KEY ADVANTAGES

  • Monitor The First Lines of Defence to Food
  • Convenient Saliva Test

IgA is secreted from mucous membranes of the body (in larger quantities than any other antibody class) to assist with binding to foreign organisms and particles, to prevent their potential transport into the body, where they could cause tissue harm and inflammation.

However it should be noted that IgA does not activate the Complement cascade in the way that IgG antibodies do, and therefore IgA specific antigens will often not yield easily identifiable short term inflammatory symptoms (hence sometimes being referred to as ‘silent inflammation’), making laboratory analyses often essential to detecting their presence and potential progression to IgG sensitivities if not identified, and any immune disturbances or compromised mucous membranes (e.g. GIT) are addressed.

IgA levels are often involved in Autoimmune pathology and are heavily influenced by Cortisol/stress levels, as well as alcohol and certain pathogens, toxins and medications.

Those with Inflammatory Bowel conditions such as Crohn’s, Ulcerative Colitis and Coeliac Disease may all benefit from detecting any elevated exposures to IgA specific dietary antigens (as IgA to Gluten and its derivative proteins is a common occurrence in Coeliac Disease and is often fundamentally involved in the mechanisms of pathology). Ongoing research continues into the possible significance of other food specific IgA to certain other conditions.

IgA antibodies can be sampled and measured via blood, or via saliva samples (being secreted from alimentary membranes).

References

1. Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. May 2007;85(5):1185-1196.

2. Panula P, Karlstedt K, Sallmen T, et al. The histaminergic system in the brain: structural characteristics and changes in hibernation. Journal of chemical neuroanatomy. Feb 2000;18(1- 2):65-74.

3. Nuutinen S, Panula P. Histamine in neurotransmission and brain diseases. Advances in experimental medicine and biology. 2010;709:95-107.

4. Corazza GR, Falasca A, Strocchi A, Rossi CA, Gasbarrini G. Decreased plasma postheparin diamine oxidase levels in celiac disease. Digestive diseases and sciences. Aug 1988;33(8):956-961.

5. Schmidt WU, Sattler J, Hesterberg R, et al. Human intestinal diamine oxidase (DAO) activity in Crohn’s disease: a new marker for disease assessment? Agents and actions. Apr 1990;30(1- 2):267-270.

6. Banks WA, Robinson SM. Minimal penetration of lipopolysaccharide across the murine blood-brain barrier. Brain, behavior, and immunity. Jan 2010;24(1):102-109.
7. Yue G, Shi G, Azaro MA, et al. Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cells by suppression of
anti-oxidative and growth factor gene expression. BMC genomics. 2008;9:608.
8. Neviere R. Pathophysiology of sepsis. In: UpToDate, Manaker, S{Ed}, UpToDate, Waltham, MA,2014; Erridge, et.al. Am J Clin Nutr. 2007;86:1286-1292;

 Sample Report – coming soon