QoL Cancer Research Results
QoL, Quality of Life: Click to Expand ⟱
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Quality of Life
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Scientific Papers found: Click to Expand⟱
Glycolysis↓, 3BP targets cancer cells’ energy metabolism, both its high glycolysis (“Warburg Effect”) and mitochondrial oxidative phosphorylation.
mt-OXPHOS↓,
ATP↓, This inhibits/ blocks total energy production leading to a depletion of energy reserves. Moreover, 3BP as an “Energy Blocker”, is very rapid in killing such cells.
selectivity↑, 3BP at its effective concentrations that kill cancer cells has little or no effect on normal cells.
toxicity↝, The results obtained hold promise for 3BP as a future cancer therapeutic without apparent cyto-toxicity when formulated properly.
OS↑, The patient (Fig. 5) was able to survive a much longer period than expected with an improved quality of life, which is clearly attributable to the treatment with 3BP.
QoL↑,
toxicity↑, German police took action on 4 August after two patients from the Netherlands and one from Belgium died shortly after undergoing treatment at the Biological Cancer Centre, run by alternative practitioner Klaus Ross in the town of Brüggen, Germany
Glycolysis↓, It is believed to "starve" tumor cells to death by inhibiting glycolysis, the breakdown of glucose molecules to provide cells with energy.
eff↑, experiments on human cancer cell lines showed that combining another chemotherapeutic with 3BP increased its efficacy.
OS↑, the patient "was able to survive a much longer period than expected with an improved quality of life, which is clearly attributable to the treatment with 3BP,
QoL↑,
toxicity↝, Vogl says doctors should "absolutely" not perform systemic infusions, in which the drug circulates through the entire body. "
ChemoSen↑, This meta-analysis indicated that the combination of Astragalus-based Chinese medicines and chemotherapy may increase the efficiency of tumor response rate (TRR) for the treatment of CRC patients
chemoP↑, Astragalus-based product with chemotherapy group was found to have lower nausea and vomiting. Astragalus-based product with chemotherapy treatment suffered with a lower diarrhea
QoL↑, The results of this meta-analysis of 1,409 patients showed that Astragalus-based product combined with chemotherapy in the treatment of CRC may increase the efficiency of TRR, improve their life quality, and reduce some side effects
RenoP∅, Hepatic dysfunction (RR: 0.76; 95% CI: 0.53–1.09; p = 0.13) and renal dysfunction (RR: 0.95; 95% CI: 0.51–1.76; p = 0.87) were similar between two groups.
hepatoP∅, Astragalus-based product with chemotherapy had no improvement in the hepatic and renal dysfunction when compared with treatment of chemotherapy alone.
AntiTum↑, APS has been increasingly used in cancer therapy owing to its anti-tumor ability as it prevents the progression of prostate, liver, cervical, ovarian, and non-small-cell lung cancer by suppressing tumor cell growth and invasion and enhancing apoptosi
TumCG↓,
TumCI↓,
Apoptosis↑, after APS treatment, the apoptosis of HepG2 cells is accelerated (57).
Imm↑, APS enhances the sensitivity of tumors to antineoplastic agents and improves the body’s immunity
Bcl-2↓, Huang et al. proposed that APS induces H22 (a hepatocellular cancer [HCC] cell line) apoptosis by downregulating Bcl-2 and upregulating Bax expression (56).
BAX↑,
Wnt↓, downregulating the Wnt/β-catenin signaling pathway.
β-catenin/ZEB1↓,
TumCG↓, APS effectively inhibited the growth of MDA-MB-231 (a human breast cancer [BC] cell line) graft tumor (58)
miR-133a-3p↑, apoptosis rate of human osteosarcoma MG63 cells increased owing to the upregulation of miR-133a and inactivation of the JNK signaling pathways (71).
JNK↓,
Fas↑, Li and Shen found that APS can induce apoptosis by activating the Fas death receptor pathway.
P53↑, Zhang et al. showed that APS could activate p53 and p21 and inhibit the expression of Notch1 and Notch3 in vitro, ultimately inhibiting cell proliferation and promoting their apoptosis
P21↑,
NOTCH1↓,
NOTCH3↓,
TumCP↓,
TumCCA↑, Liu et al. found that APS induced the cell cycle of bladder cancer UM-UC-3 to stop in the G0/G1 phase, thus inhibiting its proliferation
GPx4↓, APS was found to reduce GPX4 expression, inhibit the activity of the light chain subunit SLC7A11 (xCT), and promote the formation of BECN1-xCT complex by activating AMPK/BECN1 signaling.
xCT/SLC7A11↓,
AMPK↑,
Beclin-1↑,
NF-kB↓, APS could control the proliferation of lung cancer cells (A549 and NCI-H358 cells) by inhibiting the NF-κB signaling pathway (97)
EMT↓, APS treatment led to reduced EMT markers (vimentin, AXL) and MIF levels in cells.
Vim↓,
TumMeta↓, APS inhibits Lewis lung cancer growth and metastasis in mice by significantly reducing VEGF and EGFR expression in cancerous tissues
VEGF↓,
EGFR↓,
eff↑, Nano-drug delivery systems can increase efficiency and reduce toxicity
eff↑, Jiao et al. developed selenium nanoparticles modified with macromolecular weight APS and observed positive results in hepatoma treatment
MMP↓, Subsequent investigations revealed that APS can decrease the ΔΨm values and Bcl-2, p-PI3K, P-gp, and p-AKT levels while elevating Bax expression.
P-gp/ABCB1↓,
MMP9↓, downregulation of MMP-9 expression,
ChemoSen↑, Li et al. observed that APS could enhance the sensitivity of SKOV3 ovarian cancer cells to CDDP treatment by activating the mitochondrial apoptosis pathway and JNK1/2 signaling pathway
SIRT1↓, APS significantly suppressed SIRT1 and SREBP1 expression, decreased cholesterol and triglyceride levels in PC3 and DU145, and attenuated cell proliferation.
SREBP1/SREBF1↓,
TumAuto↑, APS can induce autophagy in colorectal cancer cells by inhibiting the PI3K/AKT/mTOR axis and the development of cancer cells.
PI3K↓,
mTOR↓,
Casp3↑, Shen found that APS elevated caspase-9, caspase-3, and Bax protein levels, decreased Bcl-2 protein expression, and inhibited CD133 and CD44 co-positive colon cancer stem cell proliferation time
Casp9↑,
CD133↓,
CD44↓,
CSCs↓,
QoL↑, QOL was significantly improved as indicated by the reduction in pain and improvement in appetite
ChemoSen↑, review aims to determine the clinical efficacy and safety of Astragalus Polysaccharide Injection (APS) combined with chemoradiotherapy for cervical cancer based on existing data.
eff↑, APS combined with chemoradiotherapy improved the objective response rate (ORR, RR = 1.43, 95% CI: 1.24–1.64) and disease control rate (
RadioS↑, APS can enhance the clinical efficacy of radiotherapy and chemotherapy for cervical cancer, respectively.
