Hydrogen Water and Cardiovascular Health: What Recent Research Shows

Posted by Holy Hydrogen on May 18, 2026

The heart is the organ punished by oxidative stress the most. Every other tissue gets to rest. The cardiovascular system does not — which is why so many researchers have spent the last twenty years asking whether molecular hydrogen, an antioxidant small enough to cross every membrane in the body, might do something useful inside it.

That question is not new. The first published research on hydrogen as a therapeutic antioxidant appeared in Nature Medicine in 2007, in the context of stroke (ischemia and reperfusion damage). The cardiovascular angle followed almost immediately, because the cardiovascular system is the body's largest stage for the exact damage hydrogen was first shown to dampen. By now, the literature stretches across hamster lipid studies, human metabolic-syndrome trials, mouse atherosclerosis models, retinal vascular work, myocardial ischemia rat models, and — as of April and May 2026 — two newly-published papers that meaningfully extend the field.

This article is a research-reporting overview of where the cardiovascular hydrogen water literature stands today. It is not medical advice. It is not a prescription. It is what the published trials and reviews actually say, written for a reader who wants the substance and not the marketing.

What the research is asking about hydrogen water and cardiovascular health

The question researchers have been circling is narrow and specific. Can a small, electrically neutral molecule that diffuses into every compartment of the body — including the lumen of blood vessels, the interior of cardiomyocytes, and the mitochondria within them — selectively soften the kinds of oxidative damage that drive cardiovascular pathology over time?

Three things make hydrogen interesting as a candidate. It is the smallest molecule in chemistry, so it crosses biological membranes that other antioxidants cannot. It has a known reactivity profile (Ohsawa et al., 2007, Nature Medicine): hydrogen appears to react with the hydroxyl radical and peroxynitrite — two of the most damaging reactive oxygen species — while leaving signaling-relevant ROS like superoxide and hydrogen peroxide largely alone. And it has a safety record that, across 80-plus published clinical trials, has not produced significant adverse effects at the concentrations studied (Johnsen et al., 2023, Molecules).

None of that proves a cardiovascular benefit. It just explains why the cardiovascular system is one of the most-studied target organs in the molecular hydrogen literature — and why interest has accelerated, not faded. The broader research base — the 2,000-plus published studies on molecular hydrogen across all indications — is the context in which the cardiovascular subset has grown up.

The foundational biology — oxidative stress and the cardiovascular system

To understand why this research exists at all, it helps to look at the kind of damage hydrogen was first hypothesized to address.

How reactive oxygen species damage cardiovascular tissue

The cardiovascular system generates reactive oxygen species (ROS) at baseline, as a normal byproduct of mitochondrial respiration in the millions of contracting cells inside the heart and the endothelial lining of every blood vessel. At low levels, this is healthy and useful — ROS act as signaling molecules. At elevated levels, the same molecules behave very differently. Hydroxyl radicals abstract hydrogen atoms from the lipid bilayers of cell membranes, kicking off lipid peroxidation chains. Peroxynitrite, formed when nitric oxide collides with superoxide, attacks proteins by nitrating tyrosine residues. The endothelium loses its ability to dilate. Low-density lipoprotein oxidizes. Macrophages move in. Plaque begins.

This is the conventional story of atherosclerosis at the molecular level, and it is the door through which hydrogen entered the conversation.

The selective antioxidant hypothesis

Ohsawa et al. proposed in 2007 (PMID: 17486089) that hydrogen behaves differently from broad-spectrum antioxidants like vitamin C or vitamin E. Their finding was that hydrogen reacted preferentially with the most damaging ROS — the hydroxyl radical in particular — and did not appear to neutralize the signaling ROS that the body needs for normal adaptation. Whether this selectivity holds up across every tissue and context is still being worked out. What it implies, if true, is that hydrogen could blunt damage without flattening the redox signaling that drives, for instance, exercise adaptation or insulin sensitivity.

For cardiovascular research specifically, the selectivity question matters because the heart cannot tolerate "antioxidant blunting." Several large trials of broad-spectrum antioxidant supplements (vitamin E, beta-carotene) have failed to show cardiovascular benefit, and some have raised safety concerns. Hydrogen, if the selectivity hypothesis is right, is a different kind of molecule than those. This is one of the threads we've explored separately in our discussion of selective versus non-selective antioxidant strategies — the selectivity question is exactly what distinguishes hydrogen from the older generation of supplement antioxidants.

