Melatonan II Research

On a glandular level, scientific study that has been based on animal test subjects has determined that Melatonan II’s overall properties of engagement can be tied to the workings of the pituitary gland.  This is the pea-sized gland found at the bottom of the hypothalamus at the base of the brain whose responsibility is chiefly tied to the overall functionality and control of a host of endocrine system-related processes, like growth and metabolism.

On a more specific level, it has been determined that Melatonan II’s inherent engagement can be directly tied to the expression of a pituitary gland-based hormone known as alpha-melanocyte stimulating hormone, otherwise known as α–MSH.  In essence, this hormone is responsible for the regulation and control of hair and skin pigmentation in animal test subjects.  The particular secretion that this hormone puts forth is known as melanin, and the secretion itself has been shown to be prompted as a response to the exposure to UV rays.  This particular process is usually referred to as melanogenesis.

The overall effects that play out of melanogenesis are twofold in its nature.  The first, simple effect is the darkening of the skin’s pigment.  The second, more complex effect is that it acts as a natural protective measure, as it safeguards against the exposure to ultraviolet rays.  This by extension acts as a safeguard against a host of skin afflictions and ailments that can result from prolonged exposure to ultraviolet rays.  This can include various types of skin cancers.

Melatonan II and Boosted Processes

Unfortunately, scientific study based on animal test subjects has determined that on its own, the α–MSH hormone has an extremely brief half-life that only lasts several minutes.  This in turn means that its simple properties of pigmentation alteration and its more complex properties as a means of pathogenic protection are limited.  However, these studies have determined that Melatonan II’s operational mechanics serve to lengthen the half-life of the α–MSH hormone.  This means that the hormone can be given the capacity to produce melanin for a longer period of time, thus increasing its overall effectiveness by a substantial amount.  Furthermore, these studies have also indicated that the presence of the peptide can induce an increase in the hormone’s half-life without the presence of harmful UV rays, thus enabling its ability to safeguard from pathogens before the pathogen triggers a response.  That being said, scientific study that has been based on animal test subjects has determined that Melatonan II’s overall functional mechanics have been shown to be more effective when UV rays have been added to the process.

Some of the mechanics that scientific study on animal test subjects has been able to associate with Melatonan II have been shown to be similar to some of the associations that have been made with Melanotan I, hence the reason why the two peptides are occasionally confused with each other.  However, these studies have determined that Melatonan II has a tendency to stimulate the release the hormones that induce the process of melanogeneisis on a far more efficient basis.

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Melatonan II and Skin Cancer

Because of the way in which Melatonan II has been shown to function in relation to the protective properties of melanogenesis, scientific study that has been based on animal test subjects has honed in on its conceptual ability to be an ally in the reduction of the likelihood of skin cancer development.  The backbone behind this link is due to the notion that the peptide has shown an ability to initiate the process of melanogenesis without the presence of UV rays.  That said, it has been determined that the clinical studies have shown that while Melatonan II can conceivably be effective in lessening the presence of most skin cancers, it is not effective against the presence of the deadliest form of skin cancer, malignant melanoma.  The reason for this because it has been determined that malignant melanoma is not caused by UV ray exposure, but rather by indirect DNA damage.