Scientific Evidence

THE EFFICIENCY AND SAFETY OF MOLECULAR HYDROGEN IS PROVEN IN CLINICAL STUDIES

OVER 1,200+ SCIENTIFIC ARTICLES SUGGEST THAT HYDROGEN HAS THERAPEUTIC POTENTIAL IN OVER 170 DIFFERENT HUMAN DISEASE MODELS & ESSENTIALLY EVERY ORGAN OF THE HUMAN BODY 

Hydrogen is a colourless, tasteless and odourless gas. It is so small that it permeates the entire body and interferes with many biochemical reactions. It is the most powerful and selective antioxidant, and has anti-inflammatory and regenerative effects. It is natural to the body, formed by the bacteria of the intestinal tract, and is completely safe. There are no recorded side effects and the only intermediate product of its reactions is water, which hydrates the body.

Professor Taylor Lebrun, founder of Molecular Hydrogen Institute in Japan

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Anti-Oxidant

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are byproducts of energy metabolism during daily activities. ROS/RNS include superoxide anion (O2 -), hydroxyl radical (·OH), peroxyl radical (RO2·), alkoxyl radical (RO·), and nitric oxide radical (NO·). They play crucial roles under normal conditions in immune defense, signaling processes, and energy extraction from organic molecules. However, if the production of ROS and RNS exceeds the body's antioxidant capacity or if the antioxidant capacity decreases, oxidative stress occurs. Acute oxidative stress often occurs, for example, during a heart attack, heart and brain failure, organ transplantation, cardiac arrest, and bleeding during surgical procedures. Chronic ROS damage can occur in various pathological conditions such as malignancy, diabetes, chronic inflammatory diseases, atherosclerosis, neurodegeneration, and also in the aging process. Humans possess antioxidant defense systems to protect against the toxicity of free radicals. Antioxidants are divided into enzymatic and non-enzymatic types. Enzymatic antioxidants include superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), while non-enzymatic antioxidants include bilirubin, alpha-tocopherol (vitamin E), beta-carotene, and uric acid.

The effects of molecular hydrogen as an antioxidant are mainly mediated by the following mechanisms:

  • Molecular hydrogen has a lower molecular weight than other common antioxidants such as SOD, CAT, and α-tocopherol, which enables it to react selectively with strong oxidants and enables it to easily penetrate biological membranes such as the nuclear and mitochondrial membranes, without affecting metabolic reductive reactions. It is also able to penetrate the blood-brain barrier. Easily.

  • By stimulating nuclear factor erythroid 2-related factor 2 (Nrf2), which down-regulates and stimulates the expression of several antioxidant enzymes and proteasomes, Hg can increase heme-related oxygenase-1 (HO-1) expression. It also reduces the expression and production of ONOO-related genes and increases the activity of the antioxidant enzymes SOD, CAT, and Myeloperoxidase (MPO).

  • Molecular hydrogen can inhibit the apoptosis signal-regulated kinase 1 (ASK1) signaling pathway and the downstream signaling molecule p38 mitogen-activated protein kinase (p38-MAPK), thus inhibiting the activity of nicotinamide adenine dinucleotide (NADPH) oxidase and reducing the production of free radicals. Through these antioxidant effects, molecular hydrogen protects cells from lipid peroxidation and fatty acids.

Anti-inflammatory

The anti-inflammatory effects of molecular hydrogen are mainly mediated by the following mechanisms: It inhibits the synthesis and secretion of proinflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, nuclear factor NF-κB, and high mobility group box (HMGB-1), and increases the expression of anti-inflammatory factor IL-10, inhibits the secretion of chemokines including skin cell-derived chemokine, macrophage inflammatory protein (MIP)-1α, MIP-2, granulocyte attraction protein 1, and inhibits the secretion of intercellular fusion molecule-1 (ICAM-1) and intercellular aggregation-inducing factor Granulocyte-macrophage (GM-CSF) and granulocyte aggregation-stimulating factor (G-CSF).

