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The Burn Won't Leave. And It's Not What Your Doctor Told You It Was.

A peer-reviewed mechanism is reframing what's happening inside the stomach of every post-H. pylori patient still feeling sick six months, a year, three years after their "negative" test — and why PPIs, slippery elm, DGL, and the supplements women in their 50s have been stacking for a decade may all be aimed at the wrong target.

Published by Wellness Report

Independent Gut Health Research Editorial review by our research desk

Published by Wellness Report — Independent Gut Health Research Editorial review by our research desk

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It usually starts about six weeks after the last antibiotic capsule.


You go in for the follow-up. The nurse practitioner clicks through your chart. She says the two words you have been waiting months to hear.


"You're negative."


You wait for the relief. It does not come.


You ask the question you rehearsed in the parking lot. Then why do I still feel like this?


She shrugs, not unkindly. "Give it time. Stay on the omeprazole. If the burning keeps up, we can talk about it in six months."


You walk to the car. You sit in it for ten minutes without starting the engine. You look at the discharge paper in your lap. Eradication confirmed. No further follow-up required. Four tidy words. Zero information about the burn under your ribs. Zero information about the bloat that arrives at 4 PM whether you eat or skip lunch. Zero information about the bracing you do before every meal. Zero information about the eight pounds you lost during your antibiotic course and have not put back. Zero information about the 4 AM anxiety you never had before this started.


You drive home. You put the paperwork in a drawer. Six months later you are still in the same body, reading something like this at midnight.


And the reason you are reading this at midnight is that you are not an edge case. You are a cohort.

H. pylori is the most common chronic bacterial infection in humans. Global estimates put lifetime exposure near half of the world population. Recent U.S. data puts active infection at 18.2 percent of American adults and lifetime exposure at 36.8 percent. If you have been treated for it, you are one of roughly thirty million Americans the healthcare system has quietly stopped tracking.


The number that should be on the evening news is the one that keeps turning up in the research and keeps not making it into your follow-up appointment.


Between 17 and 30 percent of successfully eradicated patients still report burning, gnawing, gastritis, reflux, or food sensitivity at six months to five years after their final negative test.


On the low end, that is the population of Wyoming. On the high end, it is the population of Pennsylvania. Every year.


It is the Mayo Clinic Connect thread posted by a woman two years after her treatment. My follow-up was not really in depth. Nobody told me what to expect.


It is the forum user eleven months past her last antibiotic. My doctor said I am cured. I do not feel cured.


It is the patient who summarized the whole thing in one sentence. The antibiotics killed the bug and my gut. I do not know which was worse.


Thirty million people. Reading the same sentences. Living in the same limbo. And the reason, once you see it, is not complicated.

What every patient in that thirty-million cohort is actually living with is not leftover infection.

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 It is the burn that follows the cure. And the reason everything you have tried to fix it with has not held is that none of those products were ever aimed at what is actually broken.


Look at the medicine cabinet of the average post-eradication patient five years in.


Omeprazole. Pantoprazole. Pepcid. DGL licorice. Slippery elm. Marshmallow root. Mastic gum. Zinc carnosine. L-glutamine. Aloe inner-leaf juice. Three different probiotic brands, all opened, none finished. A digestive enzyme from the fridge door. A printed low-FODMAP food list under a magnet.


Some of it gave you a week of relief. A couple gave you a month. None held.


The PPI suppresses acid. It does not repair the lining. It also keeps the lining from receiving the rhythmic acid signals that tell it to renew itself every few days. Stay on the PPI long enough and you quiet the renewal.


Slippery elm and DGL coat the stomach. They give your lining a soft cushion to sit on. They do not turn the repair signal back on.


Mastic gum has activity against H. pylori. Your H. pylori is already gone. The bacteria are not what is still burning.


Zinc carnosine and glutamine feed cells that have raw materials but no instruction signal. Adding bricks to a job site nobody is running.


Probiotics seed bacteria into a landscape that cannot host them. You cannot plant seeds in a scorched field. ISAPP, the probiotic industry's own scientific association, has acknowledged that up to ninety percent of the bacteria in a stored probiotic bottle may already be dead by the end of shelf life.


Low-FODMAP hides triggers. It removes the foods that ferment hardest in a sensitized gut. Symptoms quiet down. The minute a real meal lands — pizza on vacation, pasta at her daughter's rehearsal dinner — the same reaction fires, because the underlying inflammation never left.