CEA↓, APS further reduced tumor marker levels: CEA (MD = −1.24, 95% CI: −1.58 to −0.89, p < 0.00001; heterogeneity: χ2 = 1.75, p = 0.19, I2 = 43%), SCC (
Wnt↓, Specifically, APS inhibits the cisplatin resistance pathway and regulates the cell cycle by suppressing the Wnt/β-catenin pathway via the PPARD/CDC20 axis (Liu et al., 2025)
β-catenin/ZEB1↓,
γH2AX↑, APS also influences autophagy and upregulates γH2AX expression, thereby enhancing cervical cancer sensitivity to radiotherapy
ER Stress↑, APS alleviates endoplasmic reticulum stress and promotes mitochondrial autophagy, thereby enhancing apoptosis and mitigating cisplatin-induced toxicity
mt-TumAuto↑,
QoL↑, suggested that APS combination therapy improves short-term clinical efficacy, quality of life, and immune function
Imm↑,
AntiCan↑, Preclinical studies indicate that APS exerts significant anti-liver cancer effects through multiple biological actions, including the promotion of apoptosis, inhibition of proliferation, suppression of epithelial–mesenchymal transition, regulation of
Apoptosis↑,
TumCP↓,
EMT↓,
Imm↑, improving host immune response
ChemoSen↑, APS exhibits synergistic effects when combined with conventional chemotherapeutics and interventional treatments such as transarterial chemoembolisation, improving efficacy and reducing toxicity.
BioAv↓, limitations such as low bioavailability and a lack of large-scale clinical trials remain challenges for clinical translation.
TumCG↓, APS significantly inhibited tumour growth in H22-bearing mice with a dose-dependent effect (100, 200, 400 mg/kg), with the 400 mg/kg group achieving a tumour inhibition rate of 59.01%
IL2↑, APS enhance the thymus and spleen indices and elevates the key cytokines, including IL-2, IL-12, and TNF-α.
IL12↑,
TNF-α↑,
P-gp/ABCB1↓, APS reversed chemoresistance by downregulating P-glycoprotein and MDR1 mRNA expression
MDR1↓,
QoL↑, These effects contributed to improved treatment tolerance and enhanced quality of life [39].
Casp↑, APS can activate both the intrinsic and extrinsic apoptotic pathways, leading to caspase activation and DNA fragmentation
DNAdam↑,
Bcl-2↓, Mechanistically, APS downregulate antiapoptotic proteins such as Bcl-2 while upregulating proapoptotic proteins such as Bax and cleaved caspase-3.
BAX↑,
MMP↓, APS have been shown to disrupt the mitochondrial membrane potential and promote the release of cytochrome c, thereby enhancing apoptotic cascades in hepatocellular carcinoma models.
Cyt‑c↑,
NOTCH1↓, APS (0.1, 0.5, and 1.0 mg/mL) were shown to reduce both mRNA and protein levels of Notch1 in a concentration-dependent manner.
GSK‐3β↓, APS significantly inhibited the proliferation of HepG2 cells by downregulating the expression of glycogen synthase kinase-3β (GSK-3β), with 200 μg/mL being the most effective concentration.
TumCCA↑, APS exerted these effects by inducing cell cycle arrest at the G2/M and S phases, thereby impeding tumour cell proliferation [35].
GSH↓, HepG2 cells. APS also reduced intracellular glutathione (GSH) levels, increased reactive oxygen species (ROS) and lipid peroxidation levels, and elevated intracellular iron ion concentrations—all in a dose-dependent manner.
ROS↑,
lipid-P↑,
c-Iron↑,
GPx4↓, APS treatment led to the downregulation of GPX4 and upregulation of ACSL4, indicating that APS promotes ferroptosis in liver cancer cells.
ACSL4↑,
Ferroptosis↑,
Wnt↓, inhibit the expression of key proteins involved in the Wnt/β-catenin signalling pathway
β-catenin/ZEB1↓,
cycD1/CCND1↓, by downregulating the key oncogenic targets, including β-catenin, C-myc, and cyclin D1, which subsequently reduces Bcl-2 expression and activates the apoptotic cascade in HepG2 liver cancer cells.
Akt↓, It also inhibited the Akt/p-Akt signalling pathway.
PI3K↓, APS inhibit the PI3K/AKT/mTOR signalling pathway, which is a central negative regulator of autophagy.
mTOR↓,
CXCR4↓, PS upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker vimentin and the chemokine receptor CXCR4 at both mRNA and protein levels, suggesting that APS suppress liver cancer cell growth and metastasis by inhibiting
Vim↓,
PD-L1↓, APS interfere with immune checkpoint signalling by downregulating Programmed death-ligand 1 (PD-L1) expression on tumour cells.
eff↑, The preparation of polysaccharide–SeNP composites typically involves using sodium selenite (Na2SeO3) as the precursor and ascorbic acid (Vc) as the reducing agent, with synthesis carried out via a chemical reduction method in a polysaccharide solutio
eff↑, Mechanistic investigations revealed that AASP–SeNPs elevated intracellular ROS levels and reduced the mitochondrial membrane potential (∆Ψm).
ChemoSen↑, APS enhance doxorubicin-induced endoplasmic reticulum (ER) stress by reducing O-GlcNAcylation levels, thereby promoting apoptosis of liver cancer cells.
ChemoSen↑, APS inhibited BEL-7404 human liver cancer cell growth in a concentration-dependent manner and showed stronger cytotoxicity when combined with cisplatin.
chemoP↑, APS protects against chemotherapy-induced liver injury, particularly that caused by CTX, through antiapoptotic mechanisms
fatigue↓, meta-analysis showed that the addition of Astragalus membranaceus to the control group was effective in reducing cancer-related fatigue
QoL↑, The current evidence is supportive of the efficacy of Astragalus membranaceus in patients with cancer-related fatigue and their quality of life,
Dose↝, Wang et al. study 16 showed that both doses of 500 mg and 250 mg were effective in improving fatigue.
*cachexia↓, The results of this process favored L-carnitine supplementation in patients with cancer-related cachexia.
*Apoptosis↓, inhibiting apoptosis or reversing inflammatory processes.
*Inflam↓,
QoL↑, This treatment increased plasma-free carnitine concentrations and significantly improved fatigue, which was assessed using the functional assessment of cancer therapy, fatigue, and quality of life questionnaire, as well as quality-of-life measu
Dose↝, placebo-controlled trial, in which 2 g per day of LC was administrated orally for four weeks among eligible patients.
Weight↑, advanced pancreatic cancer received either LC (4 g/day orally) or a placebo for 12 weeks. The results showed that body mass index, nutritional status (body cell mass and body fat), and quality-of-life parameters increased
OS↝, There was an insignificant increase in overall survival, a decline in length of hospital stays, and decrease in fatigue among the LC-treated patients.
fatigue↓,
eff↝, some dietary factors, such as food intake restriction and intake of LC and certain micronutrients (vitamin C, vitamin B6, and iron, which are required as cofactors for endogenous LC biosynthesis) may have some effects on the efficacy of LC sup
Weight↑, During treatment body-mass-index increased by 3,4 ± 1,4% under L-Carnitine and decreased (−1,5 ± 1,4%) in controls
QoL↑, Moreover, nutritional status (body cell mass, body fat) and quality-of-life parameters improved under L-Carnitine.
