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MyDeficiencies

Digoxin

Cardiac Glycoside

Also sold as Lanoxin.

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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.

Digoxin has essentially no classical depletion mechanism. Only about 16% of a dose is metabolized, that metabolism is not CYP450-dependent, and digoxin does not induce or inhibit any CYP450 enzyme. Fifty to seventy percent of a dose leaves the body unchanged in the urine, protein binding is low (about 25%), and there is no hepatic induction pathway through which digoxin could accelerate the clearance of any vitamin. The actual headline finding for this dossier runs the other way: digoxin's own FDA label states that hypokalemia and hypomagnesemia sensitize the heart to digoxin and can produce toxicity even when the measured digoxin level looks normal, and that hypercalcemia independently predisposes to the same toxicity. This is a nutrient-affects-drug relationship, not a drug-depletes-nutrient one, and given digoxin's narrow therapeutic index (0.8 to 2.0 ng/mL, with roughly a third of toxic patients still under 2.0 ng/mL) it is the single most consequential nutrient-related fact in this dossier.

Digitalis glycoside (cardiac glycoside) · ATC C01AA05 · also sold as Lanoxin and Lanoxicaps and Digitek · reviewed 2026-09-05, expanded 2026-09-10. 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 Digoxin 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

Potassium - toxicity-risk flag, not a depletion

Yellow — Low

Direction: reverse direction (as labelled in the source)

Digoxin does not lower potassium. Low potassium, almost always from a co-prescribed diuretic, sensitizes the heart to digoxin and raises toxicity risk even when the digoxin level looks normal.

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. reverse direction

Limits on what this shows

  • Key negative/null findings: The label attributes potassium loss to co-prescribed diuretics, not to digoxin. A consumer depletion chart reviewed for this dossier independently states digoxin "does not deplete the mineral Potassium" while still flagging the toxicity-risk relationship correctly - i.e., not all circulating material gets this backward.
  • At-risk subgroups: Concurrent loop or thiazide diuretic use, poor oral intake, vomiting or diarrhea, hyperaldosteronism, and renal impairment (which also slows digoxin clearance, compounding risk).

Regulatory status

FDA label (Tier A): hypokalemia "sensitizes the myocardium to digoxin," and toxicity "may occur despite serum digoxin concentrations below 2.0 ng/mL." Potassium-depleting diuretics are named as "a major contributing factor to digitalis toxicity."

Population evidence

No Tier A study reviewed isolates digoxin monotherapy as a cause of hypokalemia. Wang et al. (Br J Clin Pharmacol, 2010) examined digoxin-diuretic co-prescription and intoxication risk in a population-based design; named here for completeness, but full text could not be verified for this review (see Sources) and no statistic from it is used in this entry.

Mechanism

Named, and it runs from nutrient to drug: lower extracellular potassium increases digoxin's binding to and inhibition of myocardial Na+/K+-ATPase, effectively increasing the pharmacologic effect of a given digoxin concentration. No mechanism by which digoxin itself increases renal or GI potassium loss appears in the label or in the mechanistic literature reviewed.

Counter-evidence held on record

The label separates digoxin from the diuretics that cause the wasting. No study reviewed measured a potassium decline attributable to digoxin in the absence of a diuretic. Never present this as "digoxin depletes potassium." The only actionable content here is monitoring - serum potassium and serum digoxin level, especially during diuretic co-therapy - not a supplementation prompt. Correcting potassium in a digoxin-treated patient is a medical monitoring matter given the narrow therapeutic index, not a self-directed supplement decision.

Magnesium - toxicity-risk flag, not a depletion

Yellow — Low

Direction: reverse direction (as labelled in the source)

Digoxin does not lower magnesium. Low magnesium, typically from diuretics or poor intake, increases sensitivity to digoxin's cardiac effects independent of the potassium level.

