THYROID BALANCE REPORT
The thyroid is an endocrine gland in the neck that produces two thyroid hormones - triiodothyronine (T3) and thyroxine (T4), and calcitonin. Thyroid hormones control the metabolism of almost every cell in the body, with wide-ranging metabolic, developmental and cardiovascular effects.
Thyroid activity is altered by genetics and environmental factors: nutrients (tyrosine, selenium and iodine), toxins (fluoride, chlorine or moulds), psychosocial or physical stressors, bacteria and viruses. Imbalance can result in HPT axis (Hypothalamus-Pituitary-Thyroid) dysfunction, autoimmune thyroid diseases (AITDs) such as Graves’ and Hashimoto’s, thyroid sensitive cancers (although rare), and impact transport, activation and response to thyroid hormones.
Deficiency or excess of thyroid hormones can result in many different symptoms. Hypothyroidism (under activity) can cause weight gain, fatigue, low libido, cold intolerance, dry skin, constipation and depression. Symptoms of hyperthyroidism (over activity) include anxiety, heat intolerance, heart palpitations, insomnia and weight loss.
The Thyroid Balance report analyses the genes involved in the thyroid hormone lifecycle: synthesis - centrally (in the thyroid) and in activation in peripheral tissues, transport and metabolism, processing of cofactors (vitamins D and A) and inhibitors (stress and toxins). It also examines genes that confer susceptibility to inflammation and autoimmunity.
GENES INCLUDED
HPT Axis: CAPZB, FKBP5, GPX1*, PDE8B, TG*, TSHR* (*also involved in autoimmunity)
Autoimmune: CTLA4, FOXE1, HLA-DQA1, HLA-DQB1 and PTPN22
Inflammation: CD40, FCRL3, IL6, TNF, GC and VDR
Transport: SLCO1B1 and SLCO1C1
Activation: DIO1, DIO2, BCO1, GC and VDR
Metabolism: SULT1A1, SULT1E1, UGT1A1
The thyroid is an endocrine gland in the neck that produces two thyroid hormones - triiodothyronine (T3) and thyroxine (T4), and calcitonin. Thyroid hormones control the metabolism of almost every cell in the body, with wide-ranging metabolic, developmental and cardiovascular effects.
Thyroid activity is altered by genetics and environmental factors: nutrients (tyrosine, selenium and iodine), toxins (fluoride, chlorine or moulds), psychosocial or physical stressors, bacteria and viruses. Imbalance can result in HPT axis (Hypothalamus-Pituitary-Thyroid) dysfunction, autoimmune thyroid diseases (AITDs) such as Graves’ and Hashimoto’s, thyroid sensitive cancers (although rare), and impact transport, activation and response to thyroid hormones.
Deficiency or excess of thyroid hormones can result in many different symptoms. Hypothyroidism (under activity) can cause weight gain, fatigue, low libido, cold intolerance, dry skin, constipation and depression. Symptoms of hyperthyroidism (over activity) include anxiety, heat intolerance, heart palpitations, insomnia and weight loss.
The Thyroid Balance report analyses the genes involved in the thyroid hormone lifecycle: synthesis - centrally (in the thyroid) and in activation in peripheral tissues, transport and metabolism, processing of cofactors (vitamins D and A) and inhibitors (stress and toxins). It also examines genes that confer susceptibility to inflammation and autoimmunity.
GENES INCLUDED
HPT Axis: CAPZB, FKBP5, GPX1*, PDE8B, TG*, TSHR* (*also involved in autoimmunity)
Autoimmune: CTLA4, FOXE1, HLA-DQA1, HLA-DQB1 and PTPN22
Inflammation: CD40, FCRL3, IL6, TNF, GC and VDR
Transport: SLCO1B1 and SLCO1C1
Activation: DIO1, DIO2, BCO1, GC and VDR
Metabolism: SULT1A1, SULT1E1, UGT1A1