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MyDeficiencies

Magnesium hydroxide

antacid and saline (osmotic) laxative

Also sold as Phillips' Milk of Magnesia, Pedia-Lax.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Magnesium hydroxide has no classical depletion machinery of the enzyme-induction or renal-wasting kind, and the main real signal runs in the opposite direction from depletion. It is an inorganic magnesium salt that is partly absorbed (oral bioavailability about 15% in 10 healthy men [8]) and cleared by the kidney [7]. The labels tell people with kidney disease or a magnesium-restricted diet to ask a doctor first [1][2]. The one orange entry is therefore magnesium excess and retention (hypermagnesemia), bounded to renal impairment, older age, bowel obstruction and high or prolonged dosing. Case reports record serum magnesium of 9.9 and 11.0 mg/dL with one death [10], and asystole needing resuscitation in a dialysis patient [11]. This is an excess risk: extra magnesium would be the hazard, not the remedy.

antacid and saline (osmotic) laxative · ATC A02AA04, antacid, DDD 3 g (WHO ATC/DDD Index [6]) · also sold as Phillips' Milk of Magnesia and Pedia-Lax chewables; component of Maalox and Mylanta and Haley's M-O [34] · reviewed 2026-10-04. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Magnesium hydroxide in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow — Low
Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded — disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Magnesium: excess and retention (hypermagnesemia), bounded to renal impairment, older age, bowel obstruction, and high or prolonged dosing

Orange — Moderate

See study details

Direction: excess and retention, not depletion. Magnesium hydroxide is partly absorbed and renally cleared, and in people who cannot clear it, or whose bowel transit is blocked, serum magnesium can reach dangerous levels.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

  • Null findings: No severe effects in healthy volunteers [8]. In the geriatric trial only 2 of 64 patients exceeded 1.25 mmol/L and none had symptoms [9]. In magnesium oxide data, hypermagnesemia was confined to treated patients with the lowest kidney function and those with normal function stayed in range [14][16].
  • At-risk subgroups: Renal impairment or dialysis, older age, bowel obstruction or reduced motility, chronic or high-dose use. Class context (Tier C, magnesium oxide, not this drug): Ishii 2023 [15], 35 hypermagnesemia cases and 140 controls, estimated creatinine clearance at or below 28.2 mL/min a significant risk indicator; hypermagnesemia incidence 11.6% with higher dose, 27.0% with low clearance, 53.1% with both.

Regulatory status

Labels advise asking a doctor before use with kidney disease or a magnesium-restricted diet, and warn the product may interact with prescription drugs [1][2][3]. The labels do not quantify the risk.

Population evidence (Tier A, this drug)

Dolberg [8]: crossover, 10 healthy men, single oral dose of 3 x 360 mg; bioavailability about 15%, urinary magnesium up 17.7%, no severe side effects. Healthy kidneys, one dose. Kinnunen and Salokannel 1987 [9]: trial in 64 geriatric long-stay patients, mean 25 mL magnesium hydroxide daily versus a bulk laxative; two patients had serum magnesium above 1.25 mmol/L after treatment, without clinical hypermagnesemia.

Case reports (Tier B, this drug)

Jou 2023 [10]: an 82-year-old woman with end-stage renal disease on 3,000 mg/day for 2 weeks, serum magnesium 9.9 mg/dL, recovered with dialysis; a 50-year-old woman with creatinine 1.07 mg/dL, history of cerebral hemorrhage and compromised GI transit, serum magnesium 11.0 mg/dL, cardiac arrest and death. Alaini 2017 [11]: 73-year-old man on dialysis after milk of magnesia, serum magnesium above 4.1 mmol/L, bradycardia and asystole, recovered after hemodialysis. McLaughlin 1998 [12]: 42-year-old woman with normal renal function and a sigmoid obstruction, milk of magnesia and Maalox, high magnesium with low calcium, hypothermia, hypotension, fatal pulseless electrical activity. Khairi 2014 [13]: 70-year-old man with renal failure and sigmoid volvulus on over-the-counter magnesium laxatives; the retrieved abstract does not name magnesium hydroxide, so it is supportive only.

Mechanism

Named. About 15% of the dose is absorbed [8], elimination is renal [7], so reduced glomerular filtration, or slow transit that lengthens contact time, raises serum magnesium. Hypermagnesemia causes neuromuscular blockade and vasodilation by inhibiting calcium influx (StatPearls magnesium sulfate chapter, opened via fetch summary only; not cited as a numbered source).

Class cohort test

CLASS EXTRAPOLATION applies only to the quantified renal risk [14][15][16]: those cohorts studied magnesium oxide, magnesium hydroxide was not in them, and they are used as context only. The grade itself rests on the labels, the PK study and trial [8][9], and drug-specific cases [10][11][12].

Why not red

Severe events are documented in case reports (Tier B), the Tier A trial data show a low frequency of mild elevation, and the cohort estimates of renal risk are for magnesium oxide.

Counter-evidence held on record

Counter-evidence and confounding Case reports select for catastrophic outcomes and cannot give an incidence. Several reported patients had a second driver (bowel obstruction, cerebral hemorrhage, volvulus). Risk estimates by creatinine clearance come from magnesium oxide, whose absorption may differ from magnesium hydroxide. Framing caution This is an excess and retention risk. Supplementing magnesium, or using more of this drug, is the hazard, not the remedy. It must never be presented as a magnesium deficiency or a reason to increase magnesium intake. Anyone with kidney disease should ask a clinician before use, as the label says.

Phosphate: gut binding shown, hypophosphatemia is class extrapolation from aluminum-containing antacids

Yellow — Low

See study details

Direction: depletion by absorption interference. Magnesium hydroxide lowers serum phosphorus in dialysis patients, but reported phosphate depletion with bone disease involves aluminum-based antacid mixtures.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: No study reported hypophosphatemia in people taking magnesium hydroxide alone at labeled doses.
  • At-risk subgroups: Heavy long-term antacid users, alcohol use, low dietary phosphate, and advanced kidney disease on binders (context from [17][20], not drug-specific).

Regulatory status

Not mentioned in the three labels opened [1][2][3].