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. reverse direction

Limits on what this shows

  • Key negative/null findings: No mechanism identified by which digoxin itself increases renal or GI magnesium loss. Loop diuretics (and, to a lesser extent, thiazides) are the standard attributed cause of magnesium wasting in this population.
  • At-risk subgroups: Concurrent loop diuretic use, chronic diarrhea or malabsorption, alcohol use disorder, poor intake; pediatric case literature describes hypomagnesemia in relation to digoxin intoxication in children, again in the co-therapy setting.

Regulatory status

FDA label (Tier A) lists magnesium alongside potassium, directing that "normal serum potassium and magnesium concentrations" be maintained during digoxin therapy.

Population evidence

Young IS et al., "Magnesium status and digoxin toxicity," Br J Clin Pharmacol 1991, is cited in the secondary literature as a human study of magnesium status in digoxin-toxic patients. Full text could not be opened for this review (access blocked); named only in Sources, no statistic from it is cited here. No Tier A study reviewed isolates digoxin, without diuretics, as a cause of magnesium decline.

Mechanism

Named: hypomagnesemia potentiates digoxin's Na+/K+-ATPase-inhibiting effect and independently predisposes to the same ventricular arrhythmias digoxin toxicity produces. StatPearls' cardiac glycoside toxicity chapter (Tier B) lists hypomagnesemia among the disturbances that "make one more prone to toxicity."

Counter-evidence held on record

No primary source reviewed shows digoxin lowering magnesium directly; every mechanism identified runs from magnesium status toward digoxin's toxicity threshold, not the reverse. Do not present this as a depletion. The consumer-relevant message is monitoring serum magnesium alongside potassium, particularly if arrhythmia or toxicity signs appear despite a normal digoxin level and normal potassium - not a magnesium supplementation prompt.

Calcium - bidirectional toxicity/efficacy modifier, not a depletion

Yellow — Low

Direction: reverse direction (as labelled in the source)

Digoxin does not deplete calcium. The label-documented relationship runs the other way in both directions: high calcium raises digoxin toxicity risk, and low calcium can blunt digoxin's intended effect.

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. reverse direction

Limits on what this shows

  • Key negative/null findings: Nothing identified suggests digoxin itself lowers or raises serum calcium; calcium's documented role here is entirely as a modifier of digoxin's own action and toxicity, not as a nutrient digoxin acts upon.
  • At-risk subgroups: Hyperparathyroidism, malignancy-associated hypercalcemia, excess vitamin D or calcium supplementation, and any source of hypocalcemia that could blunt therapeutic effect and prompt inappropriate dose escalation.

Regulatory status

FDA label (Tier A): "Hypercalcemia from any cause predisposes the patient to digitalis toxicity," and separately, "hypocalcemia can nullify the effects of digoxin in humans; thus, digoxin may be ineffective until serum calcium is restored."

Population evidence

No Tier A or Tier B source reviewed measures a digoxin-attributable calcium decline (or rise) in a human cohort. The label's calcium statements concern how the patient's calcium status changes digoxin's action and toxicity threshold, not the reverse.

Mechanism

Named: extracellular calcium and digoxin act on overlapping myocardial calcium-handling and Na+/K+-ATPase pathways, so higher extracellular calcium potentiates the same afterdepolarization mechanism through which digoxin toxicity produces arrhythmia. Historical practice discouraged IV calcium during digitalis therapy for this reason.

Counter-evidence held on record

No source reviewed supports a depletion claim in either direction; both label statements describe calcium acting on digoxin, never digoxin acting on calcium stores. Never frame calcium as something digoxin depletes, or as something to supplement because of digoxin. The message that matters is the opposite: unsupervised high-dose calcium or vitamin D supplementation in a patient on digoxin is the thing to flag, because it can raise toxicity risk, not remedy a deficiency.

Thiamine

Yellow — Low

Evidence in: Tier B, in vitro

One in vitro study found digoxin, like furosemide, inhibits thiamine uptake by cultured cardiac cells. No human data isolates digoxin from co-prescribed diuretics as a cause of thiamine deficiency.

