Epigenetic Liver Cells Protector
Epigenetics Protects Our Liver
A dietary supplement of Applied Epigenetics with the highest possible biologically active form of S-Adenosylmethionine as coated granules, containing the necessary vitamins for its biosynthesis and a trace element in a preventive dosage in enteric-coated capsules.
Made in Germany
A normal S-adenosylmethionine (SAM, Ademetionin, AdoMet) level in liver cells is necessary for liver health. Researchers first observed a significant impairment of methionine metabolism in patients with liver cirrhosis in 1947, highlighting the crucial role of the liver in regulating methionine concentration in the blood.
Source: LW Kinsell, HA Harper, HC Marton, GD Michael, HA Weiss Science 106, 589–594 (1947).
Cantoni demonstrated that the first step in methionine metabolism is the conversion into S-adenosylmethionine (SAM, Ademetionin, AdoMet), a reaction catalyzed by the enzyme now known as methionine adenosyltransferase (MAT).
Sources:
Cantoni GL. S-Adenosylmethionine; a new intermediate formed enzymatically from L-methionine and adenosinetriphosphate. J Biol Chem. 1953 Sep;204(1):403-16. PMID: 13084611.
Schlenk F, Depalma RE. The preparation of S-adenosylmethionine. J Biol Chem. 1957 Dec;229(2):1051-7. PMID: 13502364.
with prokaryotes, bacteria, and archaea carrying out biosynthetic steps for S-adenosylmethionine (SAM, Ademetionin, AdoMet) over 3 billion years ago, as genomic analyses prove. This underscores the exceptional significance of the C1 metabolic cycle for human cell health.
Genome sequence analysis reveals that all organisms synthesize S-adenosylmethionine (SAM, Ademetionin, AdoMet), and a large portion of genes are S-adenosylmethionine-dependent methyltransferases. S-adenosylmethionine-dependent methylation has proven crucial for many biological processes. Up to 85% of all methylation reactions and even 48% of methionine metabolism occur in the liver, emphasizing the organ’s critical role in regulating blood methionine levels.
Liver-specific and non-liver-specific methionine adenosyltransferases (MATs) are products of two genes, MAT1A and MAT2A, catalyzing the formation of S-adenosylmethionine (SAM, Ademetionin, AdoMet), the primary biological methyl group donor. Mature liver expresses MAT1A, while MAT2A is expressed in extrahepatic tissues.
rendering them water-soluble for excretion. Reduced activity of liver-specific MAT is known in various liver diseases and can contribute to the pathogenesis of liver damage. Studies have shown decreased MAT1A expression in the livers of patients with various causes of liver cirrhosis.
Source: Shelly C. Lu, Luis Alvarez, Zong-Zhi Huang, and José M. Mato. Methionine adenosyltransferase 1A knockout mice are predisposed to liver injury and exhibit increased expression of genes involved in proliferation. 2001. PNAS Vol. 98 No. 10.
Source: Mato JM, Corrales FJ, Lu SC, Avila MA. S-Adenosylmethionine: a control switch that regulates liver function. FASEB J. 2002 Jan;16(1):15-26. doi: 10.1096/fj.01-0401rev. PMID: 11772932.
S-adenosylmethionine (SAM, Ademetionin, AdoMet) is a key product in the metabolism of the amino acid methionine, formed by the reaction of methionine with adenosine triphosphate (ATP) as “energized methionine.”
S-adenosyl-L-methionine (SAM, Ademetionin, AdoMet) is the singular methyl group donor for the genetic material (RNA, DNA, and histones) for methylation. The body requires S-adenosyl-L-methionine (Ademetionin) in more than 100 essential biosyntheses and metabolic processes. Therefore, undermethylation has severe health consequences.
This metabolic diversity and significance are unique.
The lack of S-adenosylmethionine (SAM, Ademetionin, AdoMet) has devastating consequences for the organism, starting from the mitochondria and cells.
Being healthy and staying healthy has a fundamental prerequisite: mitochondrial health. Health prevention is mitochondrial protection.
The deficiency of S-adenosylmethionine (SAM, Ademetionin, AdoMet) leads to the destruction of mitochondria (mitochondrial dysfunction). Without sufficient energy supply through ATP, the cellular energy carrier produced in the respiratory chain through ATP synthetase, there is oxidative breakdown of the cell’s large molecules such as RNA, DNA, histones, proteins, lipids. This, in turn, is inevitably associated with the destruction of functional cell structures. This malfunction is the basis of many organ diseases commonly referred to as “aging diseases.”
The organism has sufficient S-adenosylmethionine (SAM, Ademetionin, AdoMet) supply until early adulthood; then, the biosynthesis of S-adenosylmethionine (SAM, Ademetionin, AdoMet) decreases significantly. Replacement of S-adenosylmethionine (SAM, Ademetionin, AdoMet) becomes necessary to continue its biological benefits for metabolism and keep the body healthy.
Only the (S/S)-isomer of S-adenosylmethionine (SAM, Ademetionin, AdoMet) promotes the methylation of genetic material. The synthesis of spermidine is accomplished by S-adenosylmethionine (SAM, Ademetionin, AdoMet) synthesis through amino-propylation. Another important key molecule of cell health (autophagy induction and improved protein synthesis) becomes indispensable in S-adenosylmethionine deficiency. This is to protect cells from the cell-destructive force of Reactive Oxygen Species (ROS).
The consequence of S-adenosyl-L-methionine deficiency can be the cause of chronic liver disease. The prevalence of chronic liver disease in the European population is 20-30%.
Currently, around 30% of the world’s population suffers from non-alcoholic fatty liver disease. Therefore, the World Health Organization (WHO) classifies the disease as epidemic. Metabolic disorders can exacerbate diseases such as type 2 diabetes or cardiovascular diseases.
The number one among chronic liver diseases is non-alcoholic fatty liver and fatty liver hepatitis. Fatty liver hepatitis, in turn, carries the risk of fibrosis (liver cirrhosis), liver failure, and liver cell carcinoma.
Men are twice as likely to have fatty liver hepatitis as women. The most dangerous accompanying diseases are obesity and sleep apnea, caused by breathing interruptions during sleep, followed by pronounced daytime fatigue and an increase in blood sugar with type 2 diabetes mellitus, with its health-restricting late complications of vascular calcification and neuropathy, and possible early death from heart or kidney failure.
Together, Ademetionine, Hydroxocobalamin, Quatrefolic®, and Pyridoxal-5-Phosphate prevent an increase in blood Homocysteine levels, making a significant contribution to the safety of physical and mental health.
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
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Unsere Produkte enthalten pro Kapsel 400mg Ademetionin (S-Adenosyl-L-Methionin) in der biologisch aktiven (S,S) Form in präventiver Dosierung