What human trials have actually measured

The body of human cardiovascular research on hydrogen water is smaller than the animal literature, but it is not empty. The most-cited study is more than a decade old, and it still anchors the conversation.

The Song 2013 metabolic syndrome trial

Song et al. (2013, Journal of Lipid Research; PMID: 23610159) ran a 10-week trial in 20 patients with potential metabolic syndrome. Participants consumed 0.9 to 1.0 liters per day of hydrogen-rich water. The investigators measured serum lipids and a series of HDL-functionality assays. They reported decreases in total cholesterol and LDL-cholesterol, decreases in apolipoprotein B100 and apoE in serum, and four separate measures of improved HDL function: protection against LDL oxidation, inhibition of TNF-α-induced monocyte adhesion to endothelial cells, stimulation of cholesterol efflux from macrophage foam cells, and protection of endothelial cells from TNF-α-induced apoptosis. Antioxidant enzyme activity (superoxide dismutase) rose and a marker of lipid peroxidation (thiobarbituric acid-reactive substances) fell.

It is a small trial. Twenty people. Ten weeks. The authors themselves frame it as a study of a population with potential metabolic syndrome — meaning the lipid abnormalities and inflammatory burden were present but the population was not yet acutely ill. That framing matters because it is also the population most people drinking hydrogen water belong to. The inflammatory dimension of this picture — what hydrogen has and hasn't been observed to do to inflammatory markers in human trials — is something we covered in depth in our overview of what the clinical trials on hydrogen water and inflammation have found.

Why dyslipidemia is the right place to look

Dyslipidemia — elevated LDL, low or dysfunctional HDL, elevated apoB — sits upstream of the inflammatory and oxidative processes that drive atherosclerosis. If hydrogen acts on the oxidative side of that cascade, the lipid-and-HDL-function panel is the most sensitive readout in a healthy-but-at-risk population. Song's design was a reasonable bet at the time. The result was suggestive enough that follow-on animal and mechanistic work has continued in the years since — and the question of whether a larger, longer human trial would replicate the lipid signal remains open.

The 2026 research on atherosclerosis

One of the two most recent papers in the cardiovascular hydrogen literature was published April 30, 2026, by Meng et al. in Life Sciences (PMID: 42069299). It is an animal study — ApoE-knockout mice, the standard murine atherosclerosis model — but it is mechanistically the most interesting cardiovascular hydrogen paper of the past several years, because it links hydrogen-rich water consumption to a specific gut–vascular pathway.

The gut microbiota–propionate–macrophage axis

The investigators administered hydrogen-rich water to ApoE-knockout mice and reported attenuated plaque formation and improved plaque stability. They also analyzed the gut microbiota composition and the short-chain fatty acid profile in the cecum and serum. Hydrogen-rich water altered the microbial community structure and notably elevated propionate, a short-chain fatty acid with documented anti-inflammatory effects. When the researchers depleted the gut microbiota with antibiotics, the protective effect of hydrogen-rich water disappeared. When they performed fecal microbiota transplants from hydrogen-treated mice to untreated mice, the anti-atherosclerotic phenotype transferred. In vitro, propionate directly suppressed inflammatory responses and M1 macrophage polarization.

The implication of the experiment — within the strict limits of an animal model — is that some of hydrogen-rich water's vascular effects may be mediated indirectly through the gut microbiome rather than (or in addition to) direct radical scavenging in the bloodstream. That is a different mechanism than the field has historically focused on, and it opens a new vein of research questions.

The propionate finding is worth pausing on. Propionate is one of the three major short-chain fatty acids generated through colonic fermentation (alongside acetate and butyrate). It has documented anti-inflammatory effects, and it is one of the metabolites by which a fiber-rich diet is thought to do its cardiovascular work. If hydrogen-rich water modulates the gut microbiome in a direction that increases propionate output, it is plausibly tapping into the same axis that diet researchers have been mapping for years. The Singh et al. (2024) review explicitly explored the parallel — the Mediterranean diet, with its high fiber and flavonoid content, generates molecular hydrogen endogenously in the gut, and the authors argue that this endogenous production is part of what makes the diet cardioprotective. The Meng 2026 mechanism paper is, in some ways, a direct extension of that line of thinking.