Population evidence

Guillot et al. [18]: four-phase trial in 9 hemodialysis patients (no binder, magnesium hydroxide alone, magnesium plus aluminum hydroxide, aluminum hydroxide alone); serum phosphorus decreased significantly on magnesium hydroxide alone and was best controlled with the combination; serum magnesium stayed below 4.5 mEq/L. This is a Tier A binding signal, but in hyperphosphatemic patients it is the intended effect, not a deficit. Case report [19]: a 40-year-old woman taking about 120 tablets daily of a product delivering 12 g magnesium oxide and 60 g aluminum aminoacetate had serum phosphate 0.55 mmol/L and bilateral femoral neck fractures; phosphate recovered and fractures healed after she stopped. The product was a magnesium oxide and aluminum mixture, not magnesium hydroxide.

Mechanism

Present. Phosphate binding by the magnesium cation in the gut was shown for this drug [18]. A 1982 narrative review attributes antacid phosphate depletion syndrome to aluminum hydroxide with prolonged high-dose use, for example in alcoholics [17]; the Merck Manual names long-term, large-amount aluminum antacids [20]. Magnesium hydroxide's own contribution to hypophosphatemia in people with normal kidneys is not isolated by any source retrieved.

Class cohort test

CLASS EXTRAPOLATION for the hypophosphatemia and bone claim: aluminum-containing antacids and magnesium oxide mixtures [17][19][20]. Magnesium hydroxide as a single agent was not in those cases. It was in the dialysis trial [18], which supports binding only. Capped at yellow.

Counter-evidence held on record

Counter-evidence and confounding Osteomalacia and fracture are outcomes, not phosphate deficiency (Hard Rule 2); in the case report [19] extreme overuse and a psychiatric history confound. Aluminum, not magnesium, is the standard explanation [17][20]. Framing caution Not an expected effect at labeled doses. Do not recommend phosphate supplementation from this entry.

Calcium: low serum calcium reported only as a consequence of magnesium excess

Yellow — Low

See study details

Direction: secondary disturbance. Severe hypermagnesemia can suppress parathyroid hormone and lower calcium; no study shows magnesium hydroxide impairs calcium absorption.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: No study measured calcium in magnesium hydroxide users without hypermagnesemia. A 1982 narrative review ties hypercalciuria and milk-alkali syndrome to calcium carbonate and bicarbonate antacids, not magnesium [17].

Regulatory status

Not mentioned in the labels opened [1][2][3].

Population evidence

McLaughlin 1998 [12] (Tier B, this drug): the fatal hypermagnesemia case with normal renal function also had reduced calcium. Eisenbud 1976 [23] (Tier C, different salt): severe hypocalcemia with low PTH after magnesium sulfate for toxemia; the authors suggest hypermagnesemia directly suppressed PTH secretion and the glands responded normally to a phosphate load afterward. Calcium values were not reported in the retrieved text of the other magnesium hydroxide cases [10][11].

Mechanism

Named for severe hypermagnesemia (PTH suppression) [23]. Not shown at therapeutic exposures with normal magnesium.

Class cohort test

CLASS EXTRAPOLATION for the PTH mechanism: magnesium sulfate [23] is not magnesium hydroxide, and the magnesium hydroxide case [12] is a single report. Capped at yellow.

Counter-evidence held on record

Counter-evidence Calcium fell in an acutely ill patient with obstruction, hypothermia and shock [12], so attribution to magnesium alone is uncertain. Framing caution This is a downstream consequence of magnesium excess, not a dietary calcium deficiency and not a calcium absorption finding. It does not imply anyone should increase calcium intake.

Potassium and fluid: diarrhea-related loss, laxative class extrapolation

Yellow — Low

See study details

Direction: loss through diarrhea, a disturbance rather than a dietary deficiency. Diarrhea from laxatives, especially when abused, can cause hypokalemia; no study measured potassium in magnesium hydroxide users.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: A PubMed listing for "magnesium hydroxide" with hypokalemia returned three records (a neonate with hyperaldosteronism, a cat, camelids) and none describing human therapeutic use.

Regulatory status

The OTC label says to stop use and ask a doctor for certain symptoms and that the product is a laxative with action in 1/2 to 6 hours [1][3]. It does not mention potassium.

Population evidence

None for this drug. Merck Manual (reviewed Dec 2025) [24]: "By inducing diarrhea, laxatives, especially when abused, can cause hypokalemia", and chronic diarrhea including laxative abuse as a cause; it does not name magnesium-containing laxatives. NIH ODS [7]: high doses of magnesium from supplements or medications often cause diarrhea with nausea and cramping.

Mechanism

Present at high doses: osmotic retention of water in the bowel and watery stool. Potassium loss follows only with persistent diarrhea.

Class cohort test

CLASS EXTRAPOLATION from laxatives as a class in a narrative reference [24]. Magnesium hydroxide was not named in the source and was in no cohort. Capped at yellow.

Counter-evidence held on record

Counter-evidence Occasional labeled use rarely causes persistent diarrhea. Losses with abuse are driven by weight-loss behaviors and other contributors named in the source. Framing caution A fluid and electrolyte disturbance linked to diarrhea, not a diet-driven potassium deficiency. Diarrhea on this drug also signals magnesium load, which matters most when kidneys are impaired. Do not recommend potassium supplementation from this entry.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden

Not graded — disclosed evidence gap

See study details

No evidence on magnesium hydroxide and mitochondrial structure, electron transport or biogenesis was retrieved for the antacid or laxative.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C source support for even a yellow grade was opened, and no circulating claim of magnesium hydroxide mitochondrial harm was found. Disclosed gap, not a finding of safety. Re-check when search budget and PubMed access are restored.

What was searched

PubMed listing for "magnesium hydroxide" with mitochondria (7 records): engineered nanomaterial and layered double hydroxide scaffold papers and unrelated mitochondrial method papers, none on the pharmaceutical. Web search (before the budget cap) for magnesium hydroxide with mitochondria, oxidative phosphorylation, ATP and cytotoxicity: general magnesium and oxidative phosphorylation literature and magnesium oxide or hydroxide nanoparticle cytotoxicity papers, titles only, not opened and not the antacid. DailyMed labels [1][2][3] opened: no mitochondrial content.

