrity
  • Inhibit pathogenic bacteria via decreasing
    luminal pH, decreasing
  • epithelial binding, and decreasing
    epithelial invasion
  • Metabolism of certain drugs
  • Holzapfel WH, et al. Int J Food
    Microbiol 19984185-101.
  • Noack J, et al. J Nutr
    19981281385-1391.
  • Gibson GR, Roberfroid MB. J Nutr
    19951251401-1412.
  • Sartor, RB. J. Clin. Gastro
    200741537-543


7

Intestinal Dysbiosis (cont) c. Causes of
Intestinal Dysbiosis I.
Antibiotics-based on spectrum of activity, route
of excretion, dosage, length of use. Hawrelak,
JA Alternative Medicine Review Vol 9, No 2 2004

8
Effects of Antibiotics on Intestinal Flora
Antibiotics Entero-bacteria Entero-cocci Anaerobic ResistantStrains Lactobacilli/Bifidus Candida
Ampicillin
Amoxicillin
Cefaclor
Ceftriaxone
Ciprofloxacin
Clindamycin
Doxycycline
Metronidazole
Moxalactam
Ofloxacin
Hawrelak, JA Alternative Medicine Review Vol 9,
No 2 2004
9
  • c. Causes of Intestinal Dysbiosis (cont)
  • II. Stress
  • Altered gut motility and increased bicarbonate
    production
  • potentially leading to decreased
    survival/adherence/replication of
  • healthy flora
  • Lenz HJ. Et al.
    Gastroenterology 198894598-602.
  • Lenz HJ. Proc Natl Acad Sci
    U S A 1989861417-1420.
  • Decreased mucin and mucopolysaccharide production
    leading to
  • increased adherence and
    replication of dysbiotic flora


10
  • c. Causes of Intestinal Dysbiosis (cont)
  • III. Lyme and Coinfections
  • Lyme is well documented to invade and
    multiply in the GI tract
  • Fried MD, et al
    Gastrointestinal pathology in children with Lyme
    disease. Jour. of Spirochetal
  • Tick-Borne Diseases
    1996 3101-04
  • Lyme and more commonly ehrlichiosis, tick
    borne relapsing fever,
  • Rocky Mountain Spotted Fever
    are commonly associated with
  • diarrhea and intestinal
    dysbiosis.
  • Reisinger EC. et al. Nat.
    Clin. Pract. Gastrenterol. Hepatol. 2005 May
    2(5)216-22.
  • Zaidi SA. et al. Clin.
    Infect. Dis. 2002 May 134(9)1206-12


11
  • c. Causes of Intestinal Dysbiosis (cont)
  • IV. Maldigestion
  • Pancreatic exocrine deficiency
  • Fecal elastase marker for pancreatic
    enzyme production
  • Gallbladder dysfunction with decreased
    bile production -gt fat
  • maldigestion
  • Consider fecal fat
    testing
  • Increased intestinal permeability/inflamma
    tion
  • Microscopically
    characterized by blunting/loss of micro-villi and
  • compromised tight
    junctions between cells
  • Corresponding loss of
    disaccharidases resulting in carbohydrate
  • maldigestion,
    increased disaccharide load to colon, and
    resulting
  • dysbiosis.


12
  • c. Causes of Intestinal Dysbiosis (cont)
  • V. Diet - Composition of diet affects type
    and metabolic activity of
  • gut flora
  • Gibson GR. Dietary
    modulation of the human gut microflora using
    prebiotics. Br J Nutr
  • 199880S209-S212.
  • High Protein Diet Typical American diet
    contains 100g of protein per

  • day. Up to 12g can escape digestion become

  • available for fermentation by colonic bacteria.

  • The resulting harmful byproducts include ammonia,

  • sulfides, indoles, phenols amines-gt migraines,

  • carcinogens, damage lining, contribute to portal

  • encephalopathy.