What this opens up for future investigation

Several follow-on questions become obvious from this design. Does the same gut-mediated pathway operate in humans? Which microbial taxa specifically respond to hydrogen exposure in the gut? How does daily oral hydrogen-rich water consumption compare to a single concentrated dose in terms of microbiome remodeling? None of these has been answered in human trials yet. The 2026 result is the kind of finding that catalyzes the next round of work — not the kind that ends the conversation.

The 2026 research on acute aortic dissection

The second very recent paper, published May 7, 2026, comes from a hydrogen-medicine research group at the Tokyo Metropolitan Institute for Geriatrics and Gerontology. Iketani et al., writing in Life Sciences (PMID: 42105975), investigated whether inhaled hydrogen gas could attenuate the severity of acute aortic dissection — a life-threatening cardiovascular event in which inflammation drives the propagation of a tear through the aortic wall.

How researchers built the model

The study used a murine model: male C57BL/6J mice pretreated with β-aminopropionitrile and then given a continuous infusion of angiotensin II to induce aortic dissection. Mice received either 2% hydrogen gas or a control gas for 24 hours. The investigators measured 24-hour survival, locomotor activity, aortic rupture frequency, false lumen enlargement, and a panel of inflammatory mediators in plasma and the aortic wall.

Inflammatory mediator findings

Hydrogen inhalation was associated with improved 24-hour survival and reduced rupture frequency, without altering systolic blood pressure. In plasma, IL-6 and G-CSF dropped significantly; MMP-9 and CXCL1 trended downward. In the aortic wall itself, MMP-9 and CXCL1 expression decreased, and the number of Ly-6B.2-positive cells — a neutrophil marker — fell. The bone marrow data suggested hydrogen attenuated the AAD-associated suppression of neutrophil populations. The authors framed the result as evidence that hydrogen inhalation may modulate neutrophil-associated acute inflammation without affecting hemodynamic drivers of the disease.

The translational distance from an angiotensin-II mouse model to human aortic dissection is, of course, considerable. What the paper establishes is a mechanism — neutrophil-mediated inflammation in the aortic wall is plausibly hydrogen-responsive — that earlier work had only sketched.

Ischemia and reperfusion — the most-studied cardiovascular area

If you wanted to map the cardiovascular hydrogen literature by topic, the largest single cluster of papers is ischemia-reperfusion injury. This is the damage that happens when blood flow is restored to a tissue after a period of oxygen deprivation: paradoxically, the rush of oxygen back into the starved tissue generates a burst of reactive oxygen species that often does more damage than the ischemic event itself.

Why this area developed first

The Ohsawa 2007 paper was, technically, an ischemia-reperfusion paper. The original demonstration of hydrogen's selective antioxidant behavior was in a rat brain ischemia model, with hydrogen inhaled during reperfusion. The cardiovascular literature picked up the same model design almost immediately, because the heart's biggest single oxidative event is myocardial ischemia-reperfusion — what happens during a heart attack and during the reperfusion that follows treatment. Animal models of myocardial ischemia-reperfusion have been the workhorse experiment in cardiovascular hydrogen research for almost two decades. Singh et al. (2024, Reviews in Cardiovascular Medicine; PMID: 39077646) reviewed the field and described "mounting evidence" that both endogenous gut-derived hydrogen and exogenously administered hydrogen have anti-inflammatory effects across a range of cardiovascular and metabolic processes.

The 2026 acoustic hydrogen delivery study

One of the more creative recent papers — Wang et al. (2026, Biomaterials Advances; PMID: 41671925) — addressed a long-standing challenge in this field: hydrogen has limited solubility in blood, and its therapeutic effect depends on getting enough of it to the right tissue at the right time. The investigators built lipid microbubbles loaded with hydrogen gas and used ultrasound to trigger their destruction at the target tissue (the heart) in a rat myocardial ischemia-reperfusion model. The result was improved ejection fraction and fractional shortening, reduced infarct size, and downregulation of several cell-death pathway mediators (cleaved caspase-1, GSDMD, cleaved caspase-3/8, p-RIPK1, p-RIPK3, p-MLKL).