OS↑, There was a trend towards an increased overall survival in the L-Carnitine group (median 519 ± 50 d versus 399 ± 43 d, not significant) and towards a reduced hospital-stay (36 ± 4d versus 41 ± 9d,n.s.).
fatigue↓, carnitine supplementation has been tested in preliminary studies concerning human cachexia, resulting in improved fatigue and quality of life.
QoL↑,
*GSH↑, l-carnitine treatment improved the tumor-induced decrease in muscular glutamate and glutathione levels and the increased plasma glutamate levels in tumor-bearing rodents
Dose↝, Significant improvements in fatigue were also observed in a randomized phase III clinical trial, in which l-carnitine (4 g/day) was orally given to patients with advanced cancer
*QoL↑, Some studies reported that aromatherapy significantly improved the QoL of PWD and relieved the distress and burden of caregivers, promoted a positive experience among caregivers
*Mood↑,
Imm↑, In this way, β-glucans can be exploited as adjuvant cancer therapy, in particular by a synergic action with chemotherapy or immunotherapy
ChemoSen↑, t has been demonstrated that the association of β-glucans with chemotherapy is able to enhance cytotoxicity and can improve patient clinical outcome.
LDL↑, mechanism that rules the cholesterol-lowering effects of β-glucans takes place through the gut microbiota and the production of short-chain fatty acids (SCFAs, for example propionate).
GutMicro↑,
TumCP↓, In the oncological field, β-glucans can stimulate the innate and adaptive immune response, inhibit the proliferation of cancer cells, promote apoptosis and block the angiogenesis [24–26].
Apoptosis↑,
angioG↓,
QoL↑, In this way, β-glucan demonstrate synergic effect with antitumor mAbs agents and they can have an important role to improve the therapeutic effects and the quality of life in cancer patients.
OS↑, Median survival was significantly longer in the lentinan group than in the control group (297 days vs. 199 days, p = 0.028).
QoL↑, Total QOL score, especially appetite and sleep quality, was significantly improved with the administration of lentinan.
QoL↑, Bevacizumab may improve quality of life, but not overall survival in glioblastoma: an epidemiological study
OS∅,
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NSCLC, |
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PC, |
NA |
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Trial, |
HCC, |
NA |
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Dose↝, Huachansu was administered intravenously for 14 days followed by 7 days off (1 cycle). 10 (level 1), 20 (level 2), 40 (level 3), 60 (level 4), and 90 (level 5) mL/m2.
toxicity↓, Mild adverse events were observed at each dose level; all were grade I or II and no grade III or IV toxicities were observed.
other↓, One of these patients (with hepatocellular cancer) had 20% regression (duration = 11 months) (dose level 1).
QoL↑, Quality of life improved for patients with stable disease.
OS?, Six patients had prolonged stable disease or minor tumor shrinkage.
AntiTum↑, Notably, multiple metabolites in BJ demonstrate anti-tumor effects through various signaling pathways
other↝, well-known metabolites such as Brusatol and Bruceine D.
ChemoSen↑, Multiple clinical studies have demonstrated that the co-administration of BJ with other pharmacological agents in individuals with cancer can enhance therapeutic efficacy, improve patients’ quality of life, and mitigate adverse reactions
QoL↑,
chemoP↑,
*Inflam↓, Brusatol (Zhou et al., 2018) has been shown to reduce inflammation in RAW264.7 cells
NF-kB↓, nhibition of NF-ΚB and ras homolog gene families, member A/rho-associated kinase (RhoA/ROCK) signaling pathways.
TumCP↓, Brusatol has exhibited notable effects in inhibiting proliferation, invasion, and metastasis in a murine model of liver transplantation tumor in humans.
TumCI↓,
TumMeta↓,
Hif1a↓, In colorectal cancer, Brusatol functions by facilitating the degradation process of hypoxia-inducible factor-1 (HIF-1α) (Oh et al., 2017), mediated by prolyl hydroxylase (PHD), while concurrently suppressing NRF2
NRF2↓,
STAT3↓, impede the proliferation and migration of osteosarcoma cells through the inhibition of the STAT3 signaling pathway.
COX2/PTGS2↓, BJO (Lou et al., 2010) induced apoptosis of T24 bladder cancer cells, possibly by upregulating caspase-3 and caspase-9 expression by activating the caspase pathway and inhibiting the NF-ΚB and Cyclooxygenase-2 (COX-2).
Casp3↑,
Casp9↑,
ROS↑, Figure 10
EGFR↓,
NRF2↑, brusatol and dehydrobruceine B (DHB) effectively increased the concentration of reactive oxygen species (ROS) by activating the NRF2 pathway
Apoptosis↑, BJOE induced apoptosis in Jurkat cells and were suggestive of
intrinsic apoptotic induction
Akt↓, BJOE inhibited Akt (protein kinase B) activation and upregulated its downstream targets p53 and FoxO1 (forkhead box gene, group O-1) to initiate apoptosis
P53↑,
FOXO1↑,
GSK‐3β↑, The activation of GSK3β was also involved.
TumVol↓, In a 96-case clinical trial, BJOE treatment reduced tumor size and improved the quality of life for patients with gastrointestinal cancer and cervical cancer [18].
QoL↑,
BBB↑, As shown in pharmacokinetic studies, BJOE crossed the blood-brain barrier
OS↑, In another 100-case clinical trial, BJOE prolonged the survival of patients with brain meta-
stases from lung cancer [24].
Dose↝, Currently, BJOE is intravenously administered for the clinical treatment of lung cancer [25-28]
and gastric cancer [29-31]
MMP↓, MMP collapse and ROS production in Jurkat cells were also observed following BJOE treatment.
ROS↑,
XIAP↑, we found that BJOE targeted Akt to stimulate FoxO1 and XIAP to induce apoptosis.
Casp9↑, BJOE promoted the activation of caspase-
9, caspase-8 and caspase-3.
Casp8↑,
Casp3↑,
cl‑PARP↑, The cleavage of PARP proteins
was also observed.
TumCCA↑, the sub-G1 phase cell percentages increased in all five samples in a BJOE concentration-dependent manner.
Dose↝, 100-mg dose of a dry extract of U. tomentosa three times per day in patients with advanced solid tumors
QoL↑, Treatment improved the patients' overall quality of life (p=0.0411) and social functioning
fatigue↓, Use of cat's claw might be beneficial in patients with advanced cancer by improving their quality of life and reducing fatigue.
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CRC, |
NA |
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Review, |
HNSCC, |
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EGFR↓, Cetuximab is an epidermal growth factor receptor (EGFR) inhibitor with the following FDA-approved indications: colorectal cancer, metastatic, KRAS wild-type (without mutation), and head and neck cancer (squamous cell).
