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Food sensitivity or intolerance is a contentious topic orhealthcare proessionals and patients alike. It is regularlythe subject o intense media speculation and scrutiny.This scrutiny may be due in part to the clouded denitionand misinormation o what actually constitutes a oodsensitivity or intolerance. The typical immediate allergyresponse to shrimp or peanuts, or instance, is a wellcharacterized phenomenon; classied as a Type I allergy. Incertain individuals Type I allergies can be potentially atal.For the purpose o this article, we will classiy adversereactions to ood according the ollowing denitions.
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Food allergy:1.
A response mediated by ood-triggeredbasophil or mast cell histamine release. This reaction canbe caused by either IgG or IgE ood-specic antibodies.These reactions are immediate in nature and can besevere. This response is the Type I allergic reaction.
Food sensitivity:2.
A purely immune system-mediatedresponse involving various classes o ood-specicimmunoglobulin molecules that can orm oodimmune complexes. These complexes can stimulate thecomplement cascade and localized infammation. Thesereactions tend to be delayed – rom a ew hours up to7 days ater ood consumption – in some cases. Thisresponse is a Type III allergic reaction.
Food intolerance3.
: A non-immunological mechanism o adverse ood response. Examples would include lactoseintolerance and MSG sensitivity.
Which IgG Test – 1, 4 or All?
The misinormation and lack o mechanistic explanationsabout IgG-mediated ood sensitivity is refected in thenumber o dierent IgG tests available to healthcarepractitioners. Tests measuring total IgG subclasses (i.e.,1 through 4), IgG
1
, IgG
4
or both IgG
1
&
4
are available.During their tenure at university or medical school,most doctors are not educated on the properties o thedierent IgG subclass antibodies; which ones activate thecomplement cascade; or their behavior ater continuedantigen exposure. Such inormation is vital whendetermining the most appropriate IgG subclass antibody tomeasure or assessment o IgG-mediated ood sensitivity.
Subclasses Explained
There are our subclasses o IgG, 1 through 4, o whichIgG
1
and IgG
4
appear to be the most dominating subclassesto ood antigens.
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IgG
1
antibodies are the initialIgG class responders to a new ood antigen. IgG
2
andIgG
3
are generally not produced to ood antigens. Insteadthey react to cell surace oligosaccharides o viruses andprotozoa, respectively. Once IgG
1
binds to the antigen,the antibody-antigen complex is quickly destroyed bythe Kuper cells in the liver and other macrophages. TheIgG
1
-antigen complex can also stimulate the complementcascade and attendant infammation. This cascade o eventsis associated with the general malaise experienced rom theinfammatory response.
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IgG4 Immune Complex Formation
Upon continued exposure to the antigen, it is proposedthat IgG
1
antibody production will “class switch” to IgG
4
.
3
Interestingly, IgG
4
antigen complexes do not activate thecomplement cascade. IgG
4
acts as a blocking agent againstthe actions o IgE and can orm small complexes as antigenexposure increases.
4
These IgG
4
ood immune complexeshave a relatively long hal-lie and are subject to alterationsthat would aect the structure enough to present as a “new”antigen.
5
It is thought that IgG
1
is then produced to attackthis complex. Thus begins a whole new cycle: IgG
1
→
IgG
4
→
complex
→
modication
→
IgG
1
→
IgG
4
. Consequently,the complexes can get larger and larger. These largercomplexes can activate the complement cascade, initiatinginfammatory responses in the body. It is this infammatoryresponse to a ood that is thought to be the root causeo symptoms in this type o adverse ood reaction. Thesymptoms resulting rom ood sensitivities, thereore, cancome rom the activation o complement via IgG
1
/IgG
4
ood immune complex. Deposition o these complexescan also occur in tissue or organs, leading to damage. Thissequence o events is thought to be the most common wayindividuals develop adverse reactions to oods they eat on aregular basis.
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In support o the above theory, researchers rom Norwayrecently published ndings suggesting a particular role orIgG
4
in patients with delayed, non-IgE-mediated cow’s milkallergy (CMA).
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The authors measured beta-lactoglobulin(b-LG) specic IgE, IgG, IgA, IgG
1
and IgG
4
levels in bothclinically reactive and tolerized IgE-mediated and non-IgE-mediated CMA patients. Compared with tolerized patients,levels o b-LG-specic IgG
4
levels in clinically reactive CMA
Understanding IG4 Food Sensitivities
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