Repair-pass searches

Repair pass 2026-10-04, all phrasings aimed at oral pharmaceutical use. WebSearch: "magnesium hydroxide" laxative or antacid with mitochondrial function or ATP in vivo (results: general magnesium-hydroxide drug and consumer pages, none on mitochondria). PubMed listing pages via fetch: "milk of magnesia" with oxidative, antioxidant, mitochondria or ATP returned 9 records (LactMed entry, colorectal surgery length of stay, the near-death case report [10], prostate-motion MRI bowel regimen, PEG 3350 versus milk of magnesia in children, constipation in dementia, alginate versus antacid reflux, hysterectomy bowel stimulation, a 1973 glycidol assay), none on mitochondria. Crossref title search for magnesium hydroxide with oral, mitochondrial respiration, ATP and liver returned plant bioenergetics, anesthetic and dentin-desensitizing papers, none on this drug. Nothing opened supported even a Tier C or Tier B yellow grade.

Channel outcomes

WebSearch reached its 200-call shared cap during the repair pass, so no further phrasings could run. Further PubMed listing requests were refused with HTTP 429 and the fetch tool asked not to retry; PMC article pages returned a bot challenge; Europe PMC returned 429 and an over-length URL error; OpenAlex search returned 429 on three tries; Crossref returned 429 on some queries; Bing and DuckDuckGo result pages and Springer and MDPI site-search pages are blocked by robots.txt. Outbound curl to PubMed, Crossref, Europe PMC and similar hosts was not attempted (org policy). Mixed result: a clean zero on the channels that answered, plus tooling-limited access to primary databases. Probably a genuine literature gap for the pharmaceutical (the 7 PubMed records seen earlier were nanomaterial or method papers), but not provable with the access available.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress

Not graded — disclosed evidence gap

See study details

No human or animal study of the pharmaceutical magnesium hydroxide on systemic redox markers was retrieved.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence for the drug as used, and no claim to rebut. Engineered nanomaterial studies were judged not to be this medication. Disclosed gap, tooling-limited as well as thin literature.

What was searched

PubMed listing for "magnesium hydroxide" with oxidative stress (13 records): titles were nanocomposite and biomaterial scaffold work (for example a gelatin/polymer magnesium hydroxide nanocomposite in rat Alzheimer's models), not the antacid or laxative, not opened and not used. Web search for magnesium hydroxide with malondialdehyde and glutathione returned magnesium deficiency and oxidative stress literature, which concerns low magnesium, the opposite of this drug's effect.

Repair-pass searches

Repair pass 2026-10-04. WebSearch queries: milk of magnesia or magnesium hydroxide oral administration with oxidative stress, malondialdehyde and rats; magnesium hydroxide antacid in gastric ulcer rats with lipid peroxidation, superoxide dismutase, glutathione and Maalox; magnesium hydroxide oral rats with antioxidant enzymes and liver. PubMed listing pages: "magnesium hydroxide" with gastric mucosa and antioxidant returned 7 records (compound bismuth and magnesium granules in aspirin gastric injury; nitric oxide and eicosanoid antacid gastroprotection papers from 1992 and 1993; a meperidine ion-trapping study with a magnesium-aluminum hydroxide antacid; an antacid coating agent containing magnesium trisilicate), titles only and none a redox-marker study of this drug. A PubMed listing for milk of magnesia with oxidative or antioxidant returned the 9 unrelated clinical records described under Mitochondrial burden. Crossref searches for antacid oxygen free radical scavenging, magnesium hydroxide lipid peroxidation and magnesium hydroxide supplementation with malondialdehyde and superoxide dismutase returned drug-reaction bulletins, formulary monographs and unrelated antioxidant papers.

Opened and excluded

[36] pylorus-ligation rat paper: measured MDA, SOD, glutathione peroxidase and glutathione, but no antacid or magnesium group (a disease model of oxidative stress, not this drug). [37] oral magnesium (250 mg/kg) in alloxan-diabetic rats: SOD rose, serum lipid peroxidation fell and gastric lipid peroxidation rose, but the abstract does not name the magnesium salt, so the cohort test cannot be passed and magnesium hydroxide is not confirmed. [38] magnesium sulfate 0.15 g/kg by gavage in carbon tetrachloride rats and [39] magnesium citrate in diabetic rats: other, fully soluble salts, reported as reducing oxidative markers in injury models; excluded as not this drug (magnesium hydroxide is about 15% absorbed [8]) and because the direction is protective in disease models, which would not be a depletion finding. [40] compound bismuth and magnesium granules: the abstract record lists NO, prostaglandins, TNF and interleukins but no MDA, SOD or glutathione data and no ingredient list; an earlier summarizing fetch had claimed MDA, SOD and GSH were measured, the OpenAlex abstract contradicted it, so the paper is not used. Magnesium deficiency and oxidative stress literature runs in the opposite direction from this drug and was not used. Engineered Mg(OH)2 nanoparticle and nanocomposite cytotoxicity papers were excluded as not antacid exposure.

Channel outcomes

Same access limits as Mitochondrial burden: search budget exhausted, PubMed listing 429 with a no-retry request, PMC bot-challenged, Europe PMC and OpenAlex search rate-limited, a Taylor and Francis article page 403. No circulating consumer claim about antioxidant depletion by milk of magnesia was found in the consumer pages opened [33][35]. Likely a genuine gap for a drug-specific study; tooling-limited for confirmation.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Iron: absorption interference, two small conflicting trials at simulated overdose doses

Yellow — Low

See study details

Direction: possible reduced iron absorption (drug affecting nutrient). One crossover trial found lower iron exposure after magnesium hydroxide, a second found no significant difference, and both used supratherapeutic iron.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: The second trial [22] was null. No study measured ferritin, transferrin saturation or hemoglobin in people on long-term magnesium hydroxide at ordinary doses.
  • At-risk subgroups: Not defined. Co-administration with iron therapy is the only studied context, and only at overdose-level iron.

Regulatory status

No iron-specific statement in the labels opened. The OTC label gives a general 2-hour separation from other drugs [3].