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. tier B, in vitro

Limits on what this shows

  • Key negative/null findings: Human thiamine-deficiency literature in heart failure attributes deficiency to loop diuretic therapy, not to digoxin. No human study reviewed measured thiamine status in digoxin-only patients, and heart failure patients on digoxin are almost always co-prescribed a loop diuretic, so confounding by co-medication cannot be excluded.
  • At-risk subgroups: Long-term heart failure patients on combined digoxin plus loop diuretic therapy, poor oral intake, alcohol use disorder.

Regulatory status

Not addressed anywhere in the FDA label. This entry rests entirely on non-label, Tier B evidence.

Population evidence

Zangen A, Botzer D, Zangen R, Shainberg A. "Furosemide and digoxin inhibit thiamine uptake in cardiac cells." Eur J Pharmacol 1998;361(1):151-155. Cultured cardiac cells, not a human cohort. Digoxin was tested directly (cohort test passed for a mechanistic study), alongside furosemide, and their effects were additive.

Mechanism

Named: digoxin inhibited cellular thiamine uptake in a dose-dependent fashion in cultured cardiac cells; intracellular thiamine pyrophosphate declined with a 16-19 day half-life under drug exposure (5-6 days when thiamine was also withheld from the culture medium).

Counter-evidence held on record

Every human thiamine-in-heart-failure study located during this review names furosemide or loop diuretics as the exposure studied, not digoxin; none isolates digoxin as an independent cause. This is mechanistic-only evidence from a single in vitro study, confounded by near-universal co-prescription of loop diuretics in this population. No dose or supplement recommendation is made at this grade.

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 - calcium-handling mechanism already graded, plus an unverified transporter interaction

Yellow — Low

Evidence in: Tier B, mechanistic

Digoxin's core toxicity mechanism involves mitochondrial calcium handling, which is not a nutrient it depletes; a separate, unrelated finding suggests coenzyme Q10 can interact with the same transporter digoxin depends on for absorption and clearance.

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. tier B, mechanistic

Limits on what this shows

  • Key negative/null findings: No source reviewed measures a change in coenzyme Q10, L-carnitine, riboflavin, or any other mitochondrial cofactor caused by digoxin in a human cohort. The mitochondrial calcium-sequestration finding is the same physiology already graded under Calcium above, not a second, independent deficit.
  • At-risk subgroups: None identifiable from the evidence reviewed; a human at-risk subgroup cannot be defined from a 1979 animal study and one unverified transporter paper.

Regulatory status

Not addressed in the FDA label as a nutrient-depletion pathway. The label's calcium and P-glycoprotein statements, already documented in the PK basis above, are the only label-level material this entry draws on.

Population evidence

No Tier A human study reviewed measures digoxin's effect on any mitochondrial nutrient. Revis N, Marusic N, "Sequestration of 45Ca2+ by mitochondria from rabbit heart, liver, and kidney after doxorubicin or digoxin/doxorubicin treatment," Exp Mol Pathol 1979 (Tier B, animal, digoxin tested directly), is named in bibliographic records as measuring mitochondrial calcium uptake after digoxin exposure; full text could not be opened for this review (see Sources), so no statistic from it is used here beyond its existence and title. Itagaki S, et al., "Interaction of coenzyme Q10 with the intestinal drug transporter P-glycoprotein," J Agric Food Chem 2008, is separately named as examining CoQ10 at the same transporter (P-glycoprotein) the label already identifies as controlling digoxin's absorption and clearance; full text also could not be opened for this review, so no statistic is drawn from it either.

Mechanism

Named, and it is digoxin's own established mechanism of action, not a depletion pathway: inhibiting myocardial Na+/K+-ATPase raises intracellular sodium, which slows the Na+/Ca2+ exchanger and raises intracellular, and per the 1979 finding, mitochondrial calcium. This is the same pathway already graded under the Calcium entry above, not independent evidence of a mitochondrial nutrient deficit. The CoQ10 finding, if confirmed, would be a nutrient-affects-drug transporter interaction, not digoxin depleting CoQ10, and it is not independently confirmed at full-text level here.