OS↑, Colorectal cancer, metastatic, KRAS wild-type (without mutation) - Cetuximab improves both overall survival and progression-free survival and preserves quality-of-life measures for patients with colorectal cancer
QoL↑,
Dose↝, administration of the drug is via IV infusion with a loading dose lasting over 2 hours, weekly maintenance dose over 1 hour.
eff↑, Combining cetuximab with immunotherapy and other targeted agents further expands the therapeutic landscape, offering renewed hope for mCRC patients who face the development of resistance to conventional therapies.
Half-Life↑, Pharmacokinetic differences include cetuximab’s non-linear clearance and longer half-life, while panitumumab exhibits both linear and non-linear clearance mechanisms and a shorter half-life [23].
Half-Life↑, These studies revealed that clearance from the bloodstream was relatively slow, with a median half-life of 7 days
EGFR↓, Cetuximab also aids in downregulating EGFR-dependent signaling by promoting the internalization of EGFR
OS↑, Cetuximab improved OS and PFS compared with best supportive care (BSC), while maintaining quality of life [
QoL↑,
eff↑, The BEACON trial illustrated that the combination of BRAF inhibition and anti-EGFR therapy using cetuximab yielded better results compared with irinotecan-based chemotherapy in refractory BRAF V600E mCRC patients.
KRAS↓, nhibition of KRAS G12C and Cetuximab
*Dose↝, The CP recipe includes around fifty (some times more depending on the brand) bioactive herbs (with the major ingredient, Amla or Indian gooseberry) and herbal extracts, which are processed by the traditional Ayurvedic pharmaceutical process, and the
*antiOx↑, Compelling evidences suggest that CP possess rich nutraceutical value along with potential antioxidant, anti-inflammatory, and immunomodulatory properties
*Inflam↓,
*Imm↑, In a clinical study conducted on the 15–75 years age group (with no underlying organic disease), CP was found to reduce the disease symptoms of seasonal influences, improved pulmonary functions, quality of life, and provided 3-times immunity with no
*QoL↑,
*Dose↑, In Ayurvedic Pharmacopoeia of India, the standard dose of CP is mentioned 12 g twice a day
*Dose↝, generally 12–28 g per day, with lukewarm milk or water
*Dose↝, School going healthy children between ages of 5-12 years were randomized to receive orally daily either CP (approx. 6 g) followed by a cup of milk (100 – 200 ml) or cup of milk only twice a day while continuing with their normal/routine diet.
*QoL↑, Regular consumption of CP for a period of six months could significantly improve immunity, energy levels, physical fitness, strength, stamina and quality of life in school going healthy children.
*Imm↑, Results of immunity (episodes of infections or allergy related conditions) showed more than 2 times protection from immunity related illness in CP Group
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AD, |
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Park, |
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*AntiAge↑, supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics.
*cardioP↑, Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10
*Inflam↓, Administration of CoQ10 in doses ranging from 60 to 500 mg/day for a 1-week to 4-month intervention period significantly decreased production of inflammatory cytokines
*antiOx↑,
*lipid-P↓, The concentrations of CoQ10 in the plasma of elderly people are positively correlated with levels of physical activity and cholesterol concentrations (Del Pozo-Cruz et al., 2014a,b), as well as with lower lipid oxidative damage.
*QoL↑, Older individuals given a combination of selenium and CoQ10 over a 4-year period reported an improvement in vitality, physical performance, and quality of life
*neuroP↑, health benefits in elderly people by preventing chronic oxidative stress associated with cardiovascular and neurodegenerative diseases
*Dose↝, the highest dose for CoQ10 supplementation is 1200 mg daily according to well-designed randomized, controlled human trials, although doses as high as 3000 mg/day have been used in shorter clinical trials
*BP↓, These authors interpreted the results to indicate a significant reduction in systolic blood pressure without improvements in other CVD risk factors, such as diastolic blood pressure, total cholesterol, LDL- and high-density lipoprotein (HDL)-choleste
*IGF-1↑, elderly healthy participants who received selenium and CoQ10 supplementation for over 4 years, an increase in insulin-like growth factor 1 (IGF-1) and postprandial insulin-like growth factor-binding protein 1 (IGFBP-1) levels
*IGFBP1↑,
*eff↑, A combination of CoQ10 with red yeast rice, berberina, policosanol, astaxanthin, and folic acid significantly decreased total cholesterol, LDL-cholesterol, triglycerides, and glucose in the blood while increasing HDL-cholesterol levels
*LDL↓,
*HDL↑,
*eff↑, 60 patients suffering from statin-associated myopathy were enrolled in a 3-month study to test for efficacy of CoQ10 and selenium treatment. A consistent reduction in their symptoms, including muscle pain, weakness, cramps, and fatigue was observed
*other↑, Because of its capacity to reduce the side-effects of statins, CoQ10 has been proposed to prevent and/or slow the progression of frailty and sarcopenia in the elderly chronically treated with statins.
*RenoP↑, experiments performed on rats showed a promising protective effect of ubiquinol in the kidneys
*ROS↓, 65 patients undergoing hemodialysis, supplementation with high amounts of CoQ10 (1200 mg/day) lowered F2-isoprostane plasma levels indicative of a reduction in oxidative stress
*TNF-α↓, low grade inflammation, respond well to CoQ10 supplementation with significant decrease in TNF-α plasma levels without having an effect on C-reactive protein and IL-6 production
*IL6↓, Another study reported that CoQ10 therapy in doses ranging from 60 to 300 mg/day caused no significant decrease in C-reactive protein while eliciting a significant reduction in IL-6 levels
*other↝, Preclinical studies demonstrated that CoQ can preserve mitochondrial function and reduce the loss of dopaminergic neurons in the case of Parkinson's disease
*other∅, There was no improvement observed in oxidative stress or neurodegeneration markers in a randomized clinical trial in Alzheimer's Disease patients with CoQ10 supplementation at a dose of 400 mg/day for 16 weeks
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Melanoma, |
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*OS↑, plateaued and has remained stable for the last 5 years
with good quality of life.
QoL↑, may help to improve quality of life,
Dose↑, few months later, she also embarked on a once-weekly course of hyperbaric oxygen therapy (90 min at 2 ATA) which she has maintained ever since.
Dose↑, oral curcumin complexed with bioperine (to aid absorption), as a single dose of 8 g each evening on an empty stomach.
IL6↓, curcumin prevents myeloma cell proliferation through inhibition of IL-6-induced STAT-3 phosphorylation
STAT3↓, curcumin downregulated the expression of NFkB, COX-2 and STAT3
NF-kB↓,
COX2/PTGS2↓,
other↝, Coordinated Undermining of Survival Paths, CUSP9, then are aprepitant, artesunate, auranofin, captopril, copper gluconate, disulfiram, ketoconazole, nelfinavir, sertraline, to be added to continuous low dose temozolomide.