These products are not all fraudulent. A handful of them help around the edges. The reason none of them resolve the burn permanently is that none of them are aimed at the actual layer that is broken.


This is why the post-H. pylori patient who has spent four thousand dollars on supplements feels like she is broken. She is not broken. Her products were just attacking the wrong target.

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For a stomach lining that is intact, eating is a non-event. 

Food goes in. Acid does its job. The lining renews itself every few days. The body absorbs what it needs.

7 AM, coffee on an empty stomach. The lining is already raw from yesterday. The acidity of the coffee lands on tissue that is supposed to be protected by a thick, glossy mucus layer and is not. The first burn of the day arrives before you have finished the cup.


10 AM, a granola bar at your desk. The fiber ferments in a microbiome that is still missing half its protective species from the antibiotic course. Gas builds. Pressure builds. The bloat starts. You shift in your chair.


12 PM, you eat the safe lunch. Plain chicken. Plain rice. Should be fine. It is not fine. The lining is now at peak inflammation. Anything moves the needle. You unbutton the top button of your jeans under the table.


3 PM, the gnawing arrives. Not pain exactly. Something more relentless. A constant low-level reminder that something inside is wrong.


6 PM, dinner. It does not matter what it is. By the time the plate is empty, you are bracing. By 8 PM you have your hand on your chest, half-hoping it is just gas. By 10 PM you are looking up symptoms of gastric cancer on your phone for the eleventh time this month.


11 PM, you lie in bed. You take the omeprazole you said you were going to stop taking three months ago. You sleep maybe four hours.


This pattern repeats every day. The DGL you took at breakfast did nothing. The slippery elm at lunch did nothing. The peppermint tea at 4 PM did nothing. Because nothing you did targeted the actual layer that is broken.


The actual layer has a name. It has three parts. And once you see them stacked, the entire pattern stops being mysterious.

What you are living inside of is not one problem. It is three. 

What you are living inside of is not one problem. It is three. 

Call them what they are.

Layer One. The repair switch that antibiotics left silent. Years of bacterial inflammation switched on a pro-inflammatory signaling system inside your stomach tissue. When the bacteria died, that system did not automatically reset. A cellular switchboard called Nrf2, your body's built-in anti-inflammatory repair signal, stayed muted. The burn you cannot point a doctor at is not the bacterium. It is the silence where the repair signal should be.


Layer Two. A microbiome that got cleared along with the target. A single course of clarithromycin plus amoxicillin can measurably disrupt the gut microbial community for four to eight years. The protective species collapse first. The wrong species creep back in first. Which is why so many eradicated patients develop new bloating, new reflux, new food sensitivities they never had before the treatment.


Layer Three. A proton pump that never got turned back on. The PPI you were given alongside the antibiotics was supposed to be temporary. The original FDA approval covered use up to fourteen days. The average post-eradication patient stays on it for more than three years. And when she tries to stop, the pumps come back online at a higher level than baseline. The research calls it rebound acid hypersecretion. One landmark trial put healthy, previously-asymptomatic volunteers on an eight-week PPI course. When they stopped, forty-four percent of them developed new heartburn, reflux, or dyspepsia within two months. The placebo arm saw fifteen percent. If you are a post-H. pylori patient, that rebound feels exactly like your infection coming back. It is not. It is the medication leaving. And because it feels like relapse, most patients reach for the bottle, refill the prescription, and quietly lock the cycle in for another year.


The H. pylori is gone. All three of these are still in the room.


Together they have a name. The Eradication Gap. Your discharge paper closed the first chapter. The Eradication Gap is the chapter nobody wrote.

In 1992, a pharmacologist at the Johns Hopkins School of Medicine named Dr. Paul Talalay published a paper in the Proceedings of the National Academy of Sciences that ended up on the front page of the New York Times. He had isolated a compound in cruciferous vegetables that activated the body's most powerful built-in repair pathway more strongly than anything his lab had ever tested. He named it sulforaphane.


The pathway has a formal name and an informal one. The formal name is Keap1-Nrf2. The informal one is your body's internal maintenance department. When it fires, it activates more than two hundred protective genes that quiet inflammation, rebuild the stomach lining, and restore the microscopic barrier between acid and tissue. It is the same system that lets a paper cut seal itself in three days.


During years of chronic H. pylori infection, that department gets gradually understaffed. During antibiotic therapy, it takes another hit. By the time your breath test comes back negative, the maintenance department has been operating on skeleton crew for years.