  • Significant issue in Lyme patients with

  • compromised GI function


13
  • c. Causes of Intestinal Dysbiosis (cont)
  • V. Diet (cont)
  • High Carbohydrate Diet
  • High refined carbohydrate
    diet
  • -gt slows bowel
    transit time
  • -gt increases
    bacterial fermentation
  • -gt increases exposure
    to potentially toxic bowel contents (96)
  • -gt promotion of
    fungal overgrowth (esp. in presence of multiple
  • antibiotics)
  • Lewis SJ, Heaton
    KW. Am J Gastroenterol 1999942010-2016.
  • High carbohydrate diet (esp
    gluten and casein)
  • -gt increases
    disaccharide load to colon (due to intestinal
  • inflammation and
    disaccharidase deficiency)
  • -gt abnormal bacterial
    overgrowth and fermentation


14
  • Intestinal Dysbiosis (cont)
  • d. Treatment Options for Intestinal Dysbiosis
  • Antibiotics All things being equal choose
    antibiotics with less effect on
  • gut flora.
  • Support
    intestinal flora-probiotics (research carefully)

  • prebiotics (FOS, etc.)

  • fermented foods
  • Stress Help patients manage stress
    effectively
  • Support endocrine
    systems esp. adrenals and thyroid as covered
  • earlier
  • Treat insommnia
    aggressively (melatonin, 5HTP, Ramelteon,
  • Trazodone, etc.)
  • Treat
    depression/anxiety if needed


15
  • Intestinal Dysbiosis (cont)
  • d. Treatment Options for Intestinal Dysbiosis
  • Lyme Expect improvement in gut issues as load
    of Lyme and
  • coinfections reduced
  • Maldigestion Digestive enzmes-Use broad
    spectrum digestive aids
  • that
    include protease, lipase, amylase as well as

  • disaccharidases (lactase, maltase, and sucrase)

  • Gallbladder support-Taurine, ox bile, and bile
    salts can
  • aid in
    bile production and fat digestion
  • Intestinal
    inflammation/permeability-Glutamine,
  • slippery
    elm, and DGL aid in reducing gut

  • inflammation. Eliminate allergenic/intolerant
    foods
  • consider
    desensitization


16
  • Intestinal Dysbiosis (cont)
  • d. Treatment Options for Intestinal Dysbiosis
    (cont)
  • Diet Consider decreasing protein intake if
    excessive
  • Eliminate gluten,
    casein, and refined carbohydrates
  • Consider Specific
    Carbohydrate Diet (SCD) in those severely
  • carbohydrate
    intolerant
  • Gottschall, E
    (1994). Breaking the Vicious Cycle Intestinal
    Health Through Diet,
  • Revised
    edition, Kirkton Press..


17
  • Intestinal Dysbiosis (cont)
  • 3. Liver/Gallbladder Function
  • Dysfunction/Inflammation of liver and
    gallbladder
  • I. Lyme and coinfections
  • II. Antibiotics Elevate liver
    function tests
  • Those with
    biliary excretion can result in GB dysfunction
  • Testing
  • I. Comprehensive liver
    detoxification screen to evaluate phase I II
  • function
  • II. Genomic testing
  • Hepatic nutritional support