Population evidence (Tier A design, this drug)

Wallace 1998 [21]: randomized crossover in healthy male volunteers, about 5.0 mg/kg elemental iron followed an hour later by 4.5 g magnesium hydroxide or nothing; iron area-under-curve 78 +/- 23 versus 144 +/- 33 micromol-hr/L, p=0.03. Snyder and Clark 1999 [22]: randomized, 16 fasting men, 10 mg/kg elemental iron, 8 given magnesium hydroxide (5 mg per mg elemental iron) 30 minutes later; mean peak serum iron 272.5 versus 300.8 ug/dL, P=.20, authors concluded no effect at a 5:1 ratio.

Mechanism

Proposed (alkalinization and binding in the gut), not tested in either trial. Both measured serum iron after one dose, not iron status.

Counter-evidence held on record

Counter-evidence The two trials disagree, are small, and used iron doses far above therapeutic. Iron deficiency in antacid users would also be confounded by the GI disease being treated. Acid-suppression (PPI or H2 blocker) iron data were not borrowed: neither is this drug and neither trial studied them. Framing caution An interaction signal, not an iron deficiency claim. Iron deficiency is not anemia (Hard Rule 2). No iron supplement is recommended by this entry.

Copper: class extrapolation, supplemental magnesium and apparent fecal copper loss

Yellow — Low

See study details

Direction: possible reduced copper retention. A 1989 human feeding study reported that magnesium supplementation increased apparent fecal copper losses, but the magnesium compound is unstated and copper status was not measured.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: A PubMed listing for "magnesium hydroxide" with copper returned 10 records, all materials science (adsorption hydrogels, nanoparticles, biocides, flame retardant), none concerning the drug in people.

Regulatory status

Not mentioned in the labels opened [1][2][3].

Population evidence

Kies and Harms 1989 [28] (book chapter, abstract only via fetch summarizer): in humans, calcium and potassium supplements improved copper retention while magnesium and selenium supplementation increased apparent fecal copper losses. Sample size, dose and magnesium compound were not available. No copper measurement in magnesium hydroxide users was found.

Mechanism

Plausible mineral competition or luminal binding at high magnesium load, but not demonstrated for this drug.

Class cohort test

CLASS EXTRAPOLATION from supplemental magnesium of unspecified form [28]. Whether magnesium hydroxide was in the cohort is unknown, so it is treated as Tier C. Capped at yellow.

Counter-evidence held on record

Counter-evidence Apparent fecal loss is a balance measure over a short feeding period; it is not a measure of copper status, and most of an oral magnesium hydroxide dose is not absorbed anyway. Framing caution Theoretical only. Not a deficiency claim and not a reason to supplement copper. Kept independent of the Iron entry (Hard Rule 7).

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk: animal data and class extrapolation, no human study

Yellow — Low

See study details

An osmotic laxative acts in the colon and alters stool water, so microbiome effects are plausible, but no human study of magnesium hydroxide was found.

Full detail, limits and 1 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: A PubMed listing for magnesium hydroxide with microbiota or microbiome returned only unrelated general microbiome reviews. Magnesium oxide in mice caused no alpha-diversity change [26].

Regulatory status

No microbiome statement in the labels opened [1][2][3].

Population evidence

Tier B, animal: Park 2023 [25] (fetch summary only): mice with loperamide-induced constipation; magnesium hydroxide with lactulose improved stool number and water content, increased short-chain fatty acids, and the higher dose gave higher acetic acid. The retrieved text did not report microbial composition. Class, Tier C: Omori 2021 [26], mice given magnesium oxide (not hydroxide) with inulin: composition shifted (Turicibacter markedly lower), alpha-diversity unchanged, cecal pH higher, cecal short-chain fatty acids lower than inulin alone. A 2021 review of magnesium oxide states it alters the gut microbiome and that long-term effects are unclear [16].

Mechanism

Plausible: altered luminal water, pH and transit. Not demonstrated for this drug in humans.

Class cohort test

CLASS EXTRAPOLATION for the composition findings: magnesium oxide [26][16]. Magnesium hydroxide was in the Park mouse study [25] but with lactulose, in a drug-induced constipation model. Capped at yellow.

Counter-evidence held on record

Counter-evidence Mouse models and combined treatments do not transfer to people taking intermittent doses. PPI microbiome data were not borrowed: the mechanism differs. Framing caution Not a claim of dysbiosis or a recommendation to take probiotics.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization: one confounded animal study of a combination product, no human data

Yellow — Low

See study details

No human study links magnesium hydroxide to lower hemoglobin or red-cell mass; the only retrieved source is an alcohol-injury rat model using Maalox Plus.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Null findings: No hemoglobin-lowering report for magnesium hydroxide was found in PubMed listings or the sources opened. The phrase "except at the highest magnesium doses" cannot be interpreted without the full paper.

Regulatory status

No hematologic warning in the labels opened [1][2][3].

Population evidence

Onyango 2017 [27] (fetch summary of the abstract only): 50 Wistar rats in 10 groups of 5, alcohol 5 g/kg five days a week for 28 days with Maalox Plus (magnesium hydroxide 4.25, 8.5 or 17 mg/kg) and/or a calcium supplement; red cell count, MCV, MCH and MCHC were measured. Alcohol-induced macrocytic anemia was reversed except at the highest magnesium doses. Maalox Plus is a combination product, and whether a drug-alone group existed was not confirmed.

Mechanism

None identified. Any human hematologic effect would be mediated through the Iron entry and is not counted separately (see Overlap map).

Counter-evidence held on record

Counter-evidence The model was alcohol-induced injury, not healthy animals, so a drug effect cannot be separated from recovery. The study gives no usable direction; it is graded yellow only because it is a Tier B animal study using the drug in a combination product. Framing caution Not an anemia or oxygen-delivery claim. Anemia is an outcome, not a nutrient (Hard Rule 2). Kept independent of ATP production (Hard Rule 7).

ATP production

Not graded — disclosed evidence gap

See study details

No evidence on magnesium hydroxide and cellular ATP synthesis or energy output was retrieved.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence and no circulating "low energy" claim specific to this drug found. Not a finding of safety. Kept independent of Mitochondrial burden and Oxygen delivery/utilization (Hard Rule 7).

