72 € for 60 units
Removes all heavy metals without causing demineralization ! - Protector against free radicals. Involved in all related diseases of heavy metals intoxication : Alzheimer's, Attention Deficit Disorders - Hyperactivity, Autism, Fibromyalgia, Chronic Fatigue Syndrome, Parkinson, Macrophagic Myofaciite
Adults : min - max 2 daily
Children (under 12 years) : contact us or see the sheet Use advice
Duration : min 270 days
- Age 1-4 years, 1 capsule every 2 days
- Age 4-8 years, 1 capsule daily
- Age 9-12 years, 1 and 2 capsules alternating every 2 days
In case of difficulty to swallowing, the capsule can be opened and contents mixed into the food bowl
Caution(s) : TAKING DURING THE MEALS (in the food bowl) For any question, don't hesitate to contact our pharmacist
It is an octanoic acid, a fatty acid, which the hydrogen atoms of carbons 6 and 8 are replaced by a disulfide bridge (-S - S-). It is part of B vitamins group.
Its role is crucial in energy metabolism. Indeed, it is the cofactor of pyruvate dehydrogenase and is found under the reduced form with two-SH after performing its catalytic role in the Krebs cycle.
The lipoic acid is a very powerful antioxidant but is also a sensor of heavy metals by its two thiol groups.
The glutathione is a tripeptide - the γ glutamyl-cysteinyl-glycine- cofactor of destruction of the oxygen free radicals (OFR).
In poisoning by heavy metals its activity is blocked.
Furthermore, heavy metals inhibit the metabolism of mitochondria, whose role is to reduce oxygen to water.
This inhibition of mitochondrial metabolism leads to OFR formations. A contribution of reduced glutathione (GSH) allows to maintains a normal rate of OFR.
Also note that GSH is intervenes in the synthesis of H2 prostaglandin and so in the regulation of the inflammation.
During the accumulation of hydrogen peroxide, selenium, a cofactor of membrane glutathione peroxidase and cytoplasmic, is the indispensable element to the formation of a reserve of glutathione under a glutathione disulfide form (GSSG). The cell can be resupplied in GSH by the action of glutathione reductase.
The Se allows to prevents the formation of a complex "GSH-heavy metal" as the complex GS-Hg-SG which blocks the vital activity of GSH. The choice of Se bound to methionine is motivated by the fact that methionine is an essential amino acid precursor of cysteine, another amino acid essential to the structural integrity of our proteins.
The cysteine in presence of heavy metals is unavailable, since this amino acid containing a thiol function (-SH) possesses a high affinity for metals.
The presence of vitamin E, liposoluble vitamin, allows to inhibit the oxidation of membrane fatty acids.
This enzyme is found in the mitochondria and cytoplasmic levels.
Its role is to destroy superoxide anions. The cofactors of SOD are the trace elements Mn-Zn and Cu.
Heavy metals such as Cd and Hg move these trace elements and inhibit the activity of dismutases superoxides.
Pycnogenol means a mixture of flavonoids rich in polyphenols and proanthocyanidins.
The pycnogenol has several interesting functions of a biological point of view : its components are anti-radical and have a half-life of action much longer than vitamins C and E and more, they are anti-inflammatory
On the other hand, the active ingredients of pycnogenol, water-soluble, crosses the cephalomeningitis barrier protecting the central nervous system of the effects of heavy metals involved in the etiology of certain neurodegenerative pathologies.
The addition of pycnogenol can also regenerate the ascorbyl group (vit C) B and protect GSH from oxidative stress.
The riboflavin, in the form of FAD, is the vitamin cofactor of the cytochrome C oxidase.
This enzyme situated in the mitochondrial at the end of respiratory chain, allows the purge of the free radicals that have not been destroyed upstream.
Allows the passage of the cell wall, provides a nutritious and revitalizing action, breaks the existing steel bridges at the level of the enzymes and proteins (which will allow to other substances of the first composition to make their work), Japanese studies reveal an important immuno-stimulating activity.
Possess anti-inflammatory and dechelating properties.
- Age 1-4 years, 1 capsule every two days
- Age 4-8 years, 1 capsule per day
- Age 9-12 years, 1 and 2 capsules in alternation one day on two
- Age 13 and adults : 2 times 1 capsule per day during meals by cure of 6 months minimum
Vitamin C is known for its antioxidant properties. However, in some cases vitamin C expresses a pro-oxidant activity. Is this a paradox ? In fact the mechanism of this paradoxical action, depends at the same time of its concentration and the power of ascorbic acid to reduce the metals of transition. In the presence of ferric iron, the vitamin C develops a pro-oxidant activity leading to an increase in free fatty acids and triglycerides, we also measure a strong increase of the activity of-N-acetyl-D-glucosaminidase reflecting a lysis of the lysosomal membrane with liberation of proteolytic enzymes in the cytoplasm and a delay of growth.1 Also note that vitamin C increases the production of hydrogen peroxide ( H2O2 ) intra-erythrocyte and this in a way of dose-dependent. 2 In this case, the intra-globular toxic production resulting from an excess of vitamin C is bound with inhibition of erythrocyte catalase activity by the ions Fe3 + located in extracellular compartments. The Fe3 + and peroxides oxidize the ascorbic acid, which then becomes a pro-oxidant factor. This combined action of iron and vitamin C is normally restrained by vitamin E and glutathione on condition that it remains in the reduced form GSH. We know that heavy metals blocks the activity of glutathione. It is true that ascorbic acid intake decreases the risk of oxidation, however, in certain circumstances the vitamin C can promote free radicals and lipid peroxidation. We showed for example that antioxidants, including vitamin C, are active in preventive stage, but they speed the propagation phase of LDL oxidation process once it is installed.3
1 Chen K. et al. Am J Physiol Endocrinol Metab 2000 279 : 1406-1412
2 Shalu Mendiratta et al. Biochimica et Biophysica Acta 1998 1380 : 389-395
3 Otero P. et al. Free Radical Research 1997 27 : 619-626