Hydrogen Oxygen Inhalation

The air you breathe gets into every single cell in your body and affects its functions and power . Try Inhalation therapy of a specific natural elements that approved to clean your lung , empower your cells with clear oxygenation , heals any body inflammations , treat any pains and has anticancer effect . 

hydrogen water steam inhalation ...it is done throught special device for hydrogen inhalation . The importance of hydrogen can be understood by considering its influence on how the body detoxifies, improves brain health, promotes healthy aging and longevity, impacts post-exercise recovery, and mimics exercise.”

acting as a powerful antioxidant, supporting cognitive health and athletic performance, promoting healthy metabolism, and helping in the activation of the body’s natural detoxification system.

In the brain, do the benefits of hydrogen go beyond its neuroprotective effects. Interestingly, hydrogen’s benefits highlight the role it has in supporting homeostasis in the body.

People suffering from asthma may find that hydrogen therapy provides relief using a natural approach, rather than pharmaceuticals.

Mechanism of Action of Hydrogen

Eliminates reactive oxygen species (ROS)

Several key factors in cancer, including ROS and antioxidant enzymes, are regulated by hydrogen. ROS are a group of oxygen-containing molecules that can harm DNA/RNA and proteins resulting in severe damage and apoptosis. External chemical attacks or an imbalance of regulatory systems result in excessive ROS production. During cancer, H2 inhalation selectively scavenges most cytotoxic ROS, such as hydroxyl radicals (OH) and proximities (ONOO), which play a causal role in tumor cell proliferation, invasion, and metastasis. By increasing the expression of antioxidant enzymes (SOD, HO-1, and Nrf2), hydrogen treatment enhances the elimination of ROS (Li et al., 2019)

Modulates Inflammation

Hydrogen can stop the growth and spread of tumors and lessen the negative effects of chemotherapy and radiotherapy by controlling inflammation. Tumor necrosis factors (TNFs), which are released by macrophages, and interleukins (ILs), which are released by leukocytes, are examples of typical inflammatory cytokines. Both have been linked to the development & spread of cancer, and hydrogen gas can block both ILs (especially IL-8, IL-1β) and TNFs (especially TNF-α) (Li et al., 2019).

Enhances/Restores Mitochondrial Function

H2 stimulates the gene expression of (PGC-1α) (Kamimura et al., 2016). Hydrogen can permeate into lymphocyte mitochondria as an antioxidant gas and selectively scavenge oxygen free radicals (Ohta, 2012). In 2019, Akagi and Baba observed an increase in T cells of cancer patients due to hydrogen inhalation. They further investigated whether the rise in T cell level was due to mitochondrial restoration. They were able to prove an increase in mitochondria of stage four lung cancer patients by using CoQ10 as a marker for mitochondrial restoration (Akagi and Baba, 2022).

Boosts Immune System

Hydrogen inhalation can be used for immune reconstitution. After 2 weeks of inhalation of a mixture of hydrogen and oxygen (66.7%: 33.3%) four hours per day; functional, cytotoxic, and helper T cells, NKT cells, Th1, natural killer cells, and Vδ2 cells increased in number while exhausted and senescent cytotoxic T cells decreased and restored back to the normal level (Chen et al., 2020).

Genes and Signaling Pathways associated with Lung cancer

Lung cancer accounts for 18% of all cancer-related deaths in the world (Sung et al., 2021). About 85% of lung cancers are non-small cell lung cancers (NSCLC) (Nawaz and Webster, 2016). Tobacco smoke is the cause of 85% of lung cancers. The smoke results in invasive and pre-invasive lesions, furthermore metastasis due to the gradual accumulation of irregularities in the genetic and epigenetic system. About one-fifth of the adenocarcinomas are not related to tobacco smoke at all. (Sun et al., 2007).

           The carcinogens in tobacco smoke are significantly linked to the development of lung cancer and cause genetic changes by forming DNA adducts (Hecht, 1999). However, less than 20% of smokers develop lung cancer, suggesting a genetic predisposition to the disease (Sun et al., 2007).

Immunotherapy for Lung Cancer

In cases of advanced NSCLC, when patients no longer respond to targeted therapy, Immunotherapy or a combination of chemotherapy with immunotherapy is employed (Lung cancer – Non-Small Cell- Types of Treatment, 2022).