It is a delivery experiment, not a clinical trial. It does not change what oral hydrogen-rich water does. What it does is demonstrate that the hydrogen-delivery problem is being attacked from multiple engineering angles, which suggests the underlying biology is plausible enough that researchers are willing to invest in solving the logistics around it.

One nuance the cardiovascular ischemia-reperfusion literature has surfaced over time is that hydrogen appears most useful when it is present during the reperfusion event, not pre-loaded into the tissue. That has implications for clinical protocol design — hydrogen-saturated saline has been studied in surgical contexts where the reperfusion window is predictable. For the daily-consumer use case, the picture is different: chronic, low-level oxidative stress in the cardiovascular system is continuous rather than episodic, and the relevant exposure is also continuous (daily oral hydrogen consumption) rather than acute. The two use cases — acute clinical and chronic consumer — are studied with different protocols and should be evaluated by different criteria.

What systematic reviews actually conclude

The cardiovascular hydrogen literature has, by now, accumulated enough volume that systematic reviews have started to appear. Two recent ones are worth reading carefully — partly because they are useful summaries, and partly because they show how the field talks about itself when forced to consolidate.

The 2024 systematic review

Dhillon et al. (2024, International Journal of Molecular Sciences; PMID: 38256045) conducted a PROSPERO-registered systematic review of hydrogen-rich water research. After applying their inclusion criteria, the review covered 25 articles spanning exercise capacity, physical endurance, liver function, cardiovascular disease, mental health, COVID-19, oxidative stress, and anti-aging research. Their stated conclusion was that the preliminary findings in clinical trials and studies are encouraging, but that larger sample sizes and rigorous methodologies are needed to substantiate them — and that the mechanisms behind the observed effects still need fuller characterization.

The review is not a meta-analysis with effect sizes. It is a structured narrative review, and that is the appropriate format for a field at this stage. The honest reading is: enough has been observed in small studies to warrant continued research, and the safety profile is good enough that continued research is reasonable.

The 81-trial clinical overview

Johnsen et al. (2023, Molecules; PMID: 38067515) reviewed 81 clinical trials and 64 scientific publications on human studies of hydrogen therapy. Their finding was that positive indications had been observed across major disease areas — including cardiovascular disease, cancer, respiratory diseases, central nervous system disorders, and infections — and that the regulatory and engineering question is now less about whether hydrogen does something biologically and more about how to deliver it consistently. They explicitly discussed the challenges of hydrogen's low solubility and the diversity of administration methods (hydrogen-rich water, inhalation, hydrogen-saturated saline) and pointed forward to delivery innovations.

For the cardiovascular reader, the relevant takeaway is the framing: cardiovascular disease is one of the disease areas the authors flagged as having positive clinical-trial indications. They did not claim "proven." They claimed enough activity to keep investigating.

Why equipment quality is part of the cardiovascular research question

If you spend any time reading the methods sections of the trials cited above, one thing becomes clear quickly: every published study controls the hydrogen concentration of the water (or the gas mixture) the participants receive. Song's metabolic syndrome trial specified the saturation profile of the water. Meng's atherosclerosis model used hydrogen-rich water of defined preparation. Iketani's aortic dissection paper used 2% hydrogen gas, calibrated.

The published literature does not say "drink anything labeled hydrogen water and call it good." It says: this concentration, in this preparation, produced these biological effects. That has direct implications for any consumer trying to match the protocol context at home.

Concentration matters. Purity matters at least as much.

The two dimensions on which a hydrogen water device has to perform for the published research to be relevant are concentration and purity. Concentration — dissolved hydrogen, typically expressed in ppm — is the variable the trials specify. Purity is the variable the trials assume, because clinical and laboratory water sources are clean by default. For a daily-use consumer device, both dimensions matter, because the water is being consumed every day for years and the cumulative exposure to anything that is in the water — beyond hydrogen — adds up.

The category's marketing has historically been a PPM number race. That race has the unfortunate side effect of letting low-quality devices compete on a single dimension. Professional-strength hydrogen water — the kind that resembles the conditions of the published research — requires both adequate concentration to match what the studies used and a verified purity profile that most consumer devices do not bother to test. We walked through the purity side of the question in detail in our piece on why most hydrogen water machines fail the purity test, and the concentration / electrode-engineering side in why electrode quality matters more than PPM. Both are background reading for anyone trying to translate the published research into an equipment choice.