What was searched

The same web-search and PubMed phrasing as Mitochondrial burden, including ATP and oxidative phosphorylation terms. Magnesium is a cofactor in ATP-dependent reactions, but that is physiology and not evidence that this drug changes ATP; no source linked excess magnesium from this drug to energy output.

Repair-pass searches

Repair pass 2026-10-04: the Mitochondrial burden queries were rerun with ATP, energy and oxidative phosphorylation wording (WebSearch, PubMed listing for milk of magnesia with ATP, Crossref for magnesium hydroxide with mitochondrial respiration and ATP). Hits were general magnesium and ATP synthase biochemistry in plants and isolated mitochondria, not an exposure to this drug. Magnesium as an ATP cofactor was kept out on purpose: it is physiology, not a drug effect, and the dossier's own magnesium finding is excess, not shortage. No Mg hydroxide-specific energy-metabolism source exists in what was opened.

Channel outcomes

Same as Mitochondrial burden: clean zero on the channels that answered, tooling-limited for the primary databases (429, bot challenge, robots.txt blocks, search cap reached). Probably a genuine gap, not proven.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

  • Vitamin B12 deficiency from "antacids"

    Where it comes from: News coverage of the 2013 Kaiser Permanente JAMA study, which described it as showing long-term antacid use linked to B12 deficiency [32].

    Why it fails: The study examined PPIs and H2 receptor antagonists (H2 blockers); per a fetch summary of the JAMA page, antacids such as magnesium hydroxide were not an exposure [31]. No B12 study of magnesium hydroxide or any neutralizing antacid was found. Neutralization of acid is not sustained secretory suppression, so the PPI and H2 blocker findings were not borrowed. Governance rests on rebuttal only; if an antacid-specific B12 study is found, re-grade.

  • Magnesium depletion or impaired magnesium absorption

    Where it comes from: Practitioner blog listing antacids as interfering with absorption of calcium, magnesium and iron [33].

    Why it fails: Reversed for this drug. Magnesium hydroxide is a magnesium source: about 15% is absorbed and urinary magnesium rises [8], and the clinical hazard is excess [10][11][12]. Drugs that deplete magnesium (loop and thiazide diuretics, long-term PPIs [7]) are different drugs.

  • Calcium malabsorption

    Where it comes from: The same blog [33], which also describes milk of magnesia as an antacid containing aluminum salts.

    Why it fails: No study of calcium absorption with magnesium hydroxide was found. The single-ingredient label lists only magnesium hydroxide [1], so the aluminum statement is wrong for this product. The calcium signal that does exist is low serum calcium secondary to magnesium excess (yellow entry), a different mechanism. Hypercalciuria in the antacid review is tied to calcium carbonate and bicarbonate [17].

How the body handles this medication

Metabolism and enzymes
An inorganic salt. None of the three labels opened [1][2][3] describes metabolism, CYP induction or CYP inhibition. No enzyme-induction depletion route is described.[1][2][3] DailyMed labels (OTC, no PK section)
Absorption and kinetics
Crossover study in 10 healthy men, 3 x 360 mg tablets: oral bioavailability about 15%, maximum serum concentration 0.11 mmol/L, elimination half-life 8.3 hours, clearance 5.1 L/hr, volume of distribution 60.2 L. For comparison, 30 to 40% of dietary magnesium is typically absorbed.[8] abstract (OpenAlex reconstruction); [7] NIH ODS
Elimination and renal handling
Absorbed magnesium is renally cleared; urinary magnesium rose 17.7% from baseline after the oral dose. The kidneys normally excrete about 120 mg daily. Unabsorbed drug acts in the bowel; the label says a bowel movement usually follows in 1/2 to 6 hours. No label describes an effect on renal tubular handling of water or electrolytes.[8] [7] [1]
Renal or other impairment
The labels advise asking a doctor first if there is kidney disease or a magnesium-restricted diet. NIH ODS: risk of magnesium toxicity rises with impaired renal function because the ability to remove excess magnesium is reduced or lost.[1][2] [7]
Antacid and mineral interactions (timing, not depletion)
OTC label: laxatives may affect other drugs and should be taken 2 or more hours before or after them [3]. Ciprofloxacin label: take at least 2 hours before or 6 hours after magnesium or aluminum antacids [4]. Levothyroxine label: administer at least 4 hours apart from phosphate binders such as calcium carbonate and ferrous sulfate, and antacids may reduce absorption; a summarizer also listed aluminum/magnesium hydroxides, not verified verbatim [5]. NIH ODS: bisphosphonates 2 hours; certain antibiotics 2 hours before or 4 to 6 hours after magnesium [7]. In vitro, levothyroxine adsorbed dose-dependently to aluminum hydroxide, magnesium oxide and magnesium carbonate; magnesium hydroxide was not named [30]. A crossover in 12 volunteers with 30 mL Maalox (magnesium plus aluminum hydroxide) gave rufloxacin relative bioavailability of 64% when the antacid preceded it by 5 minutes and 87% when given 4 hours after [29].
Gastric pH and dose context
As an antacid it neutralizes existing acid; it does not reduce acid secretion as PPIs and H2 blockers do. No study opened measured intragastric pH after magnesium hydroxide. A 15 mL dose of Phillips' product contains 1200 mg magnesium hydroxide, or 500 mg magnesium [1]; the NIH UL for supplemental magnesium is 350 mg/day for adults [7]. A laxative dose exceeds that figure because it is a medicinal dose, not supplementation advice.[1][2][7]

What the research says is worth watching

General information from the medication label and the studies above. It is not personal medical advice, and any change belongs with your prescriber.

  • Lab / excess risk

    Serum magnesium

    Worth checking when magnesium hydroxide is used regularly or at laxative doses by someone with reduced kidney function, older age, bowel obstruction or slowed bowel transit, or when symptoms such as weakness, low blood pressure, slow heart rate or drowsiness appear. Reported cases reached 9.9 to 11.0 mg/dL [10] and above 4.1 mmol/L [11]. This is an excess risk. It is not a reason to add magnesium.