18
Hepatic Nutritional Support
Bio-Chem Site Cause Intervention
Phase I Upregulated Dysgiosis/gut derived toxins increased intes. Permeab. environ. Toxic exposure Address source Antioxidants Support phase II
Phase I Downregulated P450 inhibitors (HM, drugs, EFA deficiency, hypothyroid, increased sat. fat intake Correct source, liver support with PC, taurine, silymarin, EFAs, antioxidants
Phase II- Glucoronidation Mitochondrial damage, Fe deficiency, drugs, genetic uniqueness (Gilberts) Address underlying condt. Cruciferous veg. to induce conjugation enzymes, B6, Mg, L-glutamine, asp acid, niacin
Glycination Hepatic disease, nutritional deficiency, genetics Glycine, alkaline foods to enhance glycination, B5, Mg, cysteine
Glutathione conjugation Glutathione depletion due to increased toxic load, nutritional deficiency, genetics Reduced glutathione, N-acetyl cysteine, glycine, L-methionine, L-glutamine
Sulfation Sulfate depletion, toxic load, hepatic disease, genetics High sulfur foods, red. Glutathione, L-methionine, L-cysteine, Zn, Cu, Se, Mg, B6, B12, Mg, FA
Patrick Hanaway, MD Genova Diagnostic
Laboratories
19
  • B. Heavy Metals
  • 1. Heavy Metals - Hg, Cd, Pb, Ar are the
    best studied
  • a. Hg
  • I. Sources
  • Thimersol (50 Hg by volume) was the preservative
    in most
  • vaccines until approx 2001.
  • Cumulative dose in vaccines from birth to age 5
    years exceeded the EPA guidelines for safety.
  • Large population of older children and young
    adults have had significant exposure.
  • Study on NYC adult population revealed 24.8 had
    bloodlevels at or exceeding 5ug/l, the NY State
    reportable level.
  • McKelvey W. Environ Health Perspect. 2007
    Oct115(10)1435-41
  • Seafood, dental amalgams, and industrial output
    account for the major sources of exposure today.
    (26,27)


20
  • 1. Heavy Metals (cont)
  • a. Hg
  • II. Toxicity
  • Low level chronic exposure can lead to nervous
    system
  • damage resulting
    in depression, anxiety cognitive loss
  • Weiss B, Clarkson
    TW, Simon W. Environ Health Perspect 2002 110
    (Suppl 5) 8514
  • Autoimmunity

  • Hultman, P. et al. The FASEB Journal Nov 1994
    1183-90
  • Paresthesias, insommnia, cognitive
    difficulties,
  • neuromuscular
    changes, headaches and anxiety.

  • http//www.epa.gov/iris/subst/0692.htm


21

1. Heavy Metals (cont)
b. Cd I. Sources Color pigment
(dyes paints)
Cigarette smoke
Ni-Cd batteries
Phosphate fertilizers
Jarup L et al. Health effects of
cadmium exposurea review of the literature and
a risk
estimate. Scand J Work Environ
Health 1998 24 (Suppl 1) 151
WHO. Cadmium.
Environmental Health Criteria, vol. 134. Geneva
World Health
Organization, 1992
II. Toxicity Kidney damage
Osteoporosis
Cancer


Jarup, L. Br. Med. Bull. 68167-182 (2003)

22

1. Heavy Metals (cont)
c. Pb I. Sources Gasoline
(Worldwide major source but not in US)
Lead in drinking water
primarily due to the presence of lead
in certain
pipes, solder, and fixtures.
In kids toys
and lead based paints in old homes
II. Toxicity Decreased IQ
Memory deterioration
Cancer
Anemia
Peripheral nerve symptoms


WHO. Lead.
Environmental Health Criteria, vol. 165. Geneva
World Health
Organization, 1995
Steenland K,
Boffetta P. Am J Ind Med 2000 38 2959

23

1. Heavy Metals (cont)
d. Ar I. Sources Wood
preservative
Fish
Pesticides/food
Industrial exposure II.
Toxicity Cancer-lung, bladder, kidney
Peripheral neuropathy
Anemia
GI Effects
WHO. Arsenic and Arsenic Compounds.
Environmental Health Criteria, vol. 224. Geneva
World Health
Organization, 2001
Chilvers DC, Peterson PJ. Global cycling of
arsenic. In Hutchinson TC, Meema KM (eds) Lead,
Mercury, Cadmium and
Arsenic in the Environment. Chichester John
Wiley Sons, 1987 279303
www.epa.gov/ttn/atw/hlthef/arsenic.html