How the Lourdes Hydrofix Premium Edition meets these criteria

Given the engineering criteria the published research implies, here is how the Lourdes Hydrofix Premium Edition addresses them. (This is the bridge from the science to the equipment — the place where research-context replication becomes a hardware question.)

You can find the Lourdes Hydrofix in our hydrogen water machine collection.

Engineering specifications

The Hydrofix is built around a separate-chamber (dual-chamber) electrolysis design, using a Multi-Layer Fibriform Polymer Membrane (MFPM) between solid titanium-platinum electrodes. The titanium itself is high-purity TP270C — a public Japanese Industrial Standard (JIS H 4600) designation — at 99.928% measured purity. Hydrogen gas output is approximately 120 mL/min, depending on usage conditions. The system is pH neutral, within about 0.1 of the source water. The machine is manufactured in Sabae, Fukui Prefecture, Japan — a region with a deep concentration of metal-working precision manufacturers — and ships with a Certificate of Authenticity attesting the individual unit's hydrogen output before it left the factory.

None of those specs are unusual on a brochure. What is unusual is that each of them is backed by a separate, independent, externally-verifiable test certificate.

The chamber design — separate-chamber, rather than single-chamber — is the engineering choice that most directly connects the machine to the published research. In a single-chamber design, oxygen, hypochlorite byproducts, and dissolved metal can mix with the hydrogen-saturated water that goes into the glass. In a separate-chamber design, the hydrogen-producing cathode side is physically isolated from the oxygen-producing anode side by an ion-exchange membrane. Only the hydrogen-saturated water flows into the pitcher. The trade-off is mechanical complexity and cost — which is part of why most of the consumer category does not bother with the architecture. The categorical reason this matters for cardiovascular use specifically: if the water you are drinking daily contains the byproducts the membrane was supposed to keep out, you have introduced a chronic, low-grade contaminant exposure into the population most likely to be drinking the water for cardiovascular reasons in the first place.

Independent verification

Three certificates anchor the machine's verifiable claims. The metallurgical certificate (No. 17-MANS-0078-B) documents the titanium composition. Japan Food Research Laboratories (JFRL) issued Certificate No. 23028707001-0201 reporting purity testing on the produced water: selected plasticizers, BPA, iron, and titanium were not detected. Masa International Corp. — a third-party hydrogen-output testing lab, not the manufacturer — measured the device's hydrogen production at approximately 134.2 mL/min under their test conditions (Test No. MM03-6024-01). The advertised marketing figure of 120 mL/min is the conservative number we publish. Every certificate referenced in this paragraph is a real document that can be looked up, and our editorial standard is that no certificate number appears in any blog article without a corresponding verifiable record.

Every certificate number in this article is one you can look up. That is not an accident — it is the editorial standard we set when we decided that transparency was the only marketing strategy that would hold up long-term. Eight substances tested, eight "Not detected" results. Most brands in this space do not test at all. The ones that do, in our reading of the public record, do not publish.

What we don't yet know

The cardiovascular hydrogen research base has gaps. A large, multi-center, long-duration human trial of hydrogen-rich water with cardiovascular outcomes as the primary endpoint has not yet been published. The optimal dose-response curve for daily oral hydrogen consumption in healthy-but-at-risk populations has not been characterized in detail. The interaction between hydrogen water and pharmacological cardiovascular interventions — statins, antihypertensives, antiplatelet agents — has not been studied in the kind of design that would let a clinician make integration recommendations.

These are the kinds of questions the next decade of research is going to take up. The point is not that the research is incomplete — every research field is incomplete — but that the active, accelerating publication trajectory (the 2024 reviews, the 2026 mechanism papers) is producing the foundation those larger trials would build on.

Frequently Asked Questions

Is hydrogen water studied as a treatment for heart disease?

No, and the published literature is careful not to frame it that way. Hydrogen water is studied as an investigational antioxidant in populations at risk of cardiovascular pathology — for example, the metabolic-syndrome population in Song et al. (2013). The trials measure mechanistic biomarkers (lipid panels, HDL function, oxidative-stress markers, inflammatory cytokines) rather than hard cardiovascular outcomes. Larger trials with hard endpoints would be needed before the research community talks about treatment in any clinical sense.

What concentrations do the published cardiovascular studies actually use?

