Autoimmune

A screen for antibodies that bind components of the cell nucleus. It's the single most common first-line test when autoimmune disease is suspected, run by immunofluorescence (titer = how dilute the serum can be and still show binding; pattern = what part of the nucleus lights up).

Food first: There's no dietary intervention proven to reverse a positive ANA. Vitamin D sufficiency and an anti-inflammatory dietary pattern are reasonable supportive measures, not a treatment for a positive screen.

When to see someone: A positive ANA is read alongside symptoms and other labs, never alone -- a low-titer positive with no symptoms is common in healthy people and usually not actionable. The titer and the pattern both carry information the raw positive/negative does not.

This marker sits in Maintain -- the cleanup and defence system, and whether it is switched on.

An old, nonspecific inflammation marker -- how fast red blood cells settle in a tube over an hour. Elevated fibrinogen and other acute-phase proteins during inflammation make cells clump and fall faster.

Food first: Correct underlying anemia (iron, B12, folate as appropriate), weight management, Mediterranean-pattern eating, smoking cessation -- the same broad levers that move CRP.

When to see someone: ESR rises with acute infection, recent surgery/dental work, pregnancy, and simple aging -- a single elevated reading isn't diagnostic of autoimmune disease without other supporting findings.

This marker sits in Maintain -- the cleanup and defence system, and whether it is switched on.

A liver-produced acute-phase inflammation marker; more specific and faster-responding than ESR, widely used both in cardiology risk assessment and as a rough gauge of systemic inflammatory burden in autoimmune disease.

Food first: Mediterranean-pattern eating, weight loss if overweight, smoking cessation.

When to see someone: In lupus specifically CRP is unreliable as a flare marker -- it can sit normal during active disease unless infection or serositis is also present, so a normal CRP does not rule out activity. Curcumin has a real interaction with blood thinners.

Two proteins of the complement immune cascade; in lupus specifically, immune complexes consume (use up) complement during active disease, so falling C3/C4 alongside rising anti-dsDNA is a classic (though imperfect) signal of a lupus flare, particularly lupus nephritis.

Food first: There is no dietary or supplement intervention proven to normalize complement levels independent of treating the underlying disease activity; curcumin and vitamin D are reasonable adjuncts to discuss with a rheumatologist, not substitutes for standard lupus management.

When to see someone: Low complement always needs clinical correlation, especially a check for kidney involvement (urinalysis, proteinuria) -- this is not a marker to try to move with supplements without the treating rheumatologist involved.

An antibody (usually IgM) directed against the Fc portion of IgG; associated with rheumatoid arthritis but also positive in Sjogren's syndrome, some infections, and a meaningful share of healthy older adults, so it's neither sensitive nor specific enough to diagnose RA alone.

Food first: Omega-3 intake (fatty fish or algae-based supplement) and vitamin D sufficiency have the best prevention-stage evidence, particularly in people genetically predisposed to RA; neither is proven to reverse an established positive RF.

When to see someone: RF alone doesn't diagnose RA -- a positive RF in someone without joint symptoms is common and not automatically actionable; interpret alongside anti-CCP and clinical exam.

Antibodies against citrullinated proteins; more specific for rheumatoid arthritis than RF, and can appear years before clinical joint symptoms develop, making it useful both for diagnosis and for identifying at-risk individuals.

Food first: Same as RF -- omega-3 and vitamin D sufficiency are the most evidence-backed levers, strongest in prevention-stage/at-risk populations rather than in reversing established disease.

When to see someone: A positive anti-CCP in an asymptomatic person with a family history of RA is a meaningful risk signal worth discussing with a rheumatologist for monitoring -- it is not something to try to "treat away" with supplements alone.

The three major immunoglobulin classes measured together as a quantitative immune-function panel -- IgG is the dominant long-term/memory antibody class, IgA is the primary mucosal-surface antibody (gut, respiratory tract), IgM is the first-responder antibody made early in an immune response.

