EBP Epigenetic Brain Protector

EBOP Epigenetic Burnout Protector 

ECP Epigenetic Cartilage Protector

Ademetionine in its biologically active Form (S,S) at a preventative dose of 400mg per capsule


Nugenis Gold Medal Iena 2015

For outstanding achievements in the protection against brain cell death


Cellular health is our most precious physical asset. To us that means preserving a youthful condition of the cell and the whole body for as long as possible. Cellular vitality, good health, and longevity all are intimately linked with this.
Working against this is acquired mitochondrial dysfunction and loss of mitochondria caused by ademetionine deficiency.
The mitochondrion is the key organelle for cellular health. Apart from their fundamental role in energy supply (ATP), mitochondria also are the principal producers of free oxygen radicals. If the defense mechanism of these antioxidants is impaired, they will trigger a cascade of damaging events in the cell.
Acquired mitochondrial dysfunction is found in many neurodegenerative diseases such as Huntington’s chorea, Parkinson’s, Alzheimer’s dementia, amyotrophic lateral sclerosis or stroke, and epilepsy. Furthermore, recent studies have supported the hypothesis of mitochondrial dysfunction in psychiatric diseases like bipolar disorder, depression as well as metabolic diseases, for example, diabetes mellitus.
The mitochondrion is directly affected by increased oxidative stress (ROS). Monoamine oxidase B (MAOB) and monoamine oxidase A (MAOA) can be found in both mitochondrial membranes and via the process of oxidative deamination of monoaminergic neurotransmitters, for example dopamine, react with highly reactive and aggressive hydroxy radicals which in turn interact with nearly all surrounding macromolecules such as lipids, proteins, desoxyribonucleic acids (DNA) and ribonucleic acids (RNA) oxidating all of these cell structures. This leads to multiple cellular injuries including damage to mitochondrial structures made from lipids, proteins, and DNA, first impairing cell vitality and ultimately the whole cell (cytotoxicity). 
Ademetionine deficiency results in increased oxidative stress (ROS and RNS) in cells.  
This oxidative stress caused by ademetionine deficiency is a result of increased degradation of important brain transmitters (oxidative deamination) initiated by excessive monoamine oxidase (MAO) expression following hypomethylation at the gene location. 
Ademetionine is the only donor of methyl groups in our metabolism which can deliver methyl groups at the gene level thereby reversing hypomethylation of the monoamine oxidase gene location. 
Ademetionine deficiency is linked to age. At approximately 35 years of age, the level of ademetionine expression is already reduced by a third and because of this ademetionine deficiency, an overexpression of monoamine oxidases (MAO-B and MAO-A) cannot be prevented anymore.
Paths to Cellular Health
Age-dependent substitution of ademetionine and age-dependent and adequate prophylactic substitution of spermidine protect cellular health.
A sufficient and age-dependent substitution of ademetionine required for the methylation of DNA and histones (genetic material) results in reduced mitochondrial damage by reducing overexpression of MAOA and MAOB.
Crucial transmitters: serotonin, dopamine, and noradrenaline are all available again to the body and especially to the brain as monoaminergic neurotransmitters are fully able to fulfill their receptor-dependent function at synapse level. Previously limited ability to feel, think and act can be re-established.
In addition, these monoaminergic transmitters also have receptor-independent functions influencing gene expression of our hereditary material (DNA) in the nucleus. Monoaminylation on its own is a way of diabetes prevention as it protects against intracellular serotonin deficiency in the pancreas and thereby maintains a healthy and physiological release of insulin. 
Sufficient and age-dependent substitution of ademetionine induces spermidine synthesis via aminopropylation in the 1-carbon cycle.
Spermidine also protects cellular health and, as a potent autophagy-inducing agent, supports the production of autophagosomes which remove misfolded proteins, viruses, and bacteria from the cell and thereby eliminate potentially toxic cell waste products.
Autophagy is the only preventative mechanism against intracellular pathogens. Autophagic degradation is an effector mechanism of the innate and adaptive immune response against intracellular microbes. 
Sufficient and age-dependent substitution of ademetionine maintains glutathione biosynthesis via transsulfuration in the 1-carbon cycle. Glutathione is the most potent antioxidant in the cell. 
Sufficient and age-dependent substitution of ademetionine protects the cell from oxidative stress to the endoplasmic reticulum ensuring regular protein synthesis.  

Note: This information is provided for educational purposes and does not substitute for professional medical advice. Always consult with healthcare providers for personalized guidance on health-related matters.

Copyright © Eduard Rappold 2024