  • Renal

    Kidney function

    Creatinine and estimated clearance before regular use. Labels advise asking a doctor first with kidney disease [1][2]. In magnesium oxide data, risk concentrated at estimated clearance of about 28 mL/min or lower [15] (context only, a different salt).

  • Timing / not depletion

    Separation from other drugs

    OTC label: 2 or more hours before or after other drugs [3]. Ciprofloxacin: at least 2 hours before or 6 hours after [4]. Levothyroxine: label separates phosphate binders and certain antacids by at least 4 hours [5]. Tetracycline-type antibiotics: 2 hours before or 4 to 6 hours after, bisphosphonates 2 hours [7]. These are drug-absorption interactions, not nutrient depletion. Follow the prescribing label of the other drug.

  • Lab / long-term heavy use

    Phosphate

    Consider serum phosphate in people using large amounts of antacid for months, particularly aluminum-containing combinations, with alcohol use or low phosphate intake [17][19][20].

  • Lab / diarrhea

    Electrolytes and fluid

    Persistent diarrhea on a magnesium laxative is a reason to stop and seek advice, and to check potassium and magnesium if it continues [24][7]. The labels say to stop use if a laxative effect does not follow a normal course or symptoms persist beyond 2 weeks [3].

  • Lab / iron therapy

    Iron co-administration

    Trials were conflicting and used overdose-level iron [21][22]. No iron-specific interval appears on the labels opened; the general 2-hour label separation is a reasonable default [3]. Ferritin and a complete blood count are worth checking if fatigue or pallor occur on long-term antacid use with other risk factors.

  • Special populations

    Pregnancy, pediatrics, renal impairment

    Repackaged label: pregnant or nursing people should seek professional advice; children 6 to 11 have reduced dosing and under 6 should ask a doctor [3]. Renal impairment is the principal documented sensitivity group (see the orange entry).

  • Dose check

    Supplement dose and upper limit

    No supplement dose is recommended anywhere in this dossier. Label doses are medicinal. The NIH upper limit for supplemental magnesium is 350 mg/day for adults [7]; a 15 mL dose of milk of magnesia provides 500 mg magnesium [1]. This is stated for transparency, not as dosing advice.

Overlap map, to prevent double counting

  • Magnesium (excess)

    Shares evidence with: Calcium

    Note: The McLaughlin hypermagnesemia case [12] supplies the magnesium hydroxide data point for both. The low-calcium finding is a consequence of the magnesium finding, not an independent signal.

  • Magnesium (excess)

    Shares evidence with: Potassium and fluid

    Note: Same GI action (osmotic diarrhea at high doses, [7]), and diarrhea with obstruction or poor clearance is the setting of magnesium accumulation. No shared study, but one underlying drug action.

  • Magnesium (excess); Phosphate; Calcium

    Shares evidence with: Herzog and Holtermuller 1982 review [17]

    Note: One narrative review is cited in three entries for different statements (renal-failure hypermagnesemia, aluminum phosphate depletion, calcium antacid effects). It counts as one source.

  • Iron

    Shares evidence with: Oxygen delivery/utilization

    Note: Any human hemoglobin effect would run through iron and is not counted separately. The rat study [27] is not independent confirmation of the iron trials [21][22].

  • Iron

    Shares evidence with: Timing interactions (levothyroxine, quinolones, tetracyclines, bisphosphonates)

    Note: The iron trials measure drug-nutrient absorption after overdose-level iron. The timing interactions in the monitoring panel [3][4][5][7][29] are drug-absorption interactions and are not nutrient depletion; they are not entries and not counted.

  • Phosphate

    Shares evidence with: Copper

    Note: Both rest on gut luminal binding by the cation as a mechanism, but no shared source. Graded separately.

  • Copper

    Shares evidence with: Iron

    Note: No shared source. The copper evidence [28] is a human feeding abstract with magnesium of unspecified form. Graded separately per Hard Rule 7.

  • Gut microbiome risk

    Shares evidence with: Potassium and fluid

    Note: Both depend on the osmotic laxative action, but microbiome rests on animal studies [25][26] and potassium on a class reference [24]. No shared source.

  • Mitochondrial burden

    Shares evidence with: ATP production; Oxidative stress (ungraded)

    Note: All three are ungraded for the same reason: the same null searches and the same nanomaterial-only hits. One gap viewed three times, not three independent gaps.