Food first: Correcting a confirmed zinc or vitamin A deficiency is the evidence-based lever; there is no good evidence that supplementing zinc or vitamin A above sufficiency raises immunoglobulin levels further in a replete, healthy person.

When to see someone: Selective IgA deficiency needs to be flagged before ordering celiac serology (see below), since it causes false-negative tTG-IgA results, and rarely carries a risk of severe transfusion/blood-product reactions -- this should be documented in a patient's chart if identified. Never chase a "low-normal" immunoglobulin number with high-dose supplements without an immunology workup if genuinely deficient.

A breakdown of total IgG into its four subclasses; ordered when someone has recurrent infections despite a normal total IgG, since a subclass can be selectively low even when the sum looks normal.

Food first: General immune-supportive nutrition (adequate protein, zinc, vitamin D) is reasonable background care, but a clinically significant IgG subclass deficiency is managed by immunology, sometimes with immunoglobulin replacement therapy, not diet.

When to see someone: Don't over-interpret an isolated low IgG subclass without a clinical history of recurrent infection -- many people with a "low" subclass on paper are asymptomatic and need no treatment.

The antibody class responsible for allergic/atopic responses (and parasitic defense); total IgE gives a general sense of allergic burden, allergen-specific IgE identifies what someone is actually reactive to.

Food first: There is no nutrient supplement with solid evidence for lowering IgE directly; standard allergy/asthma management (allergen avoidance, medical therapy) remains the evidence-based approach, with vitamin D sufficiency as reasonable general immune support rather than an IgE-lowering intervention.

When to see someone: Don't market vitamin D or any supplement as an "IgE reducer" -- the best trial evidence specifically on this endpoint is null or mixed.

This marker sits in Sense -- signals being produced, detected and acted on.

The antibodies that flag autoimmune thyroid disease (Hashimoto's thyroiditis, Graves' disease) -- see `Labs/Panels/Thyroid.md` for the full micronutrient breakdown, since this is where the strongest nutrient-antibody evidence in the entire autoimmune space lives.

Food first: See Thyroid.md -- selenium sufficiency (time-limited, not indefinite) is the most evidence-backed lever specifically for these antibodies.

When to see someone: Selenium's antibody-lowering effect fades with long-term use in some trials and should be periodically reassessed, not taken indefinitely at high doses; see Thyroid.md for the full safety discussion including selenosis risk.

Tissue transglutaminase IgA (tTG-IgA) is the first-line screening test for celiac disease, an autoimmune reaction to gluten that damages the small intestine; total IgA is run alongside it because tTG-IgA is falsely low/negative in people with selective IgA deficiency; deamidated gliadin peptide (DGP) antibodies (largely replacing the older, less specific "anti-gliadin" test) are used as an alternative, especially in IgA-deficient patients and young children, where tTG-IgA sensitivity is lower.

Food first: A confirmed celiac diagnosis is managed with strict gluten elimination, full stop -- this is one of the few places in functional/integrative nutrition where the dietary intervention itself is the guideline-level standard of care, not an adjunct.

When to see someone: Always run total IgA alongside tTG-IgA. In someone with IgA deficiency, a "negative" celiac screen is not a true negative.

Antibodies seen in autoimmune (pernicious) anemia, one of the most common causes of true vitamin B12 deficiency in adults -- intrinsic factor antibodies block the protein needed to absorb B12 in the gut; parietal cell antibodies attack the stomach cells that make both intrinsic factor and stomach acid.

Food first: Once diagnosed, B12 repletion via a route that bypasses the intrinsic-factor absorption step (IM injection, high-dose oral B12 which has a small intrinsic-factor-independent absorption pathway, or sublingual) is the standard, evidence-based approach.

When to see someone: Pernicious anemia is a lifelong condition requiring ongoing B12 monitoring/repletion, and it raises long-term risk of gastric carcinoid tumors and gastric cancer due to chronic atrophic gastritis -- this needs gastroenterology follow-up (periodic endoscopic surveillance in some cases), not just a B12 supplement.