QoL↑, The risks of pharmacological interactions and why we believe this drug mix will increase both quality of life and overall survival are reviewed.
Dose↝, Our treatment plan- termed CUSP9- aims to increase QOL and OS compared to current recurrent glioblastoma treatments by adding nine already-marketed growth factor-inhibiting drugs to low dose continuous temozolomide
QoL↑, we outline why CUSP9 can be expected to improve QOL as well versus current simpler treatments.
Dose↝, Our plan is to give temozolomide 50 mg/m2 daily without pause (or until toxicity)
OS↑, 3 cases with patients who had recurrent cancers and for whom all conventional therapies had failed
angioG↓, (1) inhibition of angiogenesis
Hif1a↝, (2) alteration of expression of hypoxia-inducible factor 1-α (HIF1-α)
pH↝, (3) alteration of pH regulators vacuolar-type H + -ATPase (V-ATPase) and monocarboxylate transporter 1 (MCT1)
QoL↑, DCA has the potential to extend life without reducing
patients’ quality of life with debilitating side effects or
compromising physiological function, even for disease in a
very advanced stage
TumCG↓, Accumulating evidence suggests that FMDs attenuate tumor growth by altering the energy metabolism of cancer cells
toxicity∅, FMD reduces risk factors and markers for aging, cardiovascular disease, diabetes, and cancer without serious adverse effects in healthy adults.
BG↓, dramatic downregulation of blood glucose
IGF-1↓, prolonged fasting downregulated IGF-1
mTOR↓, inhibits cellular mTOR activity.
M2 MC↓, In addition, alternate-day fasting inhibited colorectal cancer growth by suppressing adenosine-induced M2 macrophage polarization in the tumor microenvironment
eff↑, large prospective cohort study of breast cancer patients, a longer nightly fasting duration was associated with a decreased risk of breast cancer recurrence, so the FMD may also be beneficial after the eradication of the initial tumo
ChemoSen↑, Combining fasting cycles with chemotherapeutic agents markedly prevented the progression of subcutaneous breast cancer, melanoma, and glioma in mouse models
QoL↑, Fasting for 60 hours seemed to improve the patients' fatigue and quality of life during chemotherapy
RadioS↑, In response to stress, cancer cells engage antioxidant and DNA repair mechanisms in an energy-demanding manner, facilitating cancer cell survival. Thus, restriction of the energy supply would improve the antitumor activity of radiotherapy.
selectivity↑, Recently, short-term starvation was shown to increase the DNA damage induced by a single exposure to high-dose radiation in metastatic cancer cell lines, whereas healthy cells were not affected by starvation medium
ChemoSideEff↓, total toxicities’ score were significantly reduced. reported significantly fewer chemotherapy-induced side effects, including asthenia, fatigue and gastrointestinal problems such as vomiting and diarrhoea
QoL↑, We also observed significantly fewer chemotherapy postponements post-mSTF, reflecting improved tolerance of chemotherapy
IGF-1↓, On average, Insulin [− 169.4 ± 44.1; 95% CI -257.1 – (− 81.8); P < 0.001] and Insulin-like growth factor 1 levels [− 33.3 ± 5.4; 95% CI -44.1 – (− 22.5); P < 0.001] dropped significantly during fasting.
Insulin↓,
Risk↓, IF has shown potential for reducing cancer risk and enhancing therapeutic efficacy by sensitizing tumor cells to chemotherapy and radiotherapy.
ChemoSen↑, intermittent fasting (IF) may enhance the effectiveness of chemotherapy and targeted therapies by activating autophagy. IF enhances the effectiveness of chemotherapy, including drugs such as cisplatin, cyclophosphamide, and doxorubicin
RadioS↑, disease stabilization, improved response to radiotherapy patients with glioma
*Dose↝, 16:8—16 h of fasting with an 8 h eating window;
*Dose↝, 5:2—consuming a standard number of calories for 5 days and reducing intake to 25% of daily requirements for 2 days;
*Dose↝, Eat–Stop–Eat—complete fasting for 24–48 h.
*LDL↓, IF during Ramadan (approximately 18 h of fasting for 29–30 days) reduces LDL cholesterol levels and increases HDL cholesterol in women, as well as reducing inflammatory markers such as CRP and TNF-α
*CRP↓,
*TNF-α↓,
TumAuto↓, Intermittent fasting activates autophagy as an adaptive mechanism to nutrient deprivation, which may modulate tumor development and treatment
GLUT1↓, fasting reduces the expression of glucose transporters GLUT1/2, which slow down cancer metabolism and increase the susceptibility of cancer cells to oxidative stress
GLUT2↓,
glucose↓, studies on cell and animal models have shown that intermittent fasting reduces glucose and insulin-like growth factor (IGF-1) levels [103], as well as insulin [104,105], resulting in the inhibition of the mTOR kinase pathway (PI3K/Akt/mTOR), suppress
IGF-1↓,
Insulin↓,
mTOR↓,
mTORC1↓, suppression of mTORC1 [22], and activation of AMPK through increased ADP/ATP ratio in cells, which supports autophagy and induces apoptosis
AMPK↑,
Warburg↓, Moreover, IF counteracts the Warburg effect by promoting oxidative phosphorylation, leading to an increase in the production of reactive oxygen species (ROS) and enhanced oxidative stress in cancer cells [106,108], causing DNA damage and the activati
OXPHOS↑,
ROS↑,
DNAdam↑,
JAK1↓, fasting reduces the production of adenosine by cancer cells, inhibiting the activation of the JAK1/STAT pathway, thereby reducing cancer cell proliferation
STAT↓,
TumCP↓,
QoL↑, reduction in IGF-1 levels, improved quality of life patients with multiple cancer types
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Risk↓, Intermittent fasting (IF) has emerged as a potential adjunctive strategy in cancer prevention, mitigation, and treatment.
TumCMig↓,
IGF-1↓, IF may reduce cancer risk, including its effects on insulin-like growth factor 1 suppression, autophagy induction, and chronic inflammation reduction.
TumAuto↑,
Inflam↓, IF has been shown to reduce chronic inflammation,13,40 a risk factor for various cancers
ChemoSen↑, we discuss IF’s potential to enhance the efficacy of conventional cancer therapies by sensitizing cancer cells, promoting apoptosis, and reducing treatment-related side effects.
Apoptosis↑,
chemoP↑, IF has shown potential in protecting healthy tissues during chemotherapy.
*glucose↓, Fasting has been shown to enhance metabolic health by improving insulin sensitivity, lowering blood sugar levels, and reducing the risk of type 2 diabetes.
