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How blood biomarkers can aid in prevention and management of autoimmune processes – part 1

Autoimmunity appears to be on the rise. But what is an autoimmune condition, why does it happen, and why should we try to detect one as soon as possible? Read on to find out more in the first part of this two-part blog.

What is autoimmunity?

The immune system keeps our bodies safe by removing signs of danger: pathogens, damaged tissue and toxins to name but a few. Any protein can trigger an immune response. However, humans are largely made from proteins – so the body needs a system to ensure that the immune system does not attack the self.

This is where regulatory T cells (T-regs, sometimes written as Tregs) come in: T-regs are trained to recognise proteins that are safe, such as proteins of the body or food. T-regs prevent T cell proliferation and subsequent cytokine production that would otherwise be triggered in response to an unrecognised protein (1) regulation of the immune system is known as ‘immune tolerance’.

In an autoimmune condition, immune tolerance fails and the immune system mounts an unnecessary response to proteins of the body (auto = self in Latin). Dysregulation of T-regs is thought to be responsible for many autoimmune conditions, including multiple sclerosis (MS), type 1 diabetes, lupus and rheumatoid arthritis (1). In MS, a lack of T-regs appears to induce overstimulation of effector T cells which leads to the production of inflammatory cytokines, inflammation, and eventually neurone damage (1).

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Pathogenic infections and autoimmunity

Various pathogens have the potential to unbalance the immune system in the long term and could act as a trigger or a perpetuator of an autoimmune condition alongside other genetic and environmental factors.

Different white blood cell patterns can alert us as to whether there might be an acute infection or a chronic infection, and whether it might be viral or bacterial in nature. Crucially, it will give us information on whether there is immune activation that requires further investigation and immune balancing input.

One virus of relevance in autoimmunity is Epstein-Barr Virus (EBV). It is highly associated with thyroid autoimmune conditions such as Hashimoto’s and Graves diseases, as well as lupus, rheumatoid arthritis, and others (2). EBV is therefore a prognostic marker worth detecting in the assessment of autoimmune condition risk (2).

SARS-CoV-2 (Covid-19) is another virus associated with increased risk of autoimmune condition development: the virus can trigger immune hyperactivation which can lead to immune dysregulation and loss of tolerance (3). It is possible to test for antibodies to both of these viruses through FDX add-on

Vitamins and inflammation/immune function

Inflammation is a part of the immune response. As described above, it can be triggered by a lack of immune regulation which leads to cytokine production. However, inflammation can also be triggered indirectly by vitamin deficiencies.

The methylation cycle requires cofactors including folate (B9) and vitamins B6 and B12; if the body does not have access to adequate amounts, the methylation cycle cannot function optimally. This can result in hyperhomocysteinemia (4). Homocysteine enhances inflammatory activation and autoimmune triggering mechanisms; levels in the blood are correlated with autoimmune disease severity, and may serve as an indicator in early disease detection in combination with other markers (4).

Vitamin D plays an important role in modulating inflammation by reducing inflammatory cytokine production. Perhaps unsurprisingly, low vitamin D status is associated with autoimmune diseases (5). However, testing vitamin D alone may not be enough for ensuring the individual has optimal levels: everybody is unique and what is considered optimal for some may not be the case for others. Fortunately vitamin D testing can be combined with parathyroid hormone (PTH) for an indicator of vitamin D sufficiency: vitamin D suppresses PTH synthesis: therefore elevated PTH indicates vitamin D insufficiency (5).

Stress and autoimmunity

It is important to mention stress as a potential trigger and perpetuator of autoimmune conditions: large scale studies reveal a clear link between increased stress and increased development of autoimmune conditions (6). Interestingly, SSRI use appears to further attenuate the risk of autoimmune disease development (6).

Stress may induce immune dysregulation through the autonomic nervous system, which alters the body’s ability to resolve an inflammatory response, thus potentially predisposing the individual to autoimmune disease development (6).

Blood tests offer insight to the physiological effects of stress, including vitamin status, blood glucose dysregulation, and inflammation markers. There are also biomarkers such as electrolytes, DHEA and cortisol that can provide insight into whether someone might be experiencing acute or chronic stress.

Importance of early detection

Autoimmune conditions such as Addison’s disease can be life threatening if left undetected: however early detection is difficult because early symptoms are so general (7). Most people will develop autoimmune symptoms long after the initial immune dysregulation begins (8). It is possible to detect pre-symptomatic changes in the blood long before severe damage has been done to the body. If practitioners can detect inflammation and immune dysregulation earlier, they could intervene before severe tissue damage occurs, vastly improving a client’s quality of life.

We offer a range of markers in our tests that can serve to detect risk factors for autoimmunity.

Read part 2 of this blog here

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  1. Kondelkova, K., Vokurková, D., Krejsek, J., Borská, L., Fiala, Z. and Ctirad, A., 2010. Regulatory T cells (TREG) and their roles in immune system with respect to immunopathological disorders. Acta Medica (Hradec Kralove)53(2), pp.73-7. DOI: 10.14712/18059694.2016.63
  2. Janegova, A., Janega, P., Rychly, B., Kuracinova, K. and Babal, P., 2015. The role of Epstein-Barr virus infection in the development of autoimmune thyroid diseases. Endokrynologia Polska66(2), pp.132-136. DOI:10.5603/EP.2015.0020
  3. Talotta, R. and Robertson, E., 2020. Autoimmunity as the comet tail of COVID-19 pandemic. World Journal of Clinical Cases8(17), p.3621. DOI:10.12998/wjcc.v8.i17.3621
  4. Bonciani, D., Antiga, E., Bonciolini, V., Verdelli, A., Del Bianco, E., Volpi, W. and Caproni, M., 2016. Homocysteine serum levels are increased and correlate with disease severity in patients with lupus erythematosus. Clin Exp Rheumatol34(1), pp.76-81. DOI:
  5. Sainaghi, P.P., Bellan, M., Antonini, G., Bellomo, G. and Pirisi, M., 2011. Unsuppressed parathyroid hormone in patients with autoimmune/inflammatory rheumatic diseases: implications for vitamin D supplementation. Rheumatology50(12), pp.2290-2296. DOI:10.1093/rheumatology/ker314
  6. Song, H., Fang, F., Tomasson, G., Arnberg, F.K., Mataix-Cols, D., de la Cruz, L.F., Almqvist, C., Fall, K. and Valdimarsdóttir, U.A., 2018. Association of stress-related disorders with subsequent autoimmune disease. Jama319(23), pp.2388-2400. DOI:10.1001/jama.2018.7028
  7. Sævik, Å.B., Åkerman, A.K., Grønning, K., Nermoen, I., Valland, S.F., Finnes, T.E., Isaksson, M., Dahlqvist, P., Bergthorsdottir, R., Ekwall, O. and Skov, J., 2018. Clues for early detection of autoimmune Addison’s disease–myths and realities. Journal of Internal Medicine, 283(2), pp.190-199. DOI:10.1111/joim.12699
  8. Rosenblum, M.D., Remedios, K.A. and Abbas, A.K., 2015. Mechanisms of human autoimmunity. The Journal of clinical investigation, 125(6), pp.2228-2233. DOI:10.1172/JCI78088