EBOP® – Epigenetic Burnout Protector

A dietary supplement of Applied Epigenetics with the highest possible biologically active form of S-Adenosyl-L-Methionine as coated granules, containing the necessary vitamins for its biosynthesis and a trace element in a preventive dosage in enteric-coated capsules. Protects against burnout and enhances resilience.

Made in Germany

‘Burnout is defined by the World Health Organization (WHO) as a syndrome resulting from ‘chronic workplace stress that has not been successfully managed.’

Symptoms of Burnout:

• Physical and mental exhaustion
• Negative self-assessment of one’s own resilience and professional competence
• Negative feelings towards work
• Loss of compassionate attitude towards clients

◊ Cochrane’s evaluation of Ademetionine compared to other antidepressants: Risk ratios and effect size calculations for S-Adenosylmethionine (SAM, Ademetionin, AdoMet) compared to other antidepressants show no statistically significant difference. These results suggest that both therapies are approximately equal in their effects. AHRQ Evidence Report Summaries, Rockville.

Epigenetic Connections with Serotonin:

• A gene variant of the serotonin transporter gene (Variant ‘K’) leads to dysfunction of the serotonergic synapse with functional serotonin deficiency despite normal plasma serotonin levels.
• Serotonin, known colloquially as the ‘happiness hormone,’ serves important physiological functions in the digestive tract, bloodstream, and central nervous system.
• Serotonin acts as a neurotransmitter in the brain, transmitting signals between nerve cells. It is the phylogenetically oldest and universally acting neurotransmitter in all parts of the brain.
• A polymorphism in the promoter region of the serotonin transporter gene SLC6A4 has a shortened gene variant (Variant ‘K’) and is associated with anxiety disorders, obsessive-compulsive disorders, toxic stress, depressive disorders, and burnout. The shortened gene variant of the serotonin transporter is also found in fibromyalgia and lowered pain threshold.

Disease symptoms with serotonin deficiency:

• Suspected functional serotonin deficiency with normal serotonin levels is indicated by chronic fatigue symptoms, lack of motivation, mood narrowing, loss of affective resonance, anxiety, and sleep disorders.
• Mood narrowing, loss of affective resonance, anxiety, reduced drive, and sleep disorders are the key symptoms in diseases related to the depressive spectrum.

Metabolic diversity of serotonin:

• Serotonin is synthesized into melatonin with its sleep-inducing effect.
• Adequate serotonin in the brain leads to an increase in oxytocin and aids in social recognition. Social recognition is regulated by a network of oxytocin-sensitive neurons in the hippocampus.
• Increased activity of the neuronal stress axis as a result of toxic stress.

Neuronal stress response is adaptable and beneficial in the short term but, when excessively activated, can lead to altered physical responses to stress (toxic stress). Constant subjective stress is associated with elevated levels of norepinephrine, adrenaline, and cortisol. There is a lack of a relaxation phase, elevated heart rate and blood pressure, weakened immune competence, and toxic stress negatively impacts the life expectancy of affected individuals.

Oxidative stress is the main cause of cell aging:

• Stress increases serotonin levels in healthy individuals, as well as norepinephrine, dopamine, and cortisol levels.
• Cortisol elevation in toxic stress, mediated by the activation of the adrenergic system and α1-adrenergic receptors, leads to the release of the stress hormone CRH (Corticotropin-Releasing-Hormone), activating the subsequent stages of the HPA axis. The cortisol, being fat-soluble, easily passes the blood-brain barrier and influences the expression of numerous genes by acting as a transcription factor.
• The hippocampus, a region of the brain with dense serotonergic innervation, is crucial for stress regulation.

Toxic stress results in a decrease in neurogenesis in the dentate gyrus of the hippocampus, leading to reduced proliferation, survival rate, and differentiation of neural stem cells. Under toxic stress and in response to constantly elevated cortisol, the dentate gyrus experiences a decrease in cell count through the inhibition of neurogenesis, while physical activity and an enriched environment increase the volume of the dentate gyrus and the number of neurons.

Toxic stress also leads to hypomethylation of the glucocorticoid receptor gene locus, resulting in increased MaoB expression. MaoA and MaoB activity is increased by cortisol. The toxic byproducts formed during oxidative deamination, known as reactive oxygen species (ROS), include hyperoxide anion (O2·-), hydroxyl radical (HO·), peroxyl radical (ROO·), alkoxyl radical (RO·), and hydrogen peroxide (H2O2). These lead to mitochondrial dysfunction and subsequent neurotoxicity, resulting in neurodegeneration and astrogliosis in brain cells.

About 75% of MAO in the human brain belongs to the B-subtype (Saura Marti et al., 1990).

