Acidic Foods and Silent Reflux: Why Sour Candy Hits Your Throat

Reflux carries more than acid. It carries pepsin, a protein-digesting enzyme the stomach makes, and pepsin is the part that stays. In voice-box biopsies, pepsin turned up in the tissue of 8 of 9 people with LPR and in none of 12 people without it. Where pepsin was present, a protective protein in the vocal-fold lining, carbonic anhydrase III, was depleted².

Pepsin explains why acid still matters after a reflux episode is over. In lab work, human pepsin was most active at pH 2.0 and went quiet at pH 6.5 and above. Quiet is not gone. Held for a full day at pH 7 and body temperature, it recovered 79% of its activity once acid brought the pH back to 3. The researchers noted that the throat area averages about pH 6.8, so pepsin left there sits idle, in a form that could be "reactivated by a subsequent decrease in pH"³.

Sour candy is acid with sugar on it. In a dental lab, commercially sold sour sweets measured pH 2.30 to 3.14, against pH 3.86 for the orange juice they were compared with; lower means more acidic. Every sweet eroded tooth enamel, and some removed more than the juice did: up to 10.88 micrometers in an hour, against 5.23⁴. A second lab study found that sour candies generally cut deeper into enamel than their original flavors, and that saliva is "much less likely" to protect against the sour ones⁶.

Your teeth are the first surface that acid touches. The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) names "acidic foods, such as citrus fruits and tomatoes" among the foods commonly linked to GERD symptoms¹. Candy is not named on its list. By its pH, it belongs there.

The NIDDK lists these foods and drinks as commonly linked to GERD symptoms¹:

• Acidic foods, such as citrus fruits and tomatoes
• Alcoholic drinks
• Chocolate
• Coffee and other sources of caffeine
• High-fat foods
• Mint
• Spicy foods

Sour sweets belong next to the first item, at pH 2.30 to 3.14⁴. One LPR diet went by pH instead of by food group. In the 2011 low-acid diet study, every food and drink below pH 5 was cut, and each person was given a printed list of acceptable foods and drinks⁵.

No list can tell you which of these is yours. The throat log at the end of this page is how you find out.

Three studies looked at whole diets rather than single foods:

• A mostly plant-based, Mediterranean-style diet with alkaline water (pH above 8), plus standard reflux precautions. In a chart review, 99 people with LPR followed it for 6 weeks, and their reflux symptom score fell 39.8% on average. In a comparison group of 85 people treated with acid blockers and the same precautions it fell 27.2%⁷.
• Fresh fruit and vegetables, olive oil and fish. In a survey of 817 adults in Tirana, Albania, people who mostly ate red meat, fried food, sweets and fast food had 2.3 times the odds of GERD of people who ate a mostly Mediterranean pattern⁸.
• A low-fat, high-protein standardized anti-reflux diet, with lifestyle changes. In 44 people with LPR who followed both for 3 months, 88.6% had symptom relief and 40.9% had their symptoms resolve completely⁹.

For GERD symptoms at night or when lying down, the NIDDK says that eating meals at least 3 hours before you lie down or go to bed may improve symptoms¹. A case-control study in Osaka, Japan, compared 147 people with GERD and 294 without. Those who finished dinner less than 3 hours before bed had 7.45 times the odds of GERD of those who left 4 hours or more¹⁰.

For a throat that flares the day after, add one line to the log below: what time the last meal or snack ended.

The low-acid diet study came from Jamie Koufman of the Voice Institute of New York, who in 2011 put 20 adults with LPR on a strict version of it⁵. Every one still had symptoms despite twice-daily proton pump inhibitors (PPIs, the standard acid-blocking pills) plus a second acid reducer at bedtime. For at least two weeks, they cut every food and drink below pH 5.

Symptoms improved in 19 of the 20, and 3 had none left. The average Reflux Symptom Index fell from 14.9 to 8.6, and the throat findings scored on examination fell from 12.0 to 8.3⁵.

The pills had already failed these patients. In a UK double-blind trial for persistent throat symptoms, 346 adults took lansoprazole or a placebo for 16 weeks, and the drug did no better than the placebo¹¹.

