DNA adducts are substances or toxins of any kind, such as antibiotics, heavy metals, pesticides, plasticizers, etc., which are covalently bound to the mtDNA. The effects of a DANN adduct depend on its position on which gene or gene segment an adduct is bound. In general, DNA adducts lead to a permanent dysregulation of gene activity, i.e. a gene is decreased or increased in expression, it is blocked or overactivated. These different effects all result in altered gene activity, from which, depending on the gene segment affected, diseases (e.g. symptomatic CFS) can arise or existing diseases can be attributed to the DNA adduct. By identifying DNA-adducts, a targeted therapy can be initiated, the goal of which is to eliminate the DNA adduct and reduce the toxin load.
ATP is THE energy form of our cells and as such is required for all cellular metabolic processes. ATP is synthesized by oxidative phosphorylation in the mitochondria and must subsequently be discharged from the mitochondria in order to be available as an energy supplier throughout the cell. If the synthesis or transport of ATP in the mitochondria is impaired by toxins or unfavorable pH conditions at the mitochondrial double membrane, this has a direct influence on cellular processes; symptom complexes, such as chronic fatigue syndrome, can be the result. In the ATP profile, the availability of ATP, the synthesis of ATP from ADP and the transport/provision of ATP are investigated. An initial indication of possible toxins can also be seen in this profile. It also assesses whether the phosphorylase kinase is in the correct ratio to ATP and zinc.
Cell-free DNA is fragmented genomic DNA that is released from cells as a result of necrosis or apoptosis and circulates freely in the blood as extracellular DNA. The concentration of cell-free DNA in the blood reflects the degree of cell death and may indicate different diseases such as cancer, autoimmune diseases, CMS or inflam-
matory processes. However, the parameter is not specific.
NAD examination in erythrocytes reflects niacin status. Niacin, formerly vitamin B3, like NAD (nicotinamide adenine dinucleotide), is an important component of many coenzymes and thus necessary for many cellular processes and metabolic pathways, such as the respiratory chain, whose most important task is ATP synthesis.
In CFS patients, NAD availability is directly related to energy production. Therefore, the NAD profile is an ideal complement to the ATP profile and can be used as a progression parameter to monitor niacin supply in CFS.
In this profile, the electrical the electrical conditions of the cell membrane are correlated to the respective pH value. As a supplementary profile, it is also a good progression parameter.
Cardiolipin is a phospholipid and an important component of the mitochondrial membrane. The proportion of cardiolipin and other phospholipids such as phosphatidylcholine (PC) and phosphatidylethanolamine (PE) in the mitochondrial membrane is crucial for the maintenance of mitochondrial functions, above all the respiratory chain. Altered membrane morphology, due to toxins or an undersupply of phospholipids and fatty acids, directly affects mitochondrial functions through reduced mass transfer, among other effects. In addition, phospholipids such as PC or PE are main components of the cell membrane. They are essential for the exchange of substances and the elimination of toxins and for the fluidity of the membrane.
In the cardiolipin studies, the synthesis of cardiolipin, the availability of phospholipids (PC and PE) and, on the basis of cytochrome c oxidase, the extent of oxidative stress, are determined in the mitochondria.
Translocators are membrane-bound protein complexes that enable the exchange of substances and molecules across the mitochondrial membrane. Toxins can attach to the different translocators, educing their activity and their mass transfer. In addition to the binding of possible toxins to the translocators, mitochondrial morphology and oxidative changes in the mitochondrial membrane will be investigated. Furthermore, the status of MG53-bound potassium, magnesium and zinc at or in the mitochondrial membrane will be measured.
The GST profile examines the detoxification performance of the GST system and glutathione peroxidase. Glutathione S-transferases (GST) are enzymes that conjugate glutathione (GSH, a tripeptide of glutamate, cysteine, and glycine) to toxic substances (metabolites or xenobiotics). Toxins conjugated to GSH usually have greater water solubility, so they are cleared from the body via the kidney. If GST activity is reduced, toxic substances/xenobiotics may accumulate more intracellularly (and impair cellular processes). As a possible consequence, DNA adducts may form. In addition, the activity of glutathione peroxidase is examined in the GST profile. Glutathione peroxidase is an enzyme localized in erythrocytes that is centrally involved in the degradation of oxidative stress by reduction of hydrogen peroxide. Decreased activity of glutathione peroxidase leads to accumulation of cell toxic reactive oxygen species.
Metallothioneins are a family of cytoplasmic proteins that play an important role in the detoxification of heavy metals. They are able to bind and detoxify heavy metals such as mercury or cadmium. In addition metallothioneins can bind zinc and copper and reflect the intracellular ratio of zinc and copper (see SOD profile). The examination of metallothioneins indicates a possible load of heavy metals or an overload of the detoxification system and thus an insufficient detoxification performance. Furthermore, conclusions can be drawn about possible organ system disorders. In addition, the intracellular copper-zinc ratio is determined.