All references used above
  1. PHILLIPS ORIGINAL MILK OF MAGNESIA, liquid, Bayer HealthCare LLC, DailyMed label. — Regulatory label (Tier A). Label updated Dec 4, 2025. 1200 mg magnesium hydroxide per 15 mL; kidney disease and magnesium-restricted diet warnings; magnesium 500 mg per 15 mL. Read via summarizing fetch of the label page.
  2. Milk of Magnesia, PAI Holdings LLC (PAI Pharma), DailyMed label. — Regulatory label (Tier A). Revision January 2026. 2400 mg per 30 mL; antacid and laxative uses; kidney and magnesium-restricted diet warnings. Summarizing fetch.
  3. Magnesium hydroxide liquid, 400 mg per 5 mL, Rebel Distributors Corp (repackager), DailyMed label. — Regulatory label (Tier A), dated Feb 21, 2011, so possibly superseded. Laxative and antacid dosing; "laxatives may affect how other drugs work, so should be taken 2 or more hours before or after other drugs"; pregnancy and nursing advice. Summarizing fetch.
  4. Ciprofloxacin tablets, DailyMed label (Yiling Pharmaceutical). — Regulatory label for another drug (Tier A), revision 9/2020. Take at least 2 hours before or 6 hours after multivalent cation products including magnesium/aluminum antacids. Summarizing fetch.
  5. SYNTHROID (levothyroxine sodium), DailyMed label, AbbVie Inc. — Regulatory label for another drug (Tier A), revision February 2024, section 7. At least 4 hours apart from phosphate binders (calcium carbonate, ferrous sulfate); antacids may reduce absorption. The summarizer's list also named aluminum/magnesium hydroxides; that wording was not verified verbatim.
  6. WHO Collaborating Centre, ATC/DDD Index: magnesium hydroxide, A02AA04, DDD 3 g oral; and group A06AD (osmotically acting laxatives). — Reference index. The DDDs for antacids are based on hyperacidity and dyspepsia. Magnesium hydroxide is not listed under A06AD in the index retrieved (A06AD lists magnesium carbonate, oxide, peroxide, sulfate, citrate).
  7. NIH Office of Dietary Supplements. Magnesium: Fact Sheet for Health Professionals. — Reference (Tier B). Absorption 30 to 40% of dietary magnesium; renal excretion about 120 mg/day; toxicity risk with renal impairment; interactions with bisphosphonates, antibiotics, diuretics, PPIs; UL 350 mg supplemental. Summarizing fetch.
  8. Dolberg MKB, Nielsen LP, Dahl R. Pharmacokinetic profile of oral magnesium hydroxide. Basic Clin Pharmacol Toxicol. — Crossover PK study, 10 healthy men (Tier A, this drug). Year 2016 per the OpenAlex record (a search listing showed 2017). DOI 10.1111/bcpt.12642. Abstract reconstructed from OpenAlex.
  9. Kinnunen O, Salokannel J. Constipation in elderly long-stay patients: its treatment by magnesium hydroxide and bulk-laxative. Ann Clin Res 1987. — Trial, 64 geriatric patients (Tier A, this drug). PMID 3126699. Abstract reconstructed from OpenAlex.PubMed page not opened; OpenAlex record read.
  10. Jou DH, et al. Fatal hypermagnesemia in patients taking magnesium hydroxide. Electrolyte Blood Press 2023;21(2):66. — Case report, two patients (Tier B, this drug). Read via the journal mirror through a summarizing fetch.
  11. Alaini A, Roldan CA, Servilla K, Colombo ES. Near death by milk of magnesia. BMJ Case Rep 2017. — Case report, one patient (Tier B, this drug). PMC5372215. Summarizing fetch of the PMC page.
  12. McLaughlin SA, McKinney PE. Antacid-induced hypermagnesemia in a patient with normal renal function and bowel obstruction. Ann Pharmacother 1998. — Case report (Tier B, this drug; milk of magnesia and Maalox). PMID 9533062, DOI 10.1345/aph.17284. Abstract reconstructed from OpenAlex.PubMed returned a bot challenge; the first OpenAlex request was rate-limited (429) and a later one succeeded.
  13. Khairi T, Amer S, Spitalewitz S, Alasadi L. Severe symptomatic hypermagnesemia associated with over-the-counter laxatives in a patient with renal failure and sigmoid volvulus. Case Rep Nephrol 2014. — Case report. DOI 10.1155/2014/560746. Abstract reconstructed from OpenAlex.Wiley page returned 403. Retrieved abstract does not name magnesium hydroxide; supportive only.
  14. Horibata K, Tanoue A, Ito M, Takemura YC. Relationship between renal function and serum magnesium concentration in elderly outpatients treated with magnesium oxide. Geriatr Gerontol Int. — Observational, 44 elderly outpatients (23 constipation on magnesium oxide, 21 controls). Year 2015 per OpenAlex. DOI 10.1111/ggi.12530. Abstract reconstructed from OpenAlex.Magnesium oxide, not magnesium hydroxide. Tier C for this drug.
  15. Ishii H, Sawada R, Shiomi M, Shibuya K. A case-control study showing low creatinine clearance and high magnesium intake as risk factors for hypermagnesemia in older individuals. Magnes Res 2023. — Case-control, 35 cases and 140 controls. DOI 10.1684/mrh.2023.0513. Abstract reconstructed from OpenAlex.Magnesium oxide, not magnesium hydroxide. Tier C for this drug.
  16. Mori H, Tack J, Suzuki H. Magnesium oxide in constipation. Nutrients 2021;13(2):421. — Narrative review (Tier C). DOI 10.3390/nu13020421. Summarizing fetch of the MDPI page; hypermagnesemia prevalence and microbiome statements are the review's citations of other studies.Review of magnesium oxide; magnesium hydroxide not in the cited cohorts.
  17. Herzog P, Holtermuller KH. Antacid therapy: changes in mineral metabolism. Scand J Gastroenterol Suppl 1982. — Narrative review (Tier C). PMID 6293043. Abstract reconstructed from OpenAlex.PubMed page not opened; OpenAlex record read. No drug-level stratification.
  18. Guillot AP, Hood VL, Runge CF, Gennari FJ. The use of magnesium-containing phosphate binders in patients with end-stage renal disease on maintenance hemodialysis. Nephron 1982;30(2):114-117. — Four-phase trial, 9 hemodialysis patients (Tier A, this drug). PMID 7099318. The OpenAlex record lists year 2008; volume 30 corresponds to 1982, so the year should be verified. Abstract reconstructed from OpenAlex.PubMed page not opened.
  19. Neumann L, Jensen BG. Osteomalacia from Al and Mg antacids. Acta Orthop Scand 1989;60(3):361-362. — Case report, one patient (Tier B, magnesium oxide plus aluminum aminoacetate product, not magnesium hydroxide). Summarizing fetch of the open-access PDF.
  20. Merck Manual Professional Edition. Hypophosphatemia. — Reference (Tier C for this drug), page dated Dec 2025. Names long-term large-amount aluminum antacids as a cause; does not name magnesium hydroxide.
