Chronic Inflammatory Response Syndrome · 2020-03-10 · Key Facts 95% •of CIRS occurs in...

Chronic Inflammatory Response Syndrome

Dr Sandeep Gupta

[photo of blue-green algae or infected

waterway]

Mold Illness Made Simple © Dr Sandeep Gupta2

[photo of intensive care unit]

Stages of Sepsis

Initial infection

Bloodstream spread

Inflammatory Cascade

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Chronic Inflammatory Response Syndrome

Biotoxin exposure Chronic inflammation

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[photo of water-damaged building and a

tick]

Mold Illness Made Simple © Dr Sandeep Gupta8

Predisposition to inflammatory illnesses

Specific gene types

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Key Facts

95%

• of CIRS occurs in genetically predisposed people

HLA

• Genetic glitches lead to chaotic inflammatory response on exposure to biotoxins

CSM

• An external binding agent such as cholestyramine can allow the body to rid itself of biotoxins.

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Inflammation

Redness

Pain Swelling

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Cytokines

Redness

PainSwelling

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CIRS Inflammation

Silent

Deep-seated

Chaotic and inefficient

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Poor oxygen delivery to

tissues

Immune dysfunction

Hormonal changes

Inflammation in CIRS

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Biotoxin Illness in AustraliaEpidemic due to:

• Structure of houses

• Use of particle board

• Sub ground level basements

• Lack of curing of slabs

• Frequency of flooding due to extreme weather conditions etc

• Outdoor lifestyle/abundance of rainforest

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Surviving Mould Down Under

Essays documenting exact companies and brands to use to

implement Dr Shoemaker’s protocol in Australia

Discusses which items covered by Medicare

PBS Criteria for various medications discussed

Australian resources for treatment of tick-borne infections

discussed

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Commonly Known Biotoxins

Mycotoxins (of fungal original)

Ochratoxin A

Aflatoxin

Trichothecene

Borrelia

Babesia

Ciguatera toxin

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Common known biotoxins

Mycotoxins (of fungal origina)

Ochratoxin A

Aflatoxin

Trichothecene

Bacterial toxins

Botulinum toxin

Tetanospasmin

Exfoliatin or Enterotoxin Type B

Borrelia and co-infections ?

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Summary

A very specific pathophysiology of CIRS including defective antigen presentation in those with impaired HLA genetics followed by hyperactivity of the innate immune system has been described by Shoemaker.

As the science and experience evolves theories are springing up to explain observations not easily explainable by the main theory. It may be that no one theory explains all pieces.

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