PD-1 Pathway Inhibitors

Many cancers overexpress programmed cell death-ligand (PD-L1). The expression of Certain ligands on the surface of tumor cells helps them dodge the T cells by their action on particular immune checkpoint pathways. One such pathway is programmed cell death (PD-1). PD-1 acts as an immune checkpoint receptor on the membrane of T cells. (El-Guindy et al., 2018). Inhibition of these checkpoints (PD-1/PD-L1) with immune checkpoint inhibitors (ICIs) prevents the interaction with the receptor on T cells and the ligand on cancerous cells (Rittmeyer et al., 2017) Herbst, 2016). This inhibition has improved the prognosis of many cancers that are extremely difficult to treat. It has provided dramatic results in the treatment of small cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC) (Paz-Ares et al., 2019).

Certain tumors can be effectively treated by therapies inhibiting PD-1 that leads to an anticancer immune response by rejuvenating T cells as PD-1 is believed to suppress signal transduction via the T cell receptor (TCR). Hui et al. discovered that PD-1 acts through CD28 instead of TCR. Kamphorst et al. also discovered the same during their experiments on viral infections in mice. Lung cancer patients who received PD-1 therapy also had an increased number of CD8 T cells. CD 28/B7 pathway plays an important role in CD8 T cell proliferation while treating cancer patients with PD-1 therapy ((Kamphorst et al., 2017).

Hydrogen also helps in the restoration of CD8+ T cells by stimulation of mitochondrial PGC-1α. Nivolumab belongs to PD-1 inhibitors and exerts synergistic effects with mitochondrial stimulants. Hydrogen was studied for its synergistic effects on the activity of nivolumab in lung cancer patients. 56 patients receiving Nivolumab were included in the study, out of which 42 patients received hydrogen gas in combination with the drug. The overall survival (OS) of patients receiving combination therapy was significantly longer as compared to the control group. Exhausted CD8+ T cells lead to a poor prognosis in OS. Improvement in mitochondrial function, marked by higher CoQ10, could be linked with improvement in OS. The clinical efficacy of nivolumab is enhanced by the improvement of the mitochondrial function of CD8+ T cells (Akagi and Baba, 2022).

CD47-SIRPα pathway Inhibitors

 Another important immune checkpoint for lung cancer is the CD47-SIRPα axis. Zhao et al. discovered the overexpression of CD-47 in NSCLC tumor tissues. Potent antitumor activity of SIRPα–Fc mAb against NSCLC has also been proven by its targeting of CD-47 (Figure 2). It also triggered autophagy via Akt/mTOR pathway inactivation and acted as a cytoprotectant in NSCLC cells. Human trials for the efficacy of CD-47 inhibitors in NSCLC have not been conducted yet (Catalán et al., 2020).

Targeted Therapy for Lung Cancer 

Targeted therapy for lung cancer is directed against the specific proteins and gene targets that contribute to cancer growth and survival (Lung cancer – Non-Small Cell- Types of Treatment, 2022).

Tumor Suppressors 

PD-L1 expression is reduced by preserved p53 (pro-apoptotic protein) role. Mutations in the gene encoding for p53 result in loss of its function and are linked with higher expression of PD-L1. When mutations in KRAS and TP53 (p53 encoder) occur at the same time in NSCLC, these effects are intensified.

Mutations in Serine/threonine kinase 11 (STK11)- a tumor suppressor- are also found in lung adenocarcinoma, especially when KRAS mutations are also present. PD-L1 expression is low or non-existent in case of mutation or loss of STK11, resulting in impaired efficiency of PD-1/PD-L1 targeting ICIs (Lamberti et al., 2020).

 RAS and Mitogen-Activated Protein Kinase 

About one-third of lung adenocarcinomas have activating mutations in Kirsten Ras Sarcoma Viral Oncogene Homolog (KRAS). RAS activation stabilizes mRNA of PD-L1 and inhibits tristetraprolin, resulting in increased expression of PD-L1 in cell lines of lung cancer.

PI3K/Akt/mTOR 

PI3K/Akt/mTOR pathway is distorted in NSCLC as well as numerous types of cancers. Under normal conditions, this pathway causes autophagy of damaged self-cells. Activated mTOR leads to increased PD-L1 protein.

 Receptor Tyrosine Kinases 

The expression of PD-L1 on NSCLC cells is induced by ligand binding and subsequent activation of the epidermal growth factor receptor (EGRF). Lung adenocarcinomas have mutated EGRF in 10-20% of cases. This mutation is usually present in nonsmokers, females and Asians. Mutated EGFR can intensify the expression of PD-L1. EGFR inhibitors are included in targeted therapy for lung cancer (Lamberti et al., 2020).