*AntiDiabetic↑,
*cardioP↑, Recent studies support the cardioprotective effect of IF by reducing cholesterol levels, lowering blood pressure, and improving cardiovascular health
*LDL↓,
*BP↓,
*neuroP↑, IF may reduce the risk of neurodegenerative diseases, enhance cognitive function, and improve memory
*cognitive↑,
*memory↑,
*OS↑, some studies have suggested that IF may extend lifespan and improve overall health
*QoL↑,
Imm↑, In the context of cancer prevention, IF may directly affect the function of immune cells, reducing their production of inflammatory cytokines and promoting a more anti-inflammatory environment.5
TumCG↓, Evidence suggests that FMDs can effectively slow tumor growth by altering cancer cell metabolism, enhance the efficacy of traditional cancer therapies by reducing side effects, and potentially bolster antitumor immune surveillance
ChemoSideEff↓, IF may also help alleviate common side effects such as fatigue, nausea, and weight loss associated with cancer treatments
QoL↑, Results showed that chemotherapy-induced QoL decline was significantly less pronounced during fasting periods compared to non-fasting periods
QoL↑, . His quality of life remains excellent. He continues using dandelion root tea.
other↑, we moving into a phase I/II clinical trial examining the effect of dandelion root extract in patients with monocytic leukemias.
Dose↝, Because of previous signals of response at our centre to dandelion root tea/ water extract, and because of his current palliative diagnosis, we mentioned dandelion root tea to him.
TumCP↓, Our findings show that prior treatment with DRE, followed by VP-16, led to a decrease in cell proliferation, disruption of the mitochondrial membrane potential, production of reactive oxygen species and ultimately cell death induction, at a greater
MMP↓,
ROS↑,
TumCD↑,
ChemoSen↑, Overall, this study has the potential to reduce the dose of chemotherapy administered to patients, thereby decreasing the side effects and overall improving the quality of life of cancer patients.
chemoP↑,
QoL↑,
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*Mood↑, The current study indicates that Ellagic acid intervention has a favorable effect on depression in MS patients.
*BDNF↑, we found a significant elevation in circulating levels of BDNF and serotonin.
*5HT↑,
*antiOx↑, associated to its antioxidative, anti-inflammatory, immunomodulatory, antidiabetic, and anticancer properties (Gupta et al., 2021)
*Inflam↓,
*AntiCan↑,
*QoL↑, Ellagic acid improves bowel function and enhances the quality of life for individuals suffering from irritable bowel syndrome (IBS)
*neuroP↑, Ellagic acid may have neuroprotective effect by regulating the hypothalamic–pituitary–adrenal (HPA) axis and neurotransmitters in animal's brain
*cognitive↑, Ellagic acid supplementation may also improve mood and cognitive function like memory and learning in rats (Gupta et al., 2021).
*memory↑,
*Dose↝, 180 mg Ellagic acid
*Dose↝, 180 mg of EA per day (n = 22) or a placebo (n = 22) for 8 weeks
*MDA↓, we saw a significant decrease and increase in the MDA and TAC in the intervention group
*TAC↑,
*CRP↓, EA consumption reduced CRP and IL-6 levels, and these changes were significant in comparison with placebo group changes
*IL6↓,
*Inflam↓, EA, may help maintain intestinal health by modulating inflammation and oxidative stress and ultimately improving the quality of life in IBS patients.
*ROS↓,
*QoL↑,
*toxicity↓, In this study, we did not receive any adverse effects reports from patients about EA consumption.
cognitive↑, Treatment with 240 mg EGb 761 daily was significantly superior to placebo in cognition (p = 0.04), global assessment (p = 0.01), activities of daily living (p = 0.01) and quality of life (p = 0.02).
QoL↑,
Dose↝, 240 mg EGb 761 daily
Dose↝, 32 patients received EPA (2 g/day) and 32 became controls.
*IL1β↓, A decrease in serum levels of IL-1β, IL-6, TNF-α, and IFN-γ was observed in the experimental group, as well as regulation of body weight (-0.3 ± 5.9 vs. -2.1 ± 3.7),
*IL6↓,
*TNF-α↓,
*IFN-γ↓,
QoL↑, lean body mass (-0.2 ± 3.8 vs. -1.3 ± 3.6), body fat mass (0.2 ± 3.5 vs. -1.2 ± 3.8), and quality of life (10 ± 33 vs. 5 ± 34).
*Strength↑, All the patients of the exercise group had significantly better left upper body strength, higher aerobic endurance, and left and right balance maintenance time than those of the no-exercise group
*QoL↑, Moreover, the exercise group had significantly lesser unexpected hospitalization than the no-exercise group in the patients with mild dementia
*cognitive∅, However, in the mild and moderate dementia subgroups, age, sex, education years, and MMSE showed no significant differences between the groups
OS↑, In 2008, a cohort study of breast cancer survivors identified that patients who consistently exercised for greater than 2.5 hours per week following diagnosis had a greater than 60% reduction in the risk of all deaths compared with patients who were
IGF-1↓, Table 1, IGF1 Decreased levels, IGFBP3 Increased levels
IGFBP3↑,
BRCA1↑, BRCA1 Increased expression
BRCA2↑, BRCA2 Increased expression
RAS↓, RAS family oncogenes Suppressed activity
P53↑, P53 Enhanced activity
HSPs↑, Heat shock proteins Enhanced activity
Leptin↓, Leptin Reduced activity
Irisin↓, Irisin Enhanced activity
Resistin↓, Resistin Reduced activity
NK cell↑, NK cells Enhanced activity
CRP↓, C-reactive protein, interleukin-6, TNFα Reduced activity
IL6↓,
TNF-α↓,
PGE1↓, Prostaglandins Reduced activity
COX2/PTGS2↓, Cox-2 Reduced activity
*GSH↑, Glutathione, Catalase and Superoxide dismutase Increased activity
*Catalase↑,
*SOD↑,
*monoA↑, Monoamines Higher levels
*EndoR↑, Endorphins Increased release
*testos↑, testosterone increases immediately after vigorous exercise in some but not all studies. lasting for 20–60 minutes post-exercise
ROS↑, Physical activity, especially if strenuous, produces reactive oxidative species (ROS)
QoL↑, Adverse cancer-related symptoms, which have been shown to be alleviated by exercise, include fatigue, muscle weakness, thromboembolism, weight gain, loss of bone density, quality of life (QOL), psychological distress, incontinence and sexual dysfunct
BMD↑, the rate of decline in BMD was significantly less in the resistance exercise group, with a greater benefit seen in the aerobic exercise group
BowelM↑, Exercise reduces bowel transit time and ameliorates constipation and its associated abdominal cramps
*Mood↑, Folate deficiency is associated with depression and dementia
*cognitive↑, Impaired folate metabolism may result in a pattern of cognitive dysfunction that resembles ageing
*other↝, The duration of folate deficiency and of its treatment is as important as the degree of deficiency and the dose of folic acid
*memory↑, 38 folate deficient elderly subjects with depression, lethargy, and memory impairment, folinic acid 50 mg per week for 120 days significantly improved visuomotor performance, visuospatial memory, logical reasoning, associative memory, and activities
*QoL↑,
*Hcy/homoC↝, confirmed neuropathologically in 76 patients in whom higher plasma homocysteine was associated with a more rapid atrophy of the medial temporal lobes over a three year period
*other↝, impact of folate is slow and cumulative over many months, perhaps because blood-brain barrier mechanisms limit entry to the brain.
