aamp spring 2021 post-conference webinar

6/29/2021

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AAMP Spring 2021

Post-conference Webinar

Dr. Paul S. Anderson

June 29, 2021

(c) PS Anderson - www.ConsultDrA.com and AAMP 2021 1

PLEASE NOTE:

Much will NOT be in the slides but discussed

verbally on the recording – so - If you are just

reading these slides, you’ll miss a lot of the

content.


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How these work:

Immunoglobulin Deficiencies

Lots of questions about these.

• They revolved around:

–How long do you treat low Ig (A, G…)

–What will improve congenital CVIDS or IgG

subclass deficiency?


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Ig Deficiency:

• Main Consideration:

– Genetic

– Functional

• If functional the supportive agents like Vit A, Colostrum, Mushrooms, Thymus

extracts, lowering overall burden of infections, GI repair, etc. In my

experience will improve Ig levels in 6-18 months.

• If Genomic the levels generally do not improve – but their resistance and

health will be helped by those agents / interventions.


Mast Cell

• Favorite agents and how long to wait before returning to detox etc.?

– Stabilize with bioflavonoids (Rx like Cromolyn or OTC like Hesperidin,

Quercetin etc.), Vit C, and support HIS metabolism.

• Free Q&A I wrote and has some HIS biology slides:

https://www.consultdranderson.com/histamine-receptor-physiology-and-

atypical-reactions-cont/

• A 1.5-hour CE (with ce cost) goes more deeply into this:

https://www.consultdranderson.com/courses/07-histamine-triggers-mcas-and-

therapies/

• How long?


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https://www.consultdranderson.com/histamine-receptor-physiology-and-atypical-reactions-cont/

https://www.consultdranderson.com/courses/07-histamine-triggers-mcas-and-therapies/

6/29/2021

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IgG levels and Acute Infection??


So, how do we look at IgG as a marker of acute infection status?


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IgG and Acute Infection ?

• What were we taught?

• IgE is for Type-1 reactions and helminths etc

• IgA is secretory and protects mucous membranes

• IgM is ACUTE (and very short duration)

• IgG ONLY means a prior infection

• Is there any data which contradicts this dogma?


Gray JJ, Cohen BJ, Desselberger U. Detection of human parvovirus B19-specific IgM and IgG antibodies using a recombinant viral VP1 antigen expressed in insect cells and estimation of time of

infection by testing for antibody avidity. J Virol Methods. 1993 Sep;44(1):11-23. PMID: 8227275

Abstract• Sera from patients with symptoms of recent human parvovirus B19 (B19)

infection were tested for B19-specific IgM in an immunofluorescence assay (IFA) using insect cells expressing B19 recombinant VP1 coat protein as an antigen. A highly significant correlation (P < 0.001) was found between titres obtained in the IgM IFA and the units obtained in an IgM antibody-capture RIA using plasma derived native B19 antigen. An IgG IFA using the recombinant antigen was performed on 57 sera and the antibody avidity determined. There was a highly significant correlation (P < 0.001) between the relative amounts of low avidity B19-specific IgG antibodies and time after onset of illness.

• This finding allows the detection of IgG to be used for diagnosing acute infection.


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Baccard-Longere M et al. Multicenter evaluation of a rapid and convenient method for determination of cytomegalovirus immunoglobulin G avidity. Clin Diagn Lab

Immunol 8:429-431,2001

Summary

In summary, assessment of CMV-specific IgG avidity is a powerful tool for estimating the time of CMV infection. Such information is particularly important in the clinical management of pregnant women found to be positive for CMV antibodies at their first prenatal visit. Determining the time of primary infection can help guide decisions regarding antiviral therapy by identifying those women who should or should not be treated during pregnancy. CMV IgG avidity measurement also has broad applicability to the management of other patient groups with an increased risk of debilitating CMV disease, such as solid organ transplant recipients.


