Genetic testing

Here you will find our genetic testings. Just use the search function to get more informations.



Adrenergic receptor-2 (ADRB2)

Relevant to obesity. Indicates a higher predisposition to save fat.

Aldolase B (ALDOB, mutations A149G, A174D, N334K, Delta4E4)

The inherited fructose poisoning is an autosomal recessive genetic disease cused by a mutated AldolaseB-gen. The analysis covers 75% of the genetic intolerance.

Alpha-Actninin (ACTN3)

This Gene is for an important muscle-protein (muscle fibre), its availability takes effect on the ideal muscle function. It is a factor of being a sprinter or an persistent athletic. ("athletic performance&qout;)

Angiotensin Converting Enzyme (ACE)

This enzyme is important for the regulation of the blood pressure. It takes effect to the Renin-Angiotensin-System.

Apolipoprotein B (APOB, XbaI-Mutation)

If there is a mutation, it will influence the lipo protein degradation, thus causes a higher cholesterol level in the blood. The Atherosclerosis risk is increased.

Apolipoprotein B (APOB3500)

This mutation causes a extreme hyperlipidemia, that occure in early years often. The defective binding between the ApoB and LDL-receptor (FDB) is heavily involved at the formation of a atherosclerosis.

Apolipoprotein E (APOE)

At certain genetic constellations there is a higher risk for arteriosclerosis and/or Alzheimer's disease (variations in E2, e.g. E4). Additional variations in the interleukin protein (IL-1A and IL-1B(+3953)) can cause higher lipid peroxidation.

Östrogen-Rezeptor (ER)

Genetic variations are associated with Alzheimer's disease (also see APOE), Parkinson's disease and osteoporosis. Important for women: genetic variations are also associated with breast cancer (also see NAT2), also autoimmune disease like multiple sclerosis and rheumatoid arthritis (also see IL - 1RN).

Catechol-O-Methyltransferase (COMT)

Gene product take part in the metabolism of the catechol estrogens. Genetic variations with high risk of breast cancer.There will be chronically elevated tissue burden caused of estrogen and estrogen derivatives.

CD24

The gene-mutation has an obvious influence on the susceptibility and progressivity of Sclerosis disease.

Celiac disease: mutations HLA DQ (HLA DQ A05, HLA DQ B02, HLA DQ B0302)

The simultaneous absence of the DQB*03:02 and DQA*05 or DQB*02 alleles excludes a genetic predisposition in 99%. The simultaneous occurence of the three alleles confirms a genetic predisposition. Every other possible allelic combination suggests a risk factor. The Analysis is usefull to detect a celiac disease supposing that the analysis for the antibodies against transglutaminase and/or a intestinal villus biopsy proves to be negative or borderline.

Collagen Typ 1α1 (COL1A1)

Important bone protein. Genetic variations, which are related with osteoporosis (have a look at Vitamine-D3-receptor) and osteogenesis imperfecta.

CTLA4

Mutation associated with a stronger tendency of insulin related diabetes mellitus and autoimmune diseases at all.

Faktor II ( Prothrombin)

Genetic variations lead to higher thrombosis risk, especially if it's combined with oral contraceptives.This testing is recommended for familiar thrombophilia to clarify thrombosis and abortions.

Faktor V Leiden (APC-Resistenz)

Genetic variations lead to higher thrombosis risk, especially if it's combined with oral contraceptives.This testing is recommended for familiar thrombophilia to clarify thrombosis and abortions.

Fatty acid-binding protein (FABP2)

Genetic variation causes a strong elevated affinity for fat-acids, which are too long. Carrier of this polymorphism should significantly reduce the fat absorption.

Glutathion-Peroxidase 1 (GPX1)

The peroxidase is a Selenium dependent enzyme, that detoxifies with the help of gluthatione hydrogene peroxide and a width spectrum of organic peroxides. The mutation reduces the excitabilty of the enzyme activity by Selenium. Difference cancers are associated within (foe example lung cancer, Non-Hodgkin Lymphoma, breast cancer).

Glutathion-S-Transferase M 1 (GSTM1)

The enzyme participate in the detoxification of heavy metals, e.g. from nutrition or dental-metals like amalgam. Genetic variations correlate with varied forms of cancer, especially lung cancer, chronic bronchitis, cystic fibrosis, alcohol-induced cirrhosis, endometriosis.

Glutathion-S-Transferase M 3 (GSTM3)

he enzyme participate in the detoxification of heavy metals, e.g. from nutrition or dental-metals like amalgam.

Glutathion-S-Transferase P 1 (GSTP1)

THe genetic variation correlates with a number of chemical induced forms of cancer. The enzyme participate in the detoxification of heavy metals, e.g. from nutrition or dental-metals like amalgam.

Glutathion-S-Transferase T 1 (GSTT1)

Throat cancer (especially with tobacco smoke, stomach and colon cancer. Important: Enzyme participate in the detoxification of heavy metals, e.g. from nutrition or dental-metals like amalgam.

Hämochromatose (HFE)

Genetically based hemochromatosis, particularly damage to liver, heart and pancreas.

Interleukin 10 (IL10)

Anti-inflammatory interleukin. A deficiency comes particularly with an predisposition to Crohn's disease, autoimmune thyroiditis, ulcerative colitis, and skin diseases.