Two years after Talalay's discovery, his mentee Dr. Jed Fahey reported the finding that changed the practical picture. Three-day-old broccoli microgreens, the seedlings that come up before the mature head of broccoli forms, contain 20 to 50 times more of the sulforaphane precursor than the broccoli most people actually eat.


For most people that would have stayed an interesting antioxidant story. For post-H. pylori patients it became something far more specific.


In 2002, Fahey and colleagues published in PNAS that sulforaphane inhibited every tested strain of Helicobacter pylori in laboratory cultures, including strains resistant to clarithromycin. The same antibiotic that fails roughly one in four U.S. eradication attempts.


In 2009, Yanaka, Fahey, and colleagues published the landmark human trial in Cancer Prevention Research. Forty-eight H. pylori-infected patients ate broccoli microgreens daily for eight weeks. The sprout group saw a greater-than-forty-percent reduction in H. pylori stool antigen and measurable drops in gastric inflammation markers. The placebo arm saw nothing.


Then around 2015, the broader gut-lining research started arriving. Sulforaphane reinforced tight junction proteins in human gut tissue (PubMed 30302904). Sulforaphane reversed antibiotic-induced changes in gut permeability (Tandfonline 2021). Sulforaphane modulated the gut microbiome from the lining inward, increasing populations of Faecalibacterium and Bifidobacterium, two of the bacterial groups most depleted after antibiotic therapy (Frontiers in Physiology, 2025).


The compound that flips the Nrf2 switch back on is the same compound that quiets H. pylori-driven inflammation in human stomach tissue. One compound. Both jobs. Exactly the thing the Eradication Gap has been waiting for.


Which makes the obvious first thought. Fine. I will just eat the sprouts.


Except you cannot.

Three problems.


The first is dose. To hit the amount of sulforaphane the post-H. pylori research uses, you would need to eat three to four pounds of fresh microgreens every day. Every single day. For a stomach that already cannot tolerate large servings of cruciferous fiber, that is functionally impossible.


The second is heat. Sulforaphane does not exist pre-formed inside the plant. It is made on demand when two separate compounds meet. Glucoraphanin, the stable precursor. Myrosinase, the enzyme that converts the precursor into the active compound. Cooking destroys myrosinase. Boiling, steaming for more than five minutes, roasting. All of it kills the enzyme that does the actual conversion. Most of the broccoli sold and consumed in the United States no longer produces meaningful sulforaphane by the time it reaches the plate.


The third is soil. Sulfur content in industrial farmland has been declining for decades, which means the broccoli growing today contains measurably less glucoraphanin than the broccoli of the 1950s and 60s. The precursor itself is diminished (PMC8394606).


And there is a catch that matters even more for someone in your specific situation. Your gut, after antibiotic therapy, is worse at making the sulforaphane conversion on its own than a healthy gut. The bacteria that normally help were collateral damage in the eradication protocol. Eating more sprouts into a depleted gut is like pouring gasoline into a car with a cracked fuel line.


Which is exactly why broccoli sprout capsules exist in the first place. Concentrate the compound. Take two pills. Skip the kitchen. A fine idea.


And the reason the vast majority of them are a quiet failure is in a single piece of chemistry almost nobody explains to you.

Sulforaphane is not an ingredient you can put in a capsule. It is the product of a chemical reaction between two things.


Glucoraphanin. The raw precursor. Shelf-stable. Easy to put in a pill.


Myrosinase. The enzyme that turns glucoraphanin into sulforaphane. Fragile. Heat-sensitive. Acid-sensitive. Ruined by most manufacturing processes.


Both pieces live in a fresh microgreen, separated by a cell wall. When you chew the sprout, the wall ruptures, the two meet, and sulforaphane forms right there on the plate.


The supplement industry solved the first half of that equation a decade ago. Almost nobody bothered to solve the second half. The reason is not a mystery. Myrosinase is harder to protect, more expensive to source, and impossible to fake on a label. The industry learned quickly that consumers do not know the enzyme is supposed to be there.


So the bottles get made anyway. Glucoraphanin in. No active myrosinase. The label still says broccoli sprout extract. The price still sits between thirty and eighty dollars. You take it for six weeks. Nothing happens. You conclude, honestly and wrongly, that sulforaphane does not work for you.


It did not fail to work for you. It never actually formed.


The raw ingredient sat in your stomach. The reaction partner was missing. Which is what every patient before you is quietly experiencing when they tell their friends that the broccoli thing did not do anything.