Baccard-Longere M et al. Multicenter evaluation of a rapid and convenient method for determination of cytomegalovirus immunoglobulin G avidity. Clin Diagn Lab

Immunol 8:429-431,2001

• Bodeus M et al. Avidity of IgG antibodies distinguishes primary from non-primary cytomegalovirus infection in pregnant women. Clin Diagn Virol 9:9-16,1998

• Bodeus M, Goubau P. Predictive value of maternal-IgG avidity for congenital human cytomegalovirus infection. J Clin Virol 12:3-8,1999

• Bodeus M et al. Ability of three IgG-avidity assays to exclude recent cytomegalovirus infection. Eur J Clin Microbiol Infect Dis 20:248-252,2001

• Eggers M et al. Combination of microneutralization and avidity assays: improved diagnosis of recent primary human cytomegalovirus infection in single serum sample of second trimester pregnancy. J Med Virol 60:324-330,2000

• Fowler SL. A light in the darkness: predicting outcomes for congenital cytomegalovirus infections. J Pediatr 137:4-6,2000

• Gangeot-Keros L et al. Value of cytomegalovirus (CMV) IgG avidity index for the diagnosis of primary CMV infection in pregnant women. J Infect Dis 175:944-946,1997

• Lazzarotto T et al. Avidity of immunoglobulin G directed against human cytomegalovirus during primary and secondary infections in immunocompetent and immunocompromised subjects. Clin Diagn Lab Immunol 4:469-473,1997

• Lazzarotto T et al. Anticytomegalovirus (anti-CMV) immunoglobulin G avidity in identification of pregnant women at risk of transmitting congenital CMV infection. Clin Diagn Lab Immunol 6:127-129,1999

• Lazzarotto T et al. Maternal IgG avidity and IgM detected by blot as diagnostic tools to identify pregnant women at risk of transmitting cytomegalovirus. Viral Immunol 13:137-141,2000

• Lazzarotto T et al. Prenatal indicators of congenital cytomegalovirus infection. J Pediatr 137:90-95,2000

• Lazzarotto T et al. New advances in the diagnosis of congenital cytomegalovirus infection. J Clin Virol 41: 192-197, 2008.


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Blum A, Peleg A, Weinberg M. Anti-cytomegalovirus (CMV) IgG antibody titer in patients with risk factors to atherosclerosis. Clin Exp Med. 2003

Nov;3(3):157-60. PMID:14648230

Abstract

• Studies have demonstrated cytomegalovirus (CMV) DNA particles in restenotic lesions in atherosclerotic coronary arteries. We have shown that high (>1:800) anti-CMV IgG antibody titers in the serum are associated with active coronary disease and with post coronary angioplasty restenosis. In this study we assessed the anti-CMV antibody titer in patients with risk factors for atherosclerosis (but without documented clinical manifestations). … One Hundred and twenty six patients had high anti-CMV antibody titers (>/=1:800) compared with none in the control group. Although 80 patients (90%) in the control group were seropositive, none had anti-CMV IgG antibody titers higher than 1:400. The statistical difference between the patients and the control group was highly significant ( p<0.0001). An immunological response against CMV (expressed as an anti-CMV IgG antibody titer) could be a marker of a long-standing immunological reaction causing an inflammatory response that eventually would cause advanced clinical atherosclerosis. We suggest that anti-CMV antibody titer should be used as an early predictor of atherosclerosis. Our findings support the infectious theory and an association between CMV infection and atherosclerosis at an early stage, maybe even years before clinical events occur.


IgG as a Marker to Follow:

• As the above papers outline, IgG CAN be followed to watch treatment efficacy.

• Generally tested every 4-6 months

• One generally sees a decrease in total IgG specific to the strain which matches clinical therapy success, immune system operation and decrease in virus.


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IgG as a marker of acute infection status

and

Is it 100%... No but it can be of great help as a

serial marker in chronic cases.


Recovered Patients:

• What are the strategies you use with recovered patients to prevent

reoccurrence?

– Educate them

– Sleep

– Diet

– Movement

– Nutrient support

– Immune support


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Gadolinium

“What, other than EDTA do you do for Gd toxicity?”

“I wanted to know about Gadolinium because I am currently treating

a chiropractor that I sent in for an MRI with contrast and she has

spiraled out of control with neurological symptoms. I am currently

treating off and on with EDTA and DPMS but she feels to depleted

so I've slowed down, just would love more help with it.”

• Slides 150 – 171 in my Sunday lecture


Gadolinium


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NAC

A compound that can effectively compete with Gd3? may be

an approach to reduce any Gd3? retained by the body. N-

acetylcysteine pretreatment inhibits gadolinium-induced cell

death and endoplasmic reticulum stress in vitro.

It also protects against GBCA-induced nephrotoxicity in rats

with chronic renal failure (Pereira et al. 2012).