  21. Wallace KL, Curry SC, LoVecchio F, Raschke RA. Effect of magnesium hydroxide on iron absorption following simulated mild iron overdose in human subjects. Acad Emerg Med 1998;5(10):961-965. — Randomized crossover, healthy male volunteers (Tier A design, this drug). DOI 10.1111/j.1553-2712.1998.tb02771.x. Abstract reconstructed from OpenAlex; sample size not captured.Wiley page returned 403. A 1999 follow-up letter by the same group (Ann Emerg Med 34:685-686) had only metadata, no abstract, and is not cited.
  22. Snyder B, Clark RF. Effect of magnesium hydroxide administration on iron absorption after a supratherapeutic dose of ferrous sulfate in human volunteers: a randomized controlled trial. Ann Emerg Med 1999. — Randomized trial, 16 healthy fasting men (Tier A design, this drug). DOI 10.1016/s0196-0644(99)70303-3. Abstract read via a summarizing fetch of the ScienceDirect page.
  23. Eisenbud E. Hypocalcemia after therapeutic use of magnesium sulfate. Arch Intern Med 1976;136(6):688. — Case report, magnesium sulfate for toxemia (Tier C for this drug). PMID 1275625. Abstract reconstructed from OpenAlex.Different magnesium salt and route. PubMed page not opened.
  24. Merck Manual Professional Edition. Hypokalemia. — Reference (Tier C for this drug), page dated Dec 2025. Laxatives and laxative abuse as causes through diarrhea.Magnesium-containing laxatives not named in the source.
  25. Park et al. Coadministration of lactulose with probiotics ameliorates loperamide-induced constipation in mice. Prev Nutr Food Sci 2023. — Animal study (Tier B, includes magnesium hydroxide with lactulose). PMC10764220. Summarizing fetch only; composition data not reported in what was retrieved.
  26. Omori K, et al. The combined effects of magnesium oxide and inulin on intestinal microbiota and cecal short-chain fatty acids. Nutrients 2021;13(1):152. — Mouse study, 5 to 6 per group (Tier C for this drug). Summarizing fetch of the MDPI page.Magnesium oxide, not hydroxide.
  27. Onyango TO, Mburu DN, Ngugi MP, Kamau JK, Juma KK. Effects of Maalox Plus antacid and PureCal calcium supplements on haematological and biochemical parameters in alcohol-treated rats. J Alcohol Drug Depend 2017. — Rat study, 50 animals (Tier B, combination product). Abstract-level summarizing fetch of the Longdom page.Confounded alcohol model; title in the original may differ slightly from the page title.
  28. Kies C, Harms JM. Copper absorption as affected by supplemental calcium, magnesium, manganese, selenium and potassium. In: Copper Bioavailability and Metabolism, 1989. — Human feeding study abstract (Tier C). Summarizing fetch of the Springer page; magnesium compound, dose and n not stated.Magnesium compound unspecified; this drug not confirmed in the cohort.
  29. Lazzaroni M, et al. Effects of magnesium-aluminum hydroxide antacid on absorption of rufloxacin. Antimicrob Agents Chemother 1993. — Randomized crossover, 12 healthy volunteers, 30 mL Maalox (magnesium plus aluminum hydroxide). PMC192252. Summarizing fetch. Timing interaction, not depletion.Combination antacid; used only for the timing context.
  30. Mersebach H, Rasmussen AK, Kirkegaard L, Feldt-Rasmussen U. Intestinal adsorption of levothyroxine by antacids and laxatives: case stories and in vitro experiments. Pharmacol Toxicol 1999. — Two cases and in vitro adsorption (Tier C for this drug). PMID 10193669, DOI 10.1111/j.1600-0773.1999.tb00883.x. Abstract reconstructed from OpenAlex. In vitro adsorption was shown for aluminum hydroxide, magnesium oxide and magnesium carbonate; magnesium hydroxide was not named.Timing context only, and it is not in the Entries.
  31. Lam JR, et al. Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA 2013. — Nested case-control. Read via a summarizing fetch of the JAMA page, which stated antacids (magnesium hydroxide and others) were not an exposure; its case and control counts in the summary were not relied on.Excluded cohort: magnesium hydroxide not studied. Used only to trace the origin of a circulating claim.
  32. Medical News Today. Long-term antacid use linked to vitamin B12 deficiency (Dec 11, 2013). — Tier D. Used only as a circulating-claim origin.
  33. Integrative Cancer Care. Drugs that deplete vitamins and minerals (practitioner blog). — Tier D. Used only as a circulating-claim origin (antacids and calcium, magnesium, iron).
  34. Drugs.com. Magnesium hydroxide (ingredient page). — Tier D. Brand names and combination products only.
  35. Drugs.com. Magnesium hydroxide monograph. — Tier D. The page contains no nutrient depletion statement; lists diarrhea and an ask-a-doctor warning for kidney disease. Used only to record that no depletion claim appears there.
  36. Free radicals and antioxidant status following pylorus ligation induced gastric mucosal injury in rats. Pharmacol Res (journal and year not confirmed in the fetch). — Rat study. Abstract read via summarizing fetch of the ScienceDirect page: MDA, SOD, glutathione peroxidase and glutathione measured; antioxidant depletion by N-ethylmaleimide or aminotriazole worsened ulcers. No antacid group.Excluded: this drug not in the study. Cited only in the Oxidative stress gap record.
  37. Oral magnesium reduces gastric mucosa susceptibility to injury in experimental diabetes mellitus. (journal and year not confirmed in the fetch). — Rat study, oral magnesium 250 mg/kg in alloxan-diabetic Wistar rats. Abstract read via summarizing fetch: the magnesium salt is not named.Excluded: magnesium hydroxide not confirmed in the cohort; disease model.
  38. Antioxidant effects of magnesium in reducing oxidative stress by injected via an intraperitoneally carbon tetrachloride in the Wistar male adult rats. Armaghane Danesh, Nov 2014. — Rat study, magnesium sulfate 0.15 g/kg by intragastric tube. DOAJ record read via summarizing fetch (authors not shown).Excluded: magnesium sulfate, not magnesium hydroxide.
  39. Magnesium citrate supplementation and oxidative stress in diabetic rats. Visnyk of Taras Shevchenko National University of Kyiv, Biology, Nov 2016 (exact title not retrieved). — Rat study, magnesium citrate 100, 250 and 500 mg/kg; lipid hydroperoxides, TBARS and antioxidant enzymes measured. DOAJ record read via summarizing fetch.Excluded: magnesium citrate, not magnesium hydroxide.
  40. Protective effect of compound bismuth and magnesium granules on aspirin-induced gastric mucosal injury in rats. Zhonghua Yi Xue Za Zhi 2016. PMID 26875925. — Rat study, 12 per group. Abstract reconstructed from OpenAlex: NO, prostaglandins, TNF and interleukins measured; no MDA, SOD or glutathione; granule ingredients not stated. The PubMed page returned no abstract text.Excluded: composition unconfirmed, no redox markers.