It promotes macrophage ingestion of particles at sites of injury and inhibits the polarization of many granulosa cells and M1 macrophages to sites of injury. The anti-inflammatory effects of molecular hydrogen involve multiple signaling pathways. For example, stimulating the Nrf2/HO-1/HMGB-1 pathway ameliorates vascular dysfunction and lung injury caused by polyps. Inhibition of p38MAPK and c-Jun N-terminal kinase (JNK) attenuates lipopolysaccharide (LPS)-induced ALI. Autophagy-related pathways, such as mammalian target of rapamycin (mTOR)/transcription factor EB (TFEB) pathway and phosphatase and tensin homolog (PTEN)-induced kinase 1 (PINK1)/Parkin pathway, modulate the disturbance of vascular function in ALI and I/I injury. R in cardiac muscle.

Regulate Autophagy And Enhance Immunity

In eukaryotic cells, metabolic degradation is the degradation of intracellular components by the ubiquitin-proteasome system and liposomes. Autophagy (particularly macroautophagy) is defined as a lysosome-dependent catabolic process to maintain cellular homeostasis. However, when stress exceeds a critical duration or high intensity, it may have maladaptive effects, causing cell damage or even death. Emerging evidence suggests that hydrogen has dual roles in modulating autophagy (i.e., has a role in both promoting and inhibiting it).

Regulation Of Programmed Cell Death

Apoptosis (degradation) is a conventional form of programmed cell death that does not stimulate inflammatory responses. It is an evolutionarily conserved type of cell death that has significant effects on biological processes. The molecular mechanism underlying apoptosis involves the sequential activation of cysteine proteins, called caspases, and a series of pro-apoptotic and anti-apoptotic B-cell lymphoma family 2 (Bcl-2) proteins. In various disease and organ models, molecular hydrogen plays a protective role by regulating apoptosis.

It can prevent apoptosis by regulating apoptosis signaling pathways and apoptosis-related proteins, such as phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK3β), ASK1/JNK, Ras sarcoma (Ras)–extracellular signal-related kinase 1/2 (ERK1/2)–mitogen-activated protein kinase 1/2 (MEK1/2) and Akt pathways, and by suppression of caspase-3, -8, and -9 activation. and the X-linked Bcl-2/Bcl-2 (Bax) ratio. Molecular hydrogen also reduces the rate of apoptosis by reducing inflammation and oxidative damage and protects mitochondrial function. Inhibition of autophagy improves cell survival and prevents apoptosis. For example, in the myocardial I/R injury model, PINK-mediated autophagy attenuates inflammation and apoptosis. Accordingly, there is an overlap between molecular hydrogen, apoptosis, and autophagy.

Regulation Of Aging

Aging is a gradual loss of physiological function and is an inevitable process that ends in death. Aging is considered a major factor behind the emergence and development of various diseases, such as chronic obstructive pulmonary disease and idiopathic lung disease. Molecular hydrogen can reduce the expression of senescence-related proteins β-galactosidase, p53, and p21, suppress the down-regulation of Sirtuin 3 (Sirt3) expression, reduce oxidative stress damage, and thus prolong cell survival. Research has shown that molecular hydrogen produced by intestinal bacteria in the body prevents the increase of hydrogen peroxide (H2O2) by suppressing OH·-mediated intracellular lipid peroxide formation and cellular senescence, thus contributing to the suppression of aging. Genetic instability is one of the hallmarks of the aging process. By reducing oxidative DNA damage, hydrogen can help maintain genetic stability. For example, in cigarette smoke (CS)-induced emphysema, hydrogen led to a marked decrease in phosphorylated histone H2AX and 8-hydroxy-2′-deoxyguanosine (8-OHdG), which are markers of oxidative DNA damage. As a “philosophical molecule,” hydrogen can therefore be used to treat incurable diseases and aging.

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