24
  • B. Heavy Metals (cont)
  • 2. Testing for Heavy Metals
  • Blood levels useful for acute exposure, but
    unreliable tool for chronic
  • low level exposures.
  • Mercury has affinity for fatty
    tissue. Rarely seen in blood.
  • The half-life of Pb in blood is
    about one month whereas the
  • half-life in bone is 20-30
    years. (35)
  • WHO. Lead. Environmental
    Health Criteria, vol. 165. Geneva World Health
    Organization, 1995
  • Difficult to accurately assess total body
    burden. Urinary porphyrins
  • have some utility currently probably
    the best clinical test available.
  • Hair Mineral Analysis may be helpful, but show
    false negative in
  • individuals with compromised
    detoxification pathways
  • Provocative challenge-involves administering a
    test dose of a chelator
  • (DMPS, DMSA, or EDTA) and
    measuring pre- and post- fecal /or


25
  • B. Heavy Metals (cont)
  • 3. Treatment - best done once
    Lyme/coinfection load reduced
  • Pharmacological Chelators DMPS

  • DMSA

  • EDTA

  • Penicillamine
  • Non-pharmacological chelators Sauna

  • Alginate/Chlorella

  • Zeolite


26
  • B. Heavy Metals (cont)
  • 3. Treatment (cont)
  • Nutritional support during chelation essential
  • I. Gut binding
    agents-Bentonite

  • Charcoal

  • Cholestyramine
  • II. Mineral replacement-dependi
    ng on the chelator used, replace
  • minerals aggressively with
    special attention to Ca Mg
  • with EDTA and Cu Zn with
    DMPS/DMSA
  • III. Antioxidant
    support-necessary to quench free radicals
    generated
  • during heavy metal
    removal. Supplement with A, C, E, Zn,
  • selenium, and reduced
    glutathione.
  • IV. Hepatic support-as outlined
    earlier


27
  • B. Heavy Metals
  • 4. Assess methylation function in
    non-responders
  • Definition
  • Methylation involves transfer of methyl
    group
  • Methylation plays a role in
  • Neurotransmitter
    synthesis and breakdown
  • Renal disease
  • Cardiovascular
    disease
  • Cancer
  • Heavy metal
    detoxification
  • Anti-viral immune
    modulation


28
Methylation Cycle
5,10 MTHF
Methionine
SAM
MSR
Methionine Synthase
MTHR
SAH
5 MTHF
Homocysteine
Homocysteine
CBS
Cystathione
Cysteine
Glutathione
Taurine
29
  • B. Heavy Metals
  • 4. Assess methylation in non-responders (cont)
  • Single Nucleotide Polymorphisms (SNPs)
  • Can impair methylation
  • Commonly found in the general
    population
  • SNPs involving MTHFR C677T have a
    47 incidence among
  • Caucasians
  • Ulrich CM. et al.
    Cancer Epidemiol Biomarkers Prev. 1999
    Aug8(8)659-68
  • Heavy metals at low levels can suppress key
    enzymes involved in methylation


30
  • B. Heavy Metals
  • 4. Assess methylation in non-responders (cont)
  • Testing to assess methylation genomic testing

  • urine/serum amino acid analysis
  • Nutritional Support to open/bypass areas of
    impairment

  • Methyl B12 / Cyano B12

  • TMG (or DMG)

  • Folic/Folinic acid

  • P5P/B6

  • Reduced Glutathione


31

C. Conclusion 1. Aggressive GI support
before, during and after antibiotic treatment
can greatly assist in reducing
complications and improve outcome 2. Heavy
metals are ubiquitous. They can compromise
immune functioning, promote
overgrowth of candida as well as dysbiotic flora.
Judicial heavy metal detoxification,
once the lyme/coinfection load has been
reduced, with appropriate methylation support as
needed, may improve outcome and
potentially reduce the likelihood of relapse
Write a Comment
User Comments (0)
About PowerShow.com