According to Sjörgensen, the pH profile indicates the total free and bound protons in the erythrocytes (hemoglobin-corrected). Here, the buffer systems are placed in a direct context and assessed. Excretion parameters complete the profile at the organ level, as does ATP synthesis information.
Superoxide dismutases (SODases) are antioxidant enzymes that are responsible for the detoxification of oxygen free radicals and thus protect cells from apoptotic cell death. Superoxide dismutases convert cytotoxic superoxide anions into hydrogen peroxide, which is then converted into water and oxygen by catalases.
Copper, zinc and manganese are essential cofactors for the activity of the SODases. In the SOD profile, the three SODases SOD1, SOD2 and SOD3 are investigated. SOD1 is the cytoplasmic SOD, which is copper/zinc dependent. SOD2 is manganese-dependent and localized in the mitochondria. SOD2 allows conclusions to be drawn about chronic inflammatory processes. SOD3 is secreted into the extracellular space where it is responsible for the conversion of superoxide anions. Identified adducts can be assigned to the three SODs.
Among other things, L-carnitine is essential for the transport of fatty acids into the mitochondria for energy production by means of β-oxidation. The L-carnitine status is determined in the L-carnitine profile. A check of the L-carnitine status is recommended for dialysis patients as well as for diabetes type 2 and liver diseases.
Fructose enters the bloodstream through the basolateral cell membrane of the intestinal cells mainly with the help of the GLUT-2 transporter. Blood then flows from the small intestine to the liver via the portal vein. However, there is often a defect in fructokinase in hepatocytes. Failure of the enzyme rarely leads to disease (fructosemia and fructosuria), but it does indicate a liver defect at an early stage in the sense of liver stress, which is investigated by the fructose profile.
Food assimilation intolerances are not type I allergies. Rather, they are reactions of the immune system according to Kaufmann & Hahn in the sense of one of the allergies of the delayed type (type III). We intentionally avoid IgG-4 measurement because it is unreliable. As with toxins, foods are often tolerant or intolerant in an epigenetic sense and can be detected very well with the iEC method. As a rule, a leaky gut syndrome is always present, which can sometimes be more pronounced, sometimes less. In addition, we indicate the cross-activity of the identified food intolerances (as a negative list) and compare them. By means of a mathematical system, we can also assess individual human systems, e.g. the psyche or „soft criteria“, such as detoxification, the state of the immune system and a whole range of others.
Mycotoxins are toxic secondary metabolites formed by various molds. Food and feed can be contaminated with mycotoxins. The contamination of the harvested crop can already occur in the field or during storage. Mycotoxins are mainly ingested via food or by inhalation of contaminated dusts and pose considerable health risks as they are hepatotoxic, nephrotoxic, carcinogenic or have hormonal effects. The iEC Fungal Metabolites & Fungal Species Test is suitable for detecting exposure to mycotoxins. It detects 27 mycotoxins and 21 fungal species from the genera Aspergillus, Fusarium and Penicillium.
Inadequate detoxification or increased exposure to toxic substances can cause them to accumulate in the body and body cells. These toxins can impair cellular processes such as energy supply through the respiratory chain in the mitochondria or attach to DNA and form a DNA adduct. With the iEC examination (iEC for intracellular electrical capacity), the intracellular amount of toxins in the lymphocytes can be determined and a possible exposure can be detected at an early stage.
Three options are available for iEC examination:
- 1. 12 or 24 standard substances that frequently lead to exposure can be tested.
The 12 standard substances include: Aflatoxin B1, Aluminium, Antimony, Cadmium, Chromium VI, Formaldehyde, Fumonisin B1, Fungisterol A, Lead, Mercury inorganic, Mercury organic and Nickel.
In addition to the 12 standard substances, the 24 standard substances include: Benzoquinones, Bisphenol A (BPA), Cetyltrimethylammonium bromide (CTABr), Chlorotoluenes, Diesel Exhaust Gases, Glyphosate/AMPA, Lindanes & Isomeres, Nitrosamines, Organophosphates, Phthalates, Polybrominated Biphenyl (PBB) and Triclosan.
- The substances to be tested can be selected individually from more than 900 substances.
For the selection of the substances you can use our iEC selection tool on our website.
- Entire groups of substances listed on our order sheet can be examined.
NICO (Neuralgia Inducing Cavitational Osteonecrosis) is the term used to describe degenerative osteonecrosis of the jawbone. As a result of tooth extraction wounds that have not healed optimally, especially after wisdom tooth extractions, chronic inflammation can occur in the jawbone that progresses unnoticed for years.
Toxins and inflammatory mediators form in these areas, which can promote inflammatory diseases elsewhere in the body. Symptoms associated with NICOS are usually uncharacteristic, so the cause of the symptoms is often not associated with osteonecrosis of the jawbone. Symptoms that may indicate NICOS are:
- Chronic weakness (CFS)
- Autoimmune diseases
- Cardiovascular complaints
For the examination of NICOS, removed inflammatory tissue in high percentage isopropanol is required. The tissue is examined for inflammatory mediators (e.g. IL-1, IL-6, TNF-α, RANTES) and toxins such as tetrodotoxin and heavy metals.