Quote from Biometals 2016



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55 YO High Zn and Gd toxicity

A patient with chronic zinc poisoning from denture cream retained

gadolinium after a magnetic resonance imaging procedure, likely

due to transmetallation. During chelation therapy, high levels of

gadolinium in excreted urine (up to 89 m g/d, 29 days after

gadolinium administration) were present, indicating that gadolinium

had been retained.

Almost 2½ years after gadolinium exposure, a 24-hour urine

collection indicated that the gadolinium level remained in the

elevated range (0.6 m g/d). This single case report suggests

that patients with elevated zinc exposure may be at increased

risk of gadolinium retention.(c) PS Anderson - www.ConsultDrA.com and AAMP 2021 21

Gd and Zn

A diagnosis of zinc toxicity of unknown cause was made by his

physician.

The patient was treated during a 6-month period with oral

chelation therapy containing 2,3,-dimercaptosuccinic acid and

ethylenediaminetetraacetic acid, which was available as a dietary

supplement (CheleX; Xymogen, Orlando, Fla) at a dosage of three

to five capsules per day, and with 22 intravenous chelation

infusions with edetate disodium or edetate calcium disodium

(1500–3000 mg per infusion).


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DTPA

https://emergency.cdc.gov/radiation/dtpa.asp



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DTPA vs EDTA

• DTPA is the current ‘preferred’ Gd chelator not because it is better but

because it is what has been studied beyond DFO.

• BUT

– Availability:

– Personal case reports of tolerability:

• EDTA has an extremely high binding to Gd as well.

And recall – Neither will address the tissue

protection and repair issues.



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Gd Summary:

• Use a combined chelation program with EDTA – a

Dithiol or NAC and GSH

• Use a GI binder to catch bile released metals

• Use curcumin to support CNS elimination

• Deplete Zinc

–Discuss how and testing….

• And yes, all of the other general tissue supports


Chelation and Cancer:

• Would you chelate during cancer treatment?

Discuss:

Safety

Timing

Effect on CSC’s

• A free review on post “metal” chemo and chelation:

https://www.consultdranderson.com/monographs/6c-chelation-detoxification-

magnesium-other-mineral-levels-and-platinum-based-chemotherapies/


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Chelation questions:

• Suppository vs Oral chelation:

• Chelation post chole:

• When do you give Iron when low in a chronically ill patient (when

it aggravates ReDox) and how to balance that out?

• Chelation duration? “I have done a lot and levels don’t drop?”

– https://www.consultdranderson.com/heavy-metals-bone-

turnover-osteopenia-and-osteoporosis-assessment-and-

treatment/


Chelation questions:

• Prussian blue dose (yes, use 600 BID)

• IV or Oral? Is one better?

• Is the strontium that needs chelating the same

as that used for bone building?

• How much fluid intake during chelation and

what do you use for constipation?


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https://www.consultdranderson.com/heavy-metals-bone-turnover-osteopenia-and-osteoporosis-assessment-and-treatment/

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Detox Summary

Main Points:

• Generally, our typical chelation strategies will work

for most of these metals.

• Thallium is a “special case” and definitely needs GI

binding as well as potential monothiol avoidance.

• As no human is toxic with “just one metal” it is best

to assume poly-metallic toxicity and use a well-

rounded detoxification – depuration strategy.


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Toxin Elimination “DETOXIFICATION”


TOXINDISTRIBUTION - ELIMINATION

SKINLUNG

LIVER → PHASE-2 → KIDNEY

GB → BILE / GI → STOOL

URINE

STOOL

CHELATOR

BINDER

Toxin Elimination - PROTECTION


TOXINDISTRIBUTION - ELIMINATION

SKINLUNG

LIVER → PHASE-2 → KIDNEY

GB → BILE / GI → STOOL

URINE

STOOL

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So:

• Regardless of metals present:

–Use a multi chelator strategy (normally EDTA, GSH, and a DiThiol)

–Use chelation support in every case

• Glutathione and cofactor vitamins / minerals

• Mineral repletion

• Hydration and bowel regularity

• Sweating and other depuration aids


So:

• Regardless of metals present:

–Use GI binders in every case

• HS Psyllium or Charcoal in the case of Tl presence

–Use tissue protection strategies in every case

• The MOST helpful are Ascorbate, Curcumin,

Phospholipids, EGCG, etc.

