RESPIRATORY AIR IS PULLED INTO THE VITAL AIR DEVICE THROUGH AN AIR INLET (AIR-FILTER). IN THE BOTTLE FILLED WITH FILTERED OR BOTTLED WATER, THE AIR IS MOISTENED.
The Vital Air device has 3 or 5 activation chambers containing unique technology. This technology replicates the process that takes place in thebody to produce vital energy. PROCESS IN THE BODY Air breathed in and oxygen in its inactive state cannot be utilised by the body. Therefore it is activated in the body and hence made usable for building energy. The transformation of oxygen from inactive to active is essential to releases vital energy. This natural process of transformation is replicated by the Vital Air device. The water molecules enriched with energy are inhaled through the nasal cannula. The HRV measurement (HRV = Heart Rate Variability) can be used to show how this energy significantly improves the ability of the autonomic nervous system to control and regulate vital functions in our body.
VITAL AIR® THERAPY
OXYGEN & NATURE The oxygen in the air around us, with its share of approximately 21%, occurs in nature predominantly in an inert triplet ground state (3O2) Inert oxygen cannot be used by the body and must be activated by the body itself in order to be able to be carried into the blood by means of the lungs and to be transferred from there to the individual cells.
The reactive form of the oxygen is identified in physics as singlet oxygen (1O2). In this O2 molecule, the position of the electrons in relationship to one another is changed. From two unpaired electrons with parallel spin come paired electrons with anti-parallel spin.
ENERGY PRODUCTION
Singlet oxygen has been present for millions of years in nature as an escharotic form and is constantly formed by the body itself in order to facilitate metabolism and signal transmission. The constant activation of oxygen, so that it can be transported and “burnt“ consumes energy. In the course of our life, the ability of our cells to produce sufficient energy (ATP-adenosine triphosphate). declines due to illness and stress. The “unclean combustion” with ever-diminishing ATP production and increased oxygen radical production leads to further damaging of the cell structures and accelerated aging of cells. If sufficient energy is no longer being produced, less oxygen can thus be activated, which, in turn, results in even less ATP. Energy in the form of the energy storage molecule, adenosine triphosphate (ATP) is produced within the cells in the “miniature power stations”, the mitochondria. VITAL AIR® THERAPY TECHNOLOGY COPIES NATURAL PROCESSES
Through VA technology, an energy transfer to the water molecules of the humidity in the air takes place and is inhaled via the nasal cannula. The energy transfer is achieved by the stimulation of stable, photo-sensitive catalysts (a natural model is: plant pigment (chlorophyll, for example) by means of a specific light wave length. The singlet oxygen’s relaxation energy which is constantly released by this fluorescence / chemiluminiscence process is carried further by the water molecules of the air humidity.
SCIENCE AND RESULTS Now, what exactly happens in the body with this energy still cannot be precisely described by science. However, it can be shown with scientifically recognised measurement processes that something basically very positive is happening. For example, already after 20 minutes of use, a significant improvement in the vegetative nervous system’s regulatory ability can be shown by means of ECG measurement technology, especially the heart rate variability (HRV) measurement.
WHAT IS RELAXATION ENERGY?
It is the energy released (photons = light) when singlet oxygen returns to its ground state (triplet oxygen).
We kindly ask you to keep in mind that cheap kinetic oxygen has nothing to do with the technology and efficiency of Vital Air devices and cannot be an alternative for our therapy.
PRODUCTION OF SINGLET OXYGEN IN THE ORGANISM
In 2003, Klotz et al. and in 2002, Klotz asserted that singlet oxygen is not only toxic, but can also trigger a cellular stress response, either through the formation of positive regulators or by rendering negative regulators inactive.
Already in 1997, Briviba et al. pointed out that singlet oxygen can trigger signalling cascades, e.g. the activation of the AP-2 transcription factor of cjun-N-terminal kinases and the NK-kappa-B system.
There are references to the fact that oxygen can only bond to haemoglobin in its diamagnetic form, thus in the form of singlet oxygen. However, there are too “competing” ideas about the bonding of oxygen. One originates from Pauling and the other from R. Weiss. Pauling represents the view that oxygen becomes bonded as singlet oxygen when the oxidation level +II of the iron in the haemoglobin is attained. According to Weiss, on the other hand, the bonding of the oxygen amounts to the transfer of electrons between the iron and the oxygen. During that process, the iron changes its oxidation level to +III and the simple negatively charged, radical super oxide is born of the oxygen. Today, we tend to think that the “truth” lies somewhere between the two theories (Prof. Rehder, Organic Chemistry, Uni Hamburg - personal message).
In 2005, Snyder et al. referred to the fact, that, according to their experiments, singlet oxygen in cells is primarily deactivated due to interaction with the solvent(!), and less through interaction with cellular components such as proteins. Scientists from the Fraunhofer-Institut in Freiburg indicate that singlet oxygen is promptly decontaminated in the presence of water (radiation-free quenching) Singlet oxygen is the essential oxidant in the neutrophil respiratory (oxidative) burst, thus has an essential function in the defence of bacteria and pathogens (Tatsuzawa et al. in 1999). Earlier it was thought that super oxide radicals and oxygen peroxide would be formed during the respiratory burst in experiments. In 1999, Kiryu et al. showed that singlet oxygen in neutrophils is formed under physiological conditions with the involvement of the myeloperoxidase (MPO)-H2O2-Cl(-)-system. In 2005, Zivkovic et al. were able to show most recently that neutrophils with their respiratory burst (with the formation of singlet oxygen) have anti-tumour effects in the early phase of tumour development. In COPD patients and asymptomatic smokers, the intracellular respiratory burst of the blood leukocytes is reduced (Wehlin et al. in 2005). Singlet oxygen modifies important haemostatic factors in human blood (fibrinogen, factor V, factor VIII; factor X) and is thus decisively involved in the regulation of haemostasis (Stief et al. in 2000, Stief, in 2004). Chloramines thus seem to be the most important physiological producers of singlet oxygen (Stief, in 2004). Other findings of the working group around Stief which show that singlet oxygen triggers blood platelet aggregates (Stief et al. 2001a) and inhibits the agonist-induced P-selectin expression and the aggregation of blood platelets (Stief et al. 2001b) point in the same direction. Based on these data, Stief put forward the hypothesis that singlet oxygen is an anti-arteriosclerosis agent.
In 2003, Garvin et al. described in a review how reactive oxygen species like singlet oxygen are important in the regulation of renal tubular transport and this has an immediate effect on the regulation of salt and water balance. However, the authors emphasise that there has been little information up to now about where and how these regulators work along the nephron. It could be shown that singlet oxygen can render free and bonded a2-macroglobulin (and thus the essential wide spectrum protease inhibitors) in plasma inactive (Stief et al in 2000). The authors surmise that phagocytes release HOCl and chloramines and that this, in turn, leads to the formation of large quantities of singlet oxygen. Thus, singlet oxygen can contribute to the activation of proteases at the site of an inflammation, for example. In 1999, Gillesen et al. emphasised that reactive oxygen species also have a series of physiological functions such as the activation of the cellular formation of cytokines and eicosanoides, leukotrien B4, interleukin 8, and TNFa, and the activation of adhesion molecules (ICAM-1), the formation of arachidonic acid epoxides, the release of peptide hormones, the regulation of transcription processes in the cell nucleus and the initiation of an increased formation of antioxidants (especially SOD).
CONCLUSION: VITAL AIR® THERAPY TECHNOLOGY USES ONLY THE RELAXATION ENERGY OF SINGLET OXYGEN FOR THERAPY!