Diet has a ceiling too. A 2026 NYU Langone review of 208 people on a 96-hour pH monitor compared a high-acid day with a low-acid day. Average esophageal acid exposure time was 41% lower on the low-acid day, from 12.51% to 7.33% of the time¹². Of those whose monitor showed reflux disease, only 24.7% reached a normal reading on a low-acid day¹².

Throat clearing, a lump and a rough voice are the usual signs people log. For the voice, the American Academy of Otolaryngology-Head and Neck Surgery Foundation guideline says clinicians should perform laryngoscopy, a camera look at the voice box, or refer to someone who can, when hoarseness has not resolved or improved within 4 weeks, or at any point if a serious cause is suspected¹³.

Diet changes what arrives at the throat. The lining where pepsin has already settled is a separate question.

In a 2024 study of voice-box tissue and cells, pepsin expression was positively correlated with reactive oxygen species (ROS), the molecules behind oxidative stress, in the tissue. In cells, ROS rose as the pepsin dose went up. Apocynin, a ROS inhibitor, brought the ROS down, and apocynin and an NLRP3 inhibitor both suppressed damage to the cells¹⁴.

Nrf2 is a protein that switches on protective genes, and its activation induces genes involved in antioxidant defense and detoxification. A 2016 review found that sulforaphane, from broccoli, activates Nrf2 more potently than curcumin, silymarin or resveratrol, and has significantly higher bioavailability than those supplements¹⁵.

The human result closest to the throat comes from the upper airway. In a placebo-controlled dose-escalation trial at UCLA, volunteers took sulforaphane in broccoli sprout homogenate. Antioxidant Phase II enzymes rose in cells rinsed from the nose, in a dose-dependent manner, peaking at 200 g of sprouts. Alfalfa sprouts, which do not contain sulforaphane, produced no rise¹⁶.

A glucoraphanin capsule does not hold sulforaphane ready-made. Sulforaphane forms when glucoraphanin, the precursor in broccoli seed, meets myrosinase, the enzyme that converts it.

In a 2026 double-blind crossover trial, 16 people took a glucoraphanin-rich broccoli seed extract twice, once with myrosinase from mustard seed and once without. With the enzyme, sulforaphane bioavailability averaged 39.8%. Without it, 18.6%¹⁷.

So hold any label to four questions:

1. Is glucoraphanin named, with a percentage?
2. Is active myrosinase on its own line?
3. Is there an amount beside every extract, with no proprietary blend?
4. Is there a sulforaphane figure per serving?

The Sproutly label answers all four. Per two-capsule serving:

• Broccoli seed extract, 700 mg (13% glucoraphanin). The precursor.
• Broccoli sprout extract, 200 mg (active myrosinase). The enzyme, on its own line.
• Mustard seed extract, 100 mg. Mustard seed was the myrosinase source in the 2026 trial¹⁷.
• Vitamin C (ascorbic acid), 50 mg. The trial gave ascorbic acid with both of its doses too¹⁷.

The label states up to 30 mg sulforaphane per serving. The only other ingredients are the vegetable capsule (HPMC), rice flour, magnesium stearate and silica. One pouch holds 60 capsules, which is 30 servings of two.

A throat log is the food diary turned around: it tracks what you are trying to change. On day one, then once a week, write down:

• How many times you cleared your throat before noon
• Whether the lump was there when you swallowed
• How your voice sounded on the first call of the day
• How much mucus there was
• Whether you coughed when you ate

Add a line for the acidic days: candy, citrus, tomato sauce, coffee, and the time the last meal ended. If your throat flares the day after, the log shows it.

Keep everything you rely on now, the diet included, and score the log at 90 days, not at week two. Diet works on what goes in. If you would like to add something aimed at the lining, this is the one we built around sulforaphane: Sproutly broccoli sprout extract. Your first order comes with 90 days from confirmed delivery to decide.