Interleukin-1 alpha (IL-1A)

Genetic variation induces a higher activation of the immune system and therefore to a higher production of free oxygen radicals. Important: The protein is involved in conjunction with the IL-1B (+3953) in the formation of periodontitis and in conjuntion with the IL-1B (+3953) and SOD2 in the formation of diabetes mellitus (Typ 1).

Interleukin-1 beta (IL-1B (+3953))

Genetic variation causes a increased activation of the immune system and therefore a higher production of free oxygen radicals. Important: The protein is in conjunction with IL-1A responsible for the formation of periodontitis and with IL-1A and SOD2 it causes a diabetes mellitus (Typ1).

Interleukin-1 beta (IL-1B (-511))

Genetic variation causes a increased activation of the immune system and therefore a higher production of free oxygen radicals.

Interleukin-1 Rezeptor-Antagonist (IL-1RN)

Genetic variation causes a overreaction of the immune system and therefore a higher production of free oxygen radicals. Predisposition for chronic skin diseases like systematic Lupus erythematosus, alopecia areata, lichen sclerosus.

Interleukin-4 (IL-4)

IL-4 is an anti-inflammatory Interleukin, which stimulates the B-Cell-activation and the IgE-production. It is involved in the formation of atopic diseases.

Interleukin-6 (IL-6)

IL-6 has a large influence on the formation of blood. The mutation type (c-alleles) effects a reduction of the IL-6 level with a reduction of the thrombocytes and leukocytes. The risk getting an early beginning arteriosclerosis decreases. The normal type (g-alleles) increases the risk getting arteriosclerosis and arthritis. Patients with diabetes type 2 tend to kidney damage.

Katalase (CAT)

The catalase detoxifies the hydrogen peroxide build in the peroxisomes produced by the activated SODs. The promoter-mutation causes a decreased catalase activity. By that the tissue burden with H2O2 is cytotoxic and supports a lot of progressions of diseases.

Laktase (LAC C-13910-T)

Primary (congenital) lactase deficiency (lactase persistence)

LDL receptor-related protein (LRP1)

The mutant type (t-alleles) stands in a relation to breast-cancer incidence and influences intensity and aggression of carcinoma. The t-alleles also causes a better prognosis of Alzheimer's diseases, because it counteracts plaque formation.

Methylentetrahydrofolat-Reduktase (MTHFR)

Converts methyleneTHF into methylTHF for the methionine-synthesis.Genetic variations increase the risk of thrombosis and causes a higher homocysteine level.

mikrosomale Epoxidhydrolase (EPX1)

Incidence in the microsomes. It is with CYP2E1 and GSTM1 involved in the breakdown of harmful environmetnal substances. Genetic variation is putted in context with liver carcinoma, emphysema and ovarian cancer.

Multiple Drug Resistance 1 (MDR1)

Responsible for the drug metabolism. Gives prior informations on the drug metabolism. Genetic variation addicts with suitable cytochromes the degree of the breakdown of drugs.

N-Acetyltransferase 2 (NAT2)

Genetic variations are related to breasst cancer (with tobacco smoke), bladder carcinoma and colon cancer in combination with CYP1A2.

Peroxisome proliferator-activated receptor gamma (PPARG)

PPAR-gamma occurs in adipose tissue and causes if it is activated an increased expression of glucose carriers and therefore a higher absorption of glucose into the cells. The gene PPAR-gamma has a strong influence on the insulin resistance.

Plasminogenaktivator-Inhibitor (PAI-1)

Mutant has a higher risk of obesity (3 times more). The genetic variations of the Apolipoprotein E (ApoE) higher risk of atherosclerosis and diseases at the coronary artery. Other genetic variations in the interleukins increase the risk of a periodontitis. There will be a risk of thrombosis if the variation is in the clotting factors (Factor II, Factor V and MTHFR).

Sulfotransferase 1A1 (SULT1A1) )

SULT1A1 is involved in the estrogen metabolism. The genetic variation causes a increased risk of breast cancer. Therefore is the enzyme important for the detoxification of a width spectrum of substrates like n-hydroylated heterocyclic amines and polycyclic aromatic hydrocarbons. (Occurrence in cooked meat and tobacco smoke). The mutation in SULT1A1 is brought in connection with autism.

Superoxiddismutase 1 (SOD1)

The examined base-exchange causes a decrease of the activation of SOD1 in the serum and aid a destruction by superoxide radicals in some tissues, especially at vessel intima. Mutations in SOD1 are suspected to increase the risk of ALS.

Superoxiddismutase 2 Leadersequenz (SOD2 )

Occurrence in mitochondria. A higher physical activity or excessive sport causes a increased production of free oxygen radicals. Genetic variation induces oxidativ stress and in literature there is a link between: cell destruction, premature aging / skin aging, cadiovascular diseases, rheumatism /rheumatoid arthritis, neurodegenerative disorder.

Superoxiddismutase 2 T175C (SOD2 T175C)

The T175C polymorhpism reduces the stability of the active enzyme for about three times.

Superoxiddismutase 3 (SOD3)

The polymorphism is associated with a decreased antioxidant endothelial-tissue-defenses and a higher risk if ischemic heart diseases.

Tumor-Nekrosefaktor alpha (TNFA)

Genetic variation causes a increased activation of the immune system and thou a higher production of free oxygen radicals; predisposition for autoimmune diseases.

Vitamin-D3-Rezeptor (VDR3)

Involved in the regulation of the bone and calcium homeostasis. Genetic variation is putted in context with osteoporosis (have a look at collagen), dental diseases, prostate- and breast cancer.


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