Think of it as a two-key safe. Sulforaphane is locked inside the safe. It takes two keys to open. The precursor is one. The enzyme is the other. Most supplements ship the safe and one key. The safe stays locked. The compound stays trapped. The bottle goes in your supplement drawer.


This is the gap Sproutly was built to close.

Made in small batches monthy ➔

The question that drove the entire formulation was narrow. What would it take to deliver the dose of active sulforaphane the research actually uses, into a stomach that just finished antibiotic therapy, in two capsules you can swallow with your morning coffee?


The answer is a three-part system, in the proportions the peer-reviewed work points to.


700 mg of broccoli seed extract, standardized to 13 percent glucoraphanin. The concentrated precursor. A wheelbarrow of microgreens packed into a daily dose.


200 mg of broccoli sprout extract carrying active, protected myrosinase. The enzyme that makes the reaction actually happen inside you. The piece the rest of the category leaves out.


100 mg of mustard seed extract. A second, structurally different source of the same enzyme. An intentional redundancy, because a post-antibiotic stomach is unpredictable. If acid compromises the first enzyme on the way down, the second one steps in.


Plus 50 mg of Vitamin C as the cofactor for tissue repair and Nrf2 signaling.


Two capsules. Once a day. With breakfast.


Every milligram is printed on the label. No proprietary blends. No filler ingredients. Manufactured in an FDA-registered facility. Independently lab-tested for heavy metals, potency, and purity. Non-GMO. Vegan. GMP certified.


It is not a cure. It is not a detox. It is not a replacement for medical care.


It is a daily post-eradication support protocol. A full dose. The active enzyme. A backup key when the first one gets tired. The rebuild contract your discharge paper never signed.

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The one post-eradication protocol your GI visit didn't include.

A complete enzyme system. Two capsules. Two capsules. Once a day. With breakfast.

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If you sign that rebuild contract, here is what the research and customer reports suggest the next ninety days look like. Your body is your own. Your timeline will be too.

Days 1 to 14. Nothing dramatic on the outside. This is where most people get impatient. Inside, your Nrf2 pathway is registering its first real activation signal in months or years. The maintenance department is clocking back in. You will not feel this yet. It is happening anyway. Most women describe the first two weeks as I am not one hundred percent sure but something feels less angry.


Days 15 to 28. The burning starts to space out. The knot under the ribs loosens. The four PM bloat curve gets quieter, not gone, but the balloon does not fully inflate. The moment most customers remember is small. A meal they used to brace for that did not cost them later. One customer wrote, I realized on a Tuesday that I had not thought about my stomach all morning.


Weeks 5 to 8. This is the exact window the 2009 Yanaka trial directly measures. Markers of gastric inflammation drop meaningfully inside this window in the published data. Sleep returns. Food sensitivities soften. The middle-of-the-night anxiety fades. The baseline of how I feel at rest resets upward.


Weeks 9 to 12. Meals stop being a calculation. You notice, sometimes with a jolt, that you have not carried antacids in your bag for a week. Friends at dinner order from the wine list and you do not do the math first. For many post-eradication patients, this is the first time since their treatment that they stop thinking of themselves as recovering from H. pylori and start thinking of themselves as simply done with it.


At some point during this window, almost every patient who takes Sproutly seriously hits the same fork.

Path One.

 

You refill the omeprazole. You eat early. You avoid the foods you used to love. You keep antacids in your bag. You tell yourself this is who you are now, because the test was negative and the doctor said the hard part was over. The lining stays thin. The microbiome stays quiet. The rebuild contract stays unsigned. Year four looks a lot like year one.


Path Two.

 

You sign the rebuild contract. Ninety days. Two capsules a morning. You give your body the specific combination it has been waiting for since the antibiotics ended. You find out, by the end, what your stomach feels like when it is no longer being asked to function on bare studs.


You already know which path the last eight months, or three years, or eleven, have been pointing you toward. It is almost never the dramatic decisions that change a body's trajectory. It is the small ones, made on an ordinary afternoon, by someone who got tired of waiting for the system to send a rebuild crew that was never coming.


And the reason that small decision tends to actually stick is that you are not the first person to make it.

Jennifer Coleman

Breath test came back negative fourteen months ago and nobody explained why I still could not eat a normal lunch. I started Sproutly in January. Eight weeks in I realized I had not checked the omeprazole bottle in four days. I went a whole weekend without it. Then a week. My doctor signed off on a taper after I showed her my notes. That is a sentence I did not think I would get to write in 2026.

9

 David K.