1. National Institute of Diabetes and Digestive and Kidney Diseases. Eating, Diet, & Nutrition for GER & GERD. Last reviewed July 2020. https://www.niddk.nih.gov/health-information/digestive-diseases/acid-reflux-ger-gerd-adults/eating-diet-nutrition
2. Johnston N, Knight J, Dettmar PW, Lively MO, Koufman J. Pepsin and carbonic anhydrase isoenzyme III as diagnostic markers for laryngopharyngeal reflux disease. Laryngoscope. 2004;114(12):2129-34. PMID 15564833
3. Johnston N, Dettmar PW, Bishwokarma B, Lively MO, Koufman JA. Activity/stability of human pepsin: implications for reflux attributed laryngeal disease. Laryngoscope. 2007;117(6):1036-9. PMID 17417109
4. Davies R, Hunter L, Loyn T, Rees J. Sour sweets: a new type of erosive challenge? Br Dent J. 2008;204(2):E3. PMID 18084191
5. Koufman JA. Low-acid diet for recalcitrant laryngopharyngeal reflux: therapeutic benefits and their implications. Ann Otol Rhinol Laryngol. 2011;120(5):281-7. PMID 21675582
6. Wagoner SN, Marshall TA, Qian F, Wefel JS. In vitro enamel erosion associated with commercially available original-flavor and sour versions of candies. J Am Dent Assoc. 2009;140(7):906-13. PMID 19571054
7. Zalvan CH, Hu S, Greenberg B, Geliebter J. A comparison of alkaline water and Mediterranean diet vs proton pump inhibition for treatment of laryngopharyngeal reflux. JAMA Otolaryngol Head Neck Surg. 2017;143(10):1023-1029. PMID 28880991
8. Mone I, Kraja B, Bregu A, et al. Adherence to a predominantly Mediterranean diet decreases the risk of gastroesophageal reflux disease: a cross-sectional study in a South Eastern European population. Dis Esophagus. 2016;29(7):794-800. PMID 26175057
9. Lechien JR. Effectiveness of diet and lifestyle changes for the treatment of laryngopharyngeal reflux disease: a prospective study. J Voice. 2025 (online ahead of print, 18 Sep). PMID 40973508
10. Fujiwara Y, Machida A, Watanabe Y, et al. Association between dinner-to-bed time and gastro-esophageal reflux disease. Am J Gastroenterol. 2005;100(12):2633-6. PMID 16393212
11. O'Hara J, Stocken DD, Watson GC, et al. Use of proton pump inhibitors to treat persistent throat symptoms: multicentre, double blind, randomised, placebo controlled trial. BMJ. 2021;372:m4903. PMID 33414239
12. Skryd A, Pasuizaca-Yanez V, Chablaney S, et al. A low-acid diet rarely normalizes pathologic gastroesophageal reflux disease. Dis Esophagus. 2026;39(4):doag085. PMID 42585561
13. Stachler RJ, Francis DO, Schwartz SR, et al. Clinical practice guideline: hoarseness (dysphonia) (update). Otolaryngol Head Neck Surg. 2018;158(1_suppl):S1-S42. PMID 29494321
14. Tan JJ, Dai YF, Wang F, et al. Pepsin-mediated inflammation in laryngopharyngeal reflux via the ROS/NLRP3/IL-1β signaling pathway. Cytokine. 2024;178:156568. PMID 38471420
15. Houghton CA, Fassett RG, Coombes JS. Sulforaphane and other nutrigenomic Nrf2 activators: can the clinician's expectation be matched by the reality? Oxid Med Cell Longev. 2016;2016:7857186. PMID 26881038
16. Riedl MA, Saxon A, Diaz-Sanchez D. Oral sulforaphane increases Phase II antioxidant enzymes in the human upper airway. Clin Immunol. 2009;130(3):244-51. PMID 19028145
17. Mastaloudis A, Holcomb L, Fahey JW, et al. Exogenous myrosinase from mustard seed increases bioavailability of sulforaphane from a glucoraphanin-rich broccoli seed extract in a randomized clinical study. Sci Rep. 2026;16(1):9162. PMID 41692762