Introducing the DNAblue Thyroid Genetics profile from Blue Horizon Medicals – It is a DNA swab test that looks at 10 variations across 8 Genes that are either directly or indirectly linked to thyroid function.

Discover how your genes control the production of thyroid hormones, and how variations in your DNA might impact on their effectiveness, and ultimately your health.

DNAblue Thyroid Report which uncovers predispositions to:

Autoimmune thyroid conditions
Hypothyroidism / hyperthyroidism
Poor conversion of thyroid hormones (T4 to T3)
Reduced clearance of reverse T3 (rT3)
Poor TSH signalling
Indirect thyroid disruption due to stress and / or inflammation

List of investigations

Your Pituitary Gland's receptivity to TRH which stimulates the secretion of TSH

Your Thyroid Gland's receptivity to TSH

Your Thyroid Gland's receptivity to TSH signalling

Conversion of T4 to T3

The clearing of RT3 from circulation

Your Body's response to stress

Detoxification of compounds that impact thyroid hormone levels

Your Body's response and susceptibility to inflammation and infection, both of which affect thyroid function.

Gene and SNP inclusions

DIO1 - Thyroid Hormone Activation “D1” is largely expressed in the liver and kidneys. It is responsible for the clearance of rT3 from circulation, and for facilitating the conversion of T4 to T3 in plasma and surrounding tissue. This process requires selenium and iodine for optimum function. Here we look at two variants linked to poor conversion of T4 to T3 and reduced clearance of RT3.

DIO2 - Thyroid Hormone Activation “D2” is importantly expressed in the central nervous system, pituitary, brown fat tissue and muscle, and responds to changes in thyroid levels. D2 is responsible for the ‘local’ conversion of T4 to T3 in the thyroid, placenta and brain. It requires selenium and iodine to function optimally. Here we look at two different variants linked to decreased T4 and low mood in certain individuals.

COMT - Inactivation of Stress Hormones and Oestrogen COMT is one of the main inactivating enzymes of stress hormones and oestrogen in the body. COMT variants cause slow clearance of stress hormones and oestrogen leading to high oestrogen and stress hormone levels which may also be linked to thyroid hormone dysfunction.

FKBP5 - Cortisol Regulation FKBP5 is an important stress-regulating gene responsible for lowering cortisol levels after a stress response. Variants are associated with prolonged and increased symptoms of stress, which may be due to delayed lowering of cortisol levels.

PDE8B - TSH Signalling PDE8B is found in the thyroid but not the pituitary, and is involved in TSH signalling. It is thought that the variant decreases the response of the thyroid gland to TSH stimulation

TNF-a - Inflammation TNF-a is an inflammatory cytokine that helps regulate the immune reaction involved in inflammation, giving rise to fever and inhibiting tumour growth. If poorly controlled, it may be implicated in a number of autoimmune disorders. Variants in TNFa are associated with overreactive immune responses and prolonged inflammation.

TSHR - Thyroid Stimulating Hormone (TSH) Receptor The TSHR gene plays a central role in thyroid metabolism by controlling the thyroid gland’s receptivity to TSH. Variants in this gene have been linked to hyperthyroidism, particularly to Graves’ Disease (GD).

TRHR - Thyrotropin Releasing Hormone (TRH) Receptor Responsible for the body’s receptivity to TRH which stimulates the secretion of TSH from the pituitary gland. In turn, TSH stimulates the production of thyroid hormones from the thyroid gland. TRH is an important part of the negative feedback loop that ultimately regulates thyroid hormone levels. Variants have been shown to affect TSH levels.

Please see our example report - click here

Private Blood Tests in Swindon

6 x Cortisol Saliva

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Adrenal Hormones Plus Thyroid Function

Bartonella Antibodies

Extractable Nuclear Antibodies (ENA)

Cortisol Blood - 9am

DNA (Single Stranded) Antibodies

DNAblue Thyroid Genetic Traits

DHEA Sulphate

Enhanced Liver Fibrosis - ELF

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