I did everything right. Finished the quad therapy. Got the clean breath test. My life was plain chicken and rice twice a day because every other food hurt. My wife ordered me Sproutly after reading a sulforaphane study at three in the morning. I was the skeptic. By the end of week seven I had eaten pizza twice and slept flat both nights. The biochemistry explanation is what sold me. The dinner is what convinced me.

Michelle Roberts

I am an ICU nurse, twenty years in. I was treated for H. pylori in 2023. I spent the next year telling patients to give it time while my own stomach kept burning. The myrosinase argument is what made me try this. It is the first supplement I have been willing to recommend to family. Ninety days in I am sleeping flat for the first time since the antibiotics. I do not know how else to put it.

2

Darnell S

The drawer of half-opened gut supplements is real. DGL, zinc carnosine, mastic gum, slippery elm, three different probiotics. Some helped a little. None held. The difference here was that around week six I realized I had stopped scanning my chest after every meal. Stopped bracing. You stop noticing. That is the part people do not describe right. The improvement is not loud. You just stop noticing.

Mia Linburg

Post-eradication almost three years. I had decided the stomach I had was the stomach I was going to have. I was wrong. I was wrong about a lot of things. I started Sproutly in September. Week ten I ate dinner at my daughter's birthday without doing the usual math first. Thank you to whoever fought for the mustard seed line on the label.

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The Sproutly Promise

Try Sproutly for a full 90 days.

 

Not 14 days. Not 45 days. A real 90 days, because the gut lining does not rebuild itself in two weeks and any company that says otherwise has not read the research.


Take it every morning. Track the bloat curve, the 4PM moment, the sleep, the urgency, the energy. Track everything you have not been able to track for years because nothing has moved the needle long enough to bother.


If after 90 days the curve has not flattened — if it has not done for you what the research suggests it should — return the empty pouches for a full refund. Every dollar back. No questions, no friction, no thirty-page form.


If after 90 days you do feel a real difference, the simple recommendation is the one most customers arrive at on their own. Stay on it. The lining stays repaired while the input that repairs it keeps showing up.


That is the entire offer.

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The rebuild protocol for a stomach that already finished its antibiotics.

Two capsules. Once a day. With breakfast.

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LIMITED AVAILABILITY NOTICE ⚠️

To ensure quality and freshness, Sproutly is produced in small batches.

Availability may be limited based on current demand.  

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References.


1. Talalay, P. et al. Broccoli sprouts. An exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proceedings of the National Academy of Sciences, 1997.


2. Fahey, J. W., Haristoy, X., Dolan, P. M., Kensler, T. W., Scholtus, I., Stephenson, K. K., Talalay, P., Lozniewski, A. Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors. PNAS, 2002.


3. Yanaka, A., Fahey, J. W., Fukumoto, A., et al. Dietary sulforaphane-rich broccoli sprouts reduce colonization and attenuate gastritis in Helicobacter pylori-infected mice and humans. Cancer Prevention Research, 2009.


4. PMC10487861. The Rationale for Sulforaphane Favourably Influencing Gut Homeostasis and Gut-Organ Dysfunction. 2023.


5. PubMed 30302904. Sulforaphane reinforces tight junction protein expression and repairs injury to the gut mucosal epithelium.


6. Tandfonline 10.1080/21655979.2021.1952368. Sulforaphane protects intestinal epithelial cells against LPS-induced changes in permeability and inflammation.


7. Frontiers in Physiology 2025.1497566. Sulforaphane modulates microbiome composition, increasing Faecalibacterium and Bifidobacterium populations.


8. Hooi, J. K. Y., Lai, W. Y., Ng, W. K., et al. Global Prevalence of Helicobacter pylori Infection. Systematic Review and Meta-Analysis. Gastroenterology, 2017.


9. Reimer, C., Søndergaard, B., Hilsted, L., Bytzer, P. Proton-pump inhibitor therapy induces acid-related symptoms in healthy volunteers after withdrawal of therapy. Gastroenterology, 2009.


10. Lazarus, B., Chen, Y., Wilson, F. P., et al. Proton Pump Inhibitor Use and the Risk of Chronic Kidney Disease. JAMA Internal Medicine, 2016.


11. Blaser, M. J. Antibiotic use and its consequences for the normal microbiome. Science, 2016.


12. ISAPP. International Scientific Association for Probiotics and Prebiotics. Industry note on probiotic viability at end of shelf life.


13. PMC8394606. Soil sulfur depletion and declining glucoraphanin content in modern broccoli.

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