• If Tl is less an issue (or you decide they are

acceptable) ALA or NAC are very helpful as well


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More questions:

Sinus protocol question (this was Nafysa but if you can’t ask her, can Paul answer? )

• What are the specific doses (for nebulised) 1) amphotericin, 2) ibuprofen, 3)

itraconazole

• I think Tom or someone else mentioned intranasal LDN- is this correct, if so what

dose, and why would intranasal be better than buccal or oral? (Will discuss)

• Parvo B19- Paul talked about its importance in aetiology and it made me think that

perhaps I should be testing for it more. But I can’t recall if there were specific parvo

B19 treatment options that would stand out and be more specific than the regular

arsenal of antiviral approaches? Please name some if so? (See below)

• Simple one on glutathione nebuliser what dose do people like to use? 250-500mg

per nebuliser? (Yes, generally 100-200 to start with a max of 500 mg)


Parvo B-19 and Others?

• Drugs aren’t much help

• Mushrooms and immune support help a lot

• Aromatics and biofilm work can help

• Lowering overall viral burden can help a lot

• High dose Vit-A & D, and other nat meds


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No Tx was given for parasites by Dr. Gedroic

and many attendees asked about parasite Tx - so

if this could be addressed in the post-conference

• Kill

• Bind

• Mitigate side effects

• Reassess (Empiric or Labs)


Kill:

Rx:

• Albendazole 200 mg QD cc and Ivermectim 9-10 mg QD cc (ideally at two

different meals)

Also:

*If Rx as above add an antifungal to cover overgrowth (Fluconazole 150-200

QD 2-3 days a week) Nystatin 1 million units 2-3 days a week

• Duration:

– Rx daily 7 days a week for 30-60 days

– Then 3 days a week for 30-60 days

– Then cycle PRN 1-2 x a year after that


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Kill:

Nat.:

• Integrative Therapies ‘Para-Gard’ and Biotics ‘ADP’ 1-3 pills each BID cc

• Also Candibactin AR-BR same sig

• And there are many others

For both, always HS dosing of probiotics

• Duration:

– Rx daily 7 days a week for 30-60 days

– Then 3 days a week for 30-60 days

– Then cycle PRN 1-2 x a year after that


Bind:

• Hydrate a lot 2-3 L minimum daily

• Use a fiber supplement like Psyllium or a

supplement away from food daily (if no meds HS

then HS, otherwise between meals sometime.

• If they get constipated that has to be stopped so

check hydration, add Magnesium and or Ascorbate

PO to bowel tolerance


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Mitigate Side Effects:

• Hydration

• Regular BM’s

• Glutathione and support nutrients

• Boswellia

• Nutra medix “Burbur Detox” drops 5 – 15 gtt in

water PRN


(re) Assessment:

• Response to therapy

• General timeline of Rx

• Cycling Rx

• Labs


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Question:

What to do when people flare from a NAC

or ALA pre-stool test prep


48(c) PS Anderson - www.ConsultDrA.com and AAMP 2021

Advanced Integrative OncologyAAMP “HYBRID” Fall Conference

Scottsdale, Arizona

September 24th - 26th, 2021

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AAMP “HYBRID” Fall Conference

FOCUS AREAS:

• Focus-1: Integrative Oncology Updates

o Nutrigenomics and Cancer Therapies

• Focus-2: Treatment Modules on Specific Cancers

o Prostate

o Breast

o Colorectal

o Lung

• Focus-3: Food, Diet and Cancer

• Focus-4: Interventions through the Four Phases of Cancer Care

o Primary Prevention

o Diagnosis through Active Care

o Recovery from Active Care

o Secondary Prevention


AAMP “HYBRID” Fall Conference

DIAGNOSTICS AND THERAPEUTICS:

• Cancer Lab Assessment

• Nutrigenomics

• Endocrine, GI, Immune and other contributory area assessment

• Therapies using:

• Rx. agents

• Natural agents

• Rx and Natural (Herbal, Nutrient, Homeopathic, etc.) supportive therapies

• IV and Injection Therapies

• BHRT and other Compounded Medications

• Diet and Lifestyle Modifications

• Emerging and traditional therapies:

• Heat / Hyperthermia

• Photodynamic Therapies

• Immunotherapies

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AAMP FALL

CONFERENCE

September 24th-26th, 2021

CMEs for both Live In-Person or Live Remote

Streamingor Post

Conference

RESERVE PLACE TODAY Pay Balance later

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aamp spring 2021 post-conference webinar

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