Upregulation of CD47 expression was also observed in NSCLC cell lines with EGFR mutations (Catalán et al., 2020)

Genes and pathways targeted by Hydrogen?

H2 directly scavenges hydroxyl radicals (OH). H2 also has antioxidant, anti-inflammatory, and apoptotic effects by indirectly regulating gene expression. H2 may have antitumor properties through these direct and indirect actions

 In endometrial cancer, hydrogen protects normal cells while destroying cancerous cells via the pyrotrophic pathway. This pathway acts via the formation of Terminal protein gasderminn D (GSDMD) (Yang et al., 2020).

Hydrogen Inhalation in Lung cancer with Brain Metastasis

Although brain metastases are a frequent consequence of a variety of malignancies, patients with lung cancer are more likely to experience them than other cancer patients. Brain metastases are present in about 10% of individuals with newly diagnosed NSCLC. Lung cancer is the main tumor in between 40 and 50 percent of patients with brain metastases. Treatment choices for patients with brain metastases are changing for a variety of reasons, even though there are well-established management strategies for these conditions. First, many patients with advanced NSCLC live for several years, giving brain metastases and side effects from earlier treatments for brain metastases more time to develop. Second, patients with more prevalent driver mutations, notably activating mutations of the EGFR and anaplastic lymphoma kinase (ALK) rearrangements, are more likely to develop brain metastases. Third, more recent targeted treatments for EGFR and ALK have shown significantly higher intracranial efficacy, allowing for cautious consideration of systemic therapy as a preferred front-line strategy over previously recommended local treatment. (Yuan et al., 2022).

Hydrogen gas is an excellent candidate to be used in NSCLC that’s metastasized to the brain because it can easily cross the blood-brain barrier which is a limitation of standard chemotherapy. Hydrogen also shows neuroprotective effects by diminishing COX2 activity (Hou et al., 2012) or by antiapoptotic protein kinase activation (Yang et al., 2018). Inhibition of JNK and caspase-3 (proapoptotic factors) is caused by H2 (Sun et al., 2011) It downregulates many proinflammatory cytokines as well (Zhang et al., 2012).

One case study on a 44-year-old female presented evidence for the use of hydrogen monotherapy in controlling tumors. The patient initially presented with lung cancer with multiple metastases in November 2015. She received oral targeted drugs after brain metastases removal. Most of the lesions remained stable for more than 2 years. Her condition started to get worse in March 2018. Cancer had metastasized to multiple organs including the brain, adrenal gland, liver, and bones. There was an accumulation of hydrocephalus in the third and lateral ventricles (Figure 4A). The patient refused radiotherapy and brain surgery at this point. She signed informed consent for hydrogen inhalation therapy alone. She inhaled a mixture of hydrogen (67%) and oxygen (33%) using an AMS-H-03 hydrogen oxygen nebulizer from China. She experienced relief in her symptoms during the first month of hydrogen therapy. Hydrocephalus accumulation significantly reduced in the third and lateral ventricles and the brain tumors showed a significant reduction in size after four months of hydrogen monotherapy (Figure 4B). One year into the therapy, all brain tumors disappeared (Figure 4C). Liver and lung metastases showed no significant change. This data proved that hydrogen therapy helped in prolonging the survival time after the failure of standard treatments (Chen et al., 2019). 

The possible mechanism of action of hydrogen for the control of brain metastasis in NSCLC was through MAPK, TCF/LEF-1, DVL-1/3 of Wnt/β-catenin and SIRT1 (Chen et al., 2019).

 what is the Brown Gas ?

It is oxygen hydrogen mix , it is better than inhalation of hydrogen gas only . in a percentage of 30% oxygen 70% hydrogen

in Nutrimedicine , we offer the brown gas inhalation of 1500 ml/min which is the best safe effective flow rate for health

 How long is the Hydrogen session?

It is one hour session per week

How many session should I receive ?

if it is for better health , energy and brain clarity one session biweekly is enough

if it is for asthma or brinchitis one session every 3 days till improvement ( usually after the 4th session you will get full recovery)

If it is for cancer or chronic illness one session per week for 12 - 15 session is required every year .

Can I combine Hydrogen inhalation therapy with infra red sauna or red light therapy ?

Yes , you can and it will get you better results

Reserve your hydrogen inhalation session now

It is one hour session that will get you a better life

contact us +14389244664 - info@nutrimedicine.center