*Dose↝, Small doses over the long term may be preferable to larger doses in the short or long term
QoL∅, There was no significant difference in the median quality of life scores between the 2 cohorts,
QoL↑, however, when evaluating the individual quality of life metrics, 5 out of the 23 metrics showed statistically significant improvement, and none of the quality-of-life metrics declined in the oligo fucoidan group as compared to the placebo group.
Dose↝, Four standardized ginger capsules (totaling 84 mg/day active gingerols/shogaols), or placebo,
chemoPv↑, There was a clinically meaningful lower incidence of delayed nausea and vomiting in the ginger group at Cycle 2
Nausea↓,
Vomit↓,
mal↓, There was a clinically meaningful lower incidence of malnutrition in the ginger group at Cycle 3
QoL↑, Ginger supplementation was a safe adjuvant to antiemetic medications for CINV that enhanced QoL during chemotherapy treatment.
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Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.
*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,
*BG↓, Long-term administration of HRW significantly decreased FBG levels and increased BW, indicating an improvement in metabolic control.
*AntiDiabetic↑,
*BMD↑, HRW also ameliorated various DM-related complications, including diabetic cataracts, bone loss, diabetic nephropathy, erectile dysfunction, asthenozoospermia, and renal neoplasms.
*hepatoP↑, revealed significant enrichment of metabolic pathway-related genes in testis, liver, kidney, and stomach tissues, suggesting the reprogramming of metabolic functions.
*RenoP↑,
*QoL↑, The findings suggest that oral ingestion of HRW is a safe, effective, and convenient treatment that improves quality of life for DM patients by reducing blood glucose levels and alleviating diabetic complications.
chemoP↑, H2 plays a promising therapeutic role as an independent therapy as well as an adjuvant in combination therapy, resulting in an overall improvement in survivability, quality of life, blood parameters, and tumour reduction.
OS↑,
QoL↑,
TumVol↑,
ROS↑, Hydrogen, the lightest element on the earth, is an effective antioxidant that has been shown to selectively reduce harmful reactive oxygen species (ROS) in tissues
AntiTum↑, Although H2 has demonstrated significant anti-tumoural effects, the underlying mechanisms have not yet been elucidated.
other↝, Many studies have shown that H2 therapy can reduce oxidative stress. This, however, contradicts radiation therapy and chemotherapy, in which ROS are required to induce apoptosis and combat cancer.
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Inflam↑, Oxyhydrogen gas, a mixture of 66% molecular hydrogen (H2) and 33% molecular oxygen (O2) has shown exceptional promise as a novel therapeutic agent due to its ability to modulate oxidative stress, inflammation, and apoptosis.
ROS↓, neutralises reactive oxygen and nitrogen species
ChemoSen↑, enhancing existing treatments and reducing harmful oxidative states in cancer cells. boosting the effectiveness of conventional therapies
p‑PI3K↓, inhibiting the PI3K/Akt phosphorylation cascade.
p‑Akt↓,
QoL↑, Similar results have been observed in breast cancer, where patients reported improved quality of life.
GutMicro↑, improves intestinal microflora dysbiosis.
chemoP↑, reduced oxidative stress and mitigated tissue damage, suggesting its potential as a cytoprotective agent in cancer patients undergoing radiation therapy or chemotherapy
radioP↑,
*NRF2↑, documented role in activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.
*Catalase↑, consequently, hydrogen can enhance the expression of endogenous antioxidant enzymes, including catalase (CAT), glutathione peroxidase (GPx), haem oxygenase (e.g., HO-1), and superoxide dismutase (SOD) [45]
*GPx↑,
*HO-1↑,
*SOD↑,
*TNF-α↓, reducing the expression of proinflammatory mediators such as chemokines (e.g., CXCL15), cytokines (e.g., TNF-α), interleukins (e.g., IL-4, IL-6)
*IL4↓,
*IL6↓,
ChemoSen↑, further research demonstrates that oxyhydrogen gas enhanced the sensitivity of lung cancer cells to chemotherapy drugs, suggesting its potential as an adjuvant therapy
Appetite↑, inhaled oxyhydrogen gas over a minimum of 3 months. The results indicated substantial improvements in appetite, cognition, fatigue, pain, and sleeplessness
cognitive↑,
Pain↓,
Sleep↑,
other?, It is recommended that hydrogen should not exceed 4.6% in air or 4.1% by volume in pure oxygen gas (explosion risk)
| - |
in-vitro, |
Nor, |
HUVECs |
|
|
|
- |
in-vivo, |
NA, |
NA |
|
|
|
AntiTum↑, Hydrogen also has direct and indirect antitumor effects, which could be useful for the treatment of cancer patients. Hydrogen therapy improves overall survival, quality of life, blood parameters, and tumor reduction.
OS↑,
QoL↑,
TumVol↓,
radioP↑, In addition, hydrogen attenuates the risk of carcinogenesis induced by radiation.
Dose↑, Patients begin hydrogen inhalation 10 minutes prior to vitamin C injection. Patients are treated with high-dose vitamin C injection while inhaling simultaneous hydrogen
Dose↝, patients also performed the hydrogen and vitamin C combination therapy at home on their own as much as possible
eff↑, These results suggest that in normal cells, the combination of 1 mM vitamin C and hydrogen is the most effective radioprotective agent.
*Wound Healing↑, Topical ozonated olive oil significantly enhances wound healing, quality of life, glycemic control, and reduces inflammation in DFU patients.
*QoL↑, Quality of life scores improved (50.1 ± 9.5 vs. 57.8 ± 10.0,
LC↑, moderate RHT in improving local tumour control, survival outcomes and quality of life scores were observed across the different cancer subsites with minimal increase in toxicities.