Toxic stress and its role in the development of Alzheimer’s disease: Toxic stress with an overactive stress axis, described as the HPA axis (hypothalamic–pituitary–adrenal axis), also plays a significant role in the development of Alzheimer’s disease.

◊ Is dementia and depression a malfunction of neurogenesis and neuroprotection? Current concepts of depression and cerebral aging have shifted from dysfunction of neurotransmission to dysfunction of neurogenesis and neuroprotection (Bettina H. Bewernick 2013).

Neurons are unique cells that persist throughout an individual’s entire lifespan, undergoing programmed developmental changes and accumulating environmental experiences that optimize neural circuits in the brain. Neurons undergo precisely coordinated cascades of genetic regulation during development and maturation, connecting with experience to shape cellular production through progressive changes in the epigenome.

Neurogenesis (formation of new neurons): It has been shown that neurogenesis can be inhibited by physical and social stress, depression, and treatment with antidepressants. Berton O., Nestler EJ. New approaches to discovering antidepressants: beyond monoamines. Nat Rev Neurosci. 2006; 7: 137–151.

EBOP® – Epigenetic Burnout Protector consists of naturally occurring substances in the body:

• Ademetionine (S-Adenosylmethionine): The production of S-Adenosylmethionine (Ademetionine) in humans mainly occurs in the liver. A liver-healthy adult under 30 years old synthesizes approximately eight grams of S-Adenosylmethionine (SAM, Ademetionin) per day. The natural occurrence of Ademetionine in the cell and its biosynthesis in liver cells decrease with age after 35. This age-dependent Ademetionine deficiency leads to hypomethylation (undermethylation) of DNA, resulting in epigenetically caused diseases. For your benefit, we use: ADOGRAN® – a coated (acid- and water-resistant) granule of Ademetionine, and an acid-resistant capsule shell protects the integrity of the active form of S-Adenosylmethionine (SAM, Ademetionin).
• Vitamin B12: Supports the metabolic functions of our brain cells, maintaining the normal function of the nervous system and normal psychological functions (according to Regulation (EU) No 432/2012). Vitamin B12 supports Ademetionine production. For your benefit, we use: Hydroxocobalamin – Vitamin B12 in our product. Among all forms of Vitamin B12, Hydroxocobalamin has the best depot effect in brain cells. It binds particularly well to the body’s transport molecules, circulating in the blood for an extended period and spontaneously converting into one of the bioactive forms, Methylcobalamin or Adenosylcobalamin, in the organs (nerves, muscles, brain).
• Folic Acid: Contributes to normal amino acid synthesis and supports the dispositional provision of the essential amino acid methionine in the one-carbon cycle. Folic acid contributes to normal homocysteine metabolism, avoiding the risk factor of hyperhomocysteinemia. Folic acid contributes to normal psychological function, providing methionine and ensuring sufficient Ademetionine synthesis. Folic Acid contributes to the normal function of the immune system (according to Regulation (EU) No 432/2012). For your benefit, we use: QUATREFOLIC® – the glucosamine salt of 5-Methyltetrahydrofolate. Quatrefolic® is the so-called fourth generation of folates. Its high bioavailability avoids hyperhomocysteinemia. The Methyltetrahydrofolate reductase (MTHFR) catalyzes the synthesis of 5-Methyltetrahydrofolate, a methyl group donor for methionine synthesis. L-Methionine is a precursor of Ademetionine. The most common mutation variant in the Folic Acid is a point mutation at position 677. Homozygous (two identical alleles) carriers of the genetic trait, found in 5 to 20% of the population, experience a 50% loss of activity. This polymorphism in the MTHFR gene type 677T often leads to a mild to moderate increase in plasma homocysteine concentration, especially with low B12 or Folic Acid status. Hyperhomocysteinemia is an established risk factor for cardiovascular diseases, non-alcoholic fatty liver, and is proven to cause Alzheimer’s pathology.
• Vitamin B6: Contributes to normal psychological function. Vitamin B6 contributes to normal homocysteine metabolism and helps reduce tiredness and fatigue (according to Regulation (EU) No 432/2012). For your benefit, we use: VITAMIN B6 in our product in its activated form as PYRIDOXAL-5-PHOSPHATE (P5P), which breaks down Homocysteine.

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.

• Zinc: Contributes to protecting cells from oxidative stress (according to EU Regulation No 432/2012). Oxidative stress is the main cause of cell aging.

The use of EBOP® – Epigenetic Burnout Protector aims to provide a comprehensive protective shield for brain cells through these essential components, ensuring optimal cognitive function and promoting overall well-being.

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