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>Glycomarine COX Inhibition
Summary of GlycoMarine� COX Inhibition
I summarize below the COX 1 and COX 2 situation in brief, simple terms:
In arthritic joints, damage to the phospholipid cell membrane causes disruption, which allows lipase enzymes to break down the membrane producing arachidonic acid. Arachidonic acid, so produced, is then acted on by cyclo-oxygenase enzymes to produce leukotrienes. Some of the prostaglandins, prostacyclines and leukotrines are quite potent stimulators of inflammation.
There are two forms of cyclo-oxygenase enzyme, one (COX1) is a constitutive enzyme in that it is naturally present and produces prostaglandins, which are necessary for the normal physiological functions of the body. One of these functions is that of protecting the stomach from ulcerogenic damage. COX 2 enzymes, on the other hand, are not constitutive and are induced when a disease process occurs. COX 2 enzymes produce prostaglandins, which are pro-inflammatory. Hence, it is a highly desirable function for an anti-inflammatory treatment to be COX 2 selective, i.e., to inhibit the activity of COX 2 enzymes, without interfering with that of COX 1 enzymes.
Most non steroidal anti-inflammatory treatments are non selective and inhibit both COX 1 and COX 2 activity, thus having the potential to cause gastric damage, renal dysfunction and other adverse side effects.
The bioactivity of GlycoMarine in the preferential inhibition of COX 2 adn 5-lipoxygenase activity, in addition to its other anti-arthritic functions can thus be appreciated.
GlycoMarine� Cortisol Hypothesis
With regard tot he significant enhancement of vitality experienced by human and animal subjects when treated with GlycoMarine, the following hypothesis has been proposed by researchers at the Auckland University School of Medicine. Incidentally, it is interesting to note that this vitality enhancement, although frequently noted and commented on by human subjects, is most easily demonstrated or witnessed in animal subjects, thus providing objective validity for the function.
The hypothesis put forward as a possible explanation for this activity is as follows:
GlycoMarine contains an enzyme called alpha suphatase, the properties of which are to cleave to the bonds between sulphate groups and their cation counterpart. In the body, compounds formed between cortisol and sulphate groups circulate naturally. If the action of the alpha sulphatase enzyme in the GlycoMarine cleaves to the sulphate/cortisol bond, then free cortisol will be released. The free cortisol will stimulate the adrenal gland to release adrenaline, and may also stimulate the exiting activity in brain function , thus enhancing vitality and the desire for activity. The description of this phenomenon by people who have experienced it matches that of the experience of people who have experienced cortisone injections.
Although there can be adverse effects of cortisol on the normal functioning of the liver and other organs, there have been no such occurrences resulting from long-term consumption of GlycoMarine. This is possibly due to the enzymatic activity causing the release of only small amounts of the sterol, in a controlled biosynthetic manner, from an endogenous source.
John E. Croft
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