OS↑,
QoL↑,
toxicity↓,
Dose↝, Various heating methods include direct (e.g., intracavitary and whole-body waterbed), infrared, perfusional (e.g., isolated limb perfusion, intravesical and intraperitoneal), nanoparticles, ultrasound and regional radiofrequency (RF) radiation
Dose↝, Moderate HT is usually described at a range of 39–44 °C a
ROS↑, Figure 1
DNArepair↓,
EPR↑,
DNAdam↑,
HSP70/HSPA5↑,
BloodF↑,
Hypoxia↓,
Showing Research Papers: 1 to 50 of 84
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 84
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
CD47↓, 1, LC↑, 1, mal↓, 1, miR-124-3p↓, 1, Nausea↓, 1, PFS↑, 1, Vomit↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Ferroptosis↑, 1, GPx4↓, 2, GSH↓, 1, c-Iron↑, 1, lipid-P↑, 1, NRF2↓, 1, NRF2↑, 1, OXPHOS↑, 1, mt-OXPHOS↓, 1, ROS↓, 1, ROS↑, 9, xCT/SLC7A11↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, Insulin↓, 2, MMP↓, 4, PGC-1α↑, 1, XIAP↓, 1, XIAP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACSL4↑, 1, AMPK↑, 2, glucose↓, 1, GLUT2↓, 1, Glycolysis↓, 2, LDL↑, 1, SCD1↓, 1, SIRT1↓, 1, SREBP1/SREBF1↓, 1, Warburg↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 4, p‑Akt↓, 1, Apoptosis↑, 6, BAX↑, 2, Bcl-2↓, 2, Casp↑, 1, Casp3↑, 4, Casp8↑, 1, Casp9↑, 3, Cyt‑c↑, 1, Fas↑, 1, Ferroptosis↑, 1, IAP2/BIRC3↓, 1, JNK↓, 1, TumCD↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
BowelM↑, 1, EZH2↓, 1, other?, 1, other↓, 1, other↑, 1, other↝, 3,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, HSP70/HSPA5↑, 1, HSPs↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↑, 1, TumAuto↓, 1, TumAuto↑, 2, mt-TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
BRCA1↑, 1, BRCA2↑, 1, DNAdam↑, 3, DNArepair↓, 1, P53↑, 3, cl‑PARP↑, 1, γH2AX↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK4↓, 1, cycD1/CCND1↓, 1, P21↑, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CD133↓, 1, CD44↓, 1, CSCs↓, 1, EMT↓, 2, FOXO1↑, 1, GSK‐3β↓, 1, GSK‐3β↑, 1, IGF-1↓, 5, IGFBP3↑, 1, mTOR↓, 4, mTORC1↓, 1, NOTCH1↓, 2, NOTCH3↓, 1, PI3K↓, 3, p‑PI3K↓, 1, RAS↓, 1, STAT↓, 1, STAT3↓, 2, TumCG↓, 5, Wnt↓, 4,
Migration(tgid=13) ⓘ
CEA↓, 1, KRAS↓, 1, MALAT1↓, 1, miR-133a-3p↑, 1, MMP9↓, 1, TumCI↓, 3, TumCMig↓, 2, TumCP↓, 7, TumMeta↓, 2, Vim↓, 2, β-catenin/ZEB1↓, 4,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 2, EGFR↓, 4, EPR↑, 1, Hif1a↓, 2, Hif1a↝, 1, Hypoxia↓, 1, VEGF↓, 2,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1, GLUT1↓, 1, P-gp/ABCB1↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 3, CRP↓, 1, CXCR4↓, 1, IL12↑, 1, IL2↑, 1, IL6↓, 2, Imm↑, 5, Inflam↓, 1, Inflam↑, 1, JAK1↓, 1, M2 MC↓, 1, NF-kB↓, 3, NK cell↑, 2, PD-L1↓, 1, PGE1↓, 1, Resistin↓, 1, TNF-α↓, 1, TNF-α↑, 1,
Cellular Microenvironment(tgid=17) ⓘ
pH↝, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↑, 1, Irisin↓, 1, Leptin↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, ChemoSen↑, 16, Dose↑, 3, Dose↝, 18, eff↑, 12, eff↝, 1, Half-Life↑, 2, MDR1↓, 1, RadioS↑, 3, selectivity↑, 4,
Clinical Biomarkers(tgid=22) ⓘ
BG↓, 1, BloodF↑, 1, BMD↑, 1, BRCA1↑, 1, CEA↓, 1, CRP↓, 1, EGFR↓, 4, EZH2↓, 1, GutMicro↑, 2, IL6↓, 2, KRAS↓, 1, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, AntiTum↑, 4, Appetite↑, 1, chemoP↑, 9, chemoPv↑, 1, ChemoSideEff↓, 2, cognitive↑, 2, fatigue↓, 4, hepatoP∅, 1, NP/CIPN↓, 1, OS?, 1, OS↑, 12, OS↝, 1, OS∅, 1, Pain↓, 1, QoL↑, 40, QoL∅, 1, radioP↑, 4, RenoP∅, 1, Risk↓, 2, Sleep↑, 1, toxicity↓, 2, toxicity↑, 1, toxicity↝, 2, toxicity∅, 1, TumVol↓, 4, TumVol↑, 1, TumW↓, 1, Weight↑, 2,
Infection & Microbiome(tgid=24) ⓘ
CD8+↑, 2,
Total Targets: 190
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
compII↑, 1, SpO2↑, 1, Stroke↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 5, Catalase↑, 4, Fenton↓, 1, GPx↑, 2, GSH↑, 2, HDL↑, 1, HO-1↑, 3, lipid-P↓, 2, MDA↓, 3, MPO↓, 2, NOX4↓, 1, NRF2↑, 3, RNS↓, 1, ROS↓, 4, SOD↑, 4, TAC↑, 1, TBARS↓, 1, VitE↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, compIII↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, glucose↓, 1, LDL↓, 4, NADPH↓, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 2, Apoptosis↓, 2, Bcl-2↑, 1, Bcl-xL↑, 1, Casp12↓, 1, Casp3↓, 1, Casp9↓, 1, GranB/GZMB↓, 1, p‑JNK↓, 1, p38↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 2, other↝, 3, other∅, 1, tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↓, 1, p‑eIF2α↓, 1, ER Stress↓, 1, GRP78/BiP↓, 1, XBP-1↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3‑Ⅱ/LC3‑Ⅰ↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
IGF-1↑, 1, IGFBP1↑, 1, mTOR↓, 1, PI3K↑, 2, STAT3↑, 1,
Migration(tgid=13) ⓘ
APP↓, 1, TGF-β↑, 1, Treg lymp↝, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
ATF4↓, 1,
Barriers & Transport(tgid=15) ⓘ
IBI↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD25+↑, 1, CD4+↑, 2, CRP↓, 2, FOXP3↑, 1, HMGB1↓, 1, IFN-γ↓, 2, IL10↑, 2, IL1β↓, 3, IL4↓, 2, IL4↑, 1, IL6↓, 6, Imm↑, 3, Inflam↓, 8, JAK2↑, 1, LPS↓, 1, M2 MC↑, 1, MCP1/CCL2↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 6,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↑, 1, BDNF↑, 1, EndoR↑, 1, monoA↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE/β-secretase↓, 1, NLRP3↓, 2,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
testos↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↝, 1, Dose↓, 1, Dose↑, 2, Dose↝, 13, eff↑, 4,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, BG↓, 1, BMD↑, 1, BP↓, 2, creat↓, 1, CRP↓, 2, GutMicro↑, 1, Hcy/homoC↝, 1, IL6↓, 6, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 2, antiPs↑, 1, cachexia↓, 1, cardioP↑, 3, cognitive↑, 4, cognitive∅, 1, hepatoP↑, 3, memory↑, 3, Mood↑, 3, neuroP↑, 5, Obesity↓, 1, OS↑, 3, QoL↑, 11, RenoP↑, 3, Strength↑, 1, toxicity↓, 1, Weight↑, 1, Wound Healing↑, 1,
Infection & Microbiome(tgid=24) ⓘ
Sepsis↓, 1,
Total Targets: 128
Scientific Paper Hit Count for: QoL, Quality of Life
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1141 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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