Concentrations vary substantially across the field. The Song 2013 metabolic syndrome trial used approximately 0.9 to 1.0 liters per day of hydrogen-rich water. Other oral studies have used concentrations described in ppm — typically in the range of 0.5 to 1.6 ppm depending on the device used and the protocol. Inhalation studies use percentage-based mixtures (e.g., 2% hydrogen gas in the Iketani 2026 paper). The relevant point for a consumer is that any device used to approximate the research conditions has to deliver hydrogen concentrations close to what the trials specified — which is one of the reasons device quality matters.

What does the safety record look like across cardiovascular trials?

According to the Johnsen 2023 review of 81 clinical trials, no significant adverse effects have been reported from hydrogen water consumption at the concentrations studied. Hydrogen also holds FDA GRAS (Generally Recognized as Safe) status for use as a food additive. That is one of the strongest parts of the evidence base — the safety profile is well-characterized and continues to look benign across populations and protocols. None of which substitutes for a conversation with a healthcare provider about your own situation.

References

Ohsawa I, Ishikawa M, Takahashi K, et al. Hydrogen acts as a therapeutic antioxidant by selectively reducing cytotoxic oxygen radicals. Nature Medicine. 2007;13(6):688-694. PMID: 17486089. DOI: 10.1038/nm1577.
Song G, Li M, Sang H, et al. Hydrogen-rich water decreases serum LDL-cholesterol levels and improves HDL function in patients with potential metabolic syndrome. Journal of Lipid Research. 2013;54(7):1884-1893. PMID: 23610159. PMC3679390. DOI: 10.1194/jlr.M036640.
Meng F, Xue M, Li H, et al. Consumption of hydrogen-rich water ameliorates atherosclerosis by modulating gut microbiota and enhancing short-chain fatty acid levels. Life Sciences. 2026;397:124418. PMID: 42069299. DOI: 10.1016/j.lfs.2026.124418.
Iketani M, Kawata M, Ito M, et al. Inhalation of hydrogen gas reduces exacerbations of acute aortic dissection in mice. Life Sciences. 2026;397:124443. PMID: 42105975. DOI: 10.1016/j.lfs.2026.124443.
Wang SH, Li CH, Wei ZJ, et al. Acoustic hydrogen delivery to treat PANoptosis induced by myocardial ischemia/reperfusion injury in rats. Biomaterials Advances. 2026;183:214770. PMID: 41671925. DOI: 10.1016/j.bioadv.2026.214770.
Singh RB, Sumbalova Z, Fatima G, et al. Effects of Molecular Hydrogen in the Pathophysiology and Management of Cardiovascular and Metabolic Diseases. Reviews in Cardiovascular Medicine. 2024;25(1):33. PMID: 39077646. PMC11262389. DOI: 10.31083/j.rcm2501033.
Dhillon G, Buddhavarapu V, Grewal H, et al. Hydrogen Water: Extra Healthy or a Hoax? — A Systematic Review. International Journal of Molecular Sciences. 2024;25(2):973. PMID: 38256045. PMC10816294. DOI: 10.3390/ijms25020973.
Johnsen HM, Hiorth M, Klaveness J. Molecular Hydrogen Therapy — A Review on Clinical Studies and Outcomes. Molecules. 2023;28(23):7785. PMID: 38067515. PMC10707987. DOI: 10.3390/molecules28237785.
LeBaron TW, Sharpe R, Ohno K. Electrolyzed-Reduced Water: Review I. Molecular Hydrogen Is the Exclusive Agent Responsible for the Therapeutic Effects. International Journal of Molecular Sciences. 2022;23(23):14750. PMID: 36499079. PMC9738607. DOI: 10.3390/ijms232314750.
Fu Z, Zhang J, Zhang Y. Role of Molecular Hydrogen in Ageing and Ageing-Related Diseases. Oxidative Medicine and Cellular Longevity. 2022;2022:2249749. PMID: 35340218. PMC8956398. DOI: 10.1155/2022/2249749.

Holy Hydrogen products, including the Lourdes Hydrofix Premium Edition, are not medical devices and are not intended to diagnose, treat, cure, or prevent any disease. All information on this site is provided for educational and general wellness purposes only and should not be considered medical advice. Always consult a qualified healthcare provider before beginning any new wellness practice, especially if you have a medical condition, are pregnant or nursing, or take prescription medications.

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