Counter-evidence held on record

Every mechanism identified here either restates digoxin's own known cardiotoxicity pathway, already graded under Calcium, or rests on a single unverified mechanistic source on CoQ10 transport. No source shows digoxin lowering a mitochondrial nutrient in a living organism. Do not present this as "digoxin depletes CoQ10" or "digoxin damages mitochondria." The calcium-handling mechanism described here is digoxin's own mechanism of cardiotoxicity, already accounted for under the Calcium entry; repeating it here as an independent mitochondrial finding would double count the same physiology, not add new evidence.

Oxidative Stress

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

Oxidative stress - a toxicity-mechanism signal, not a measured human deficiency

Yellow — Low

Evidence in: Tier B, cell-based

One cell-based study reports digoxin-induced oxidative damage to cardiomyocytes that melatonin mitigated. This describes a candidate mechanism of digoxin's own cardiotoxicity at the exposure tested, not a demonstrated antioxidant-nutrient deficiency in treated patients.

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. tier B, cell-based

Limits on what this shows

  • Key negative/null findings: No source reviewed measures a decline in any antioxidant nutrient's circulating or tissue level attributable to digoxin. The signal identified here is a cell-culture toxicity finding, not a nutrient-status finding.
  • At-risk subgroups: Not identifiable from the evidence reviewed; a cell-culture finding does not define a human at-risk subgroup.

Regulatory status

Not addressed in the FDA label.

Population evidence

No Tier A human study reviewed measures antioxidant nutrient status (vitamin E, vitamin C, selenium, glutathione) in digoxin-treated patients. Ovey IS, Oncel CR, "The effect of melatonin on digoxin-induced cardiac damage in cardiomyocytes," Bratisl Lek Listy 2019 (Tier B, cell-based, digoxin tested directly), is named in bibliographic records as testing digoxin's effect on cardiomyocytes with and without melatonin co-treatment; full text could not be opened for this review (see Sources), so no specific marker value or effect size from it is used here.

Mechanism

Plausible but not independently confirmed at full-text level here: the cardiac glycoside toxicity literature already cited in this dossier's Sources (the StatPearls reference) describes calcium overload as part of digitalis toxicity, and calcium overload is separately linked in the general cardiac literature to secondary reactive-oxygen-species generation. This is a toxicity mechanism, not a mechanism by which digoxin depletes a dietary antioxidant.

Counter-evidence held on record

No human study reviewed measured an antioxidant nutrient's status in digoxin-treated patients, and the one Tier B source located describes a toxicity mechanism at the exposure tested, not a depletion pathway demonstrated at therapeutic dosing. Never present this as "digoxin depletes vitamin E" or "digoxin depletes antioxidants." Oxidative stress here is a candidate contributor to digoxin's own cardiotoxicity at high exposure, a safety-monitoring matter, not a reason to recommend an antioxidant supplement.

Copper and Iron Balance

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

Copper - not gradeable, no study has measured it

Not graded — disclosed evidence gap

See study details

No mechanism and no circulating claim connect digoxin to copper status. This is a genuine evidence gap, not a clean bill of health.

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: The mechanism screen found no absorption, catabolic, renal, cofactor, mitochondrial, dilutional, microbiome, intake, or utilization pathway by which digoxin plausibly affects copper status, and a targeted literature search returned no animal, in vitro, or class-level study measuring digoxin's effect on copper. Neither consumer nutrient-depletion chart already cited in this dossier (Sources 9 and 10) lists copper against digoxin, so there is no circulating claim to rebut either. Both conditions for an ungraded outcome are met: no Tier B/C evidence and no claim to fail.
  • What would fill it: A study, even a mechanistic or animal one, measuring copper status or a copper-dependent enzyme's activity before and after digoxin exposure.

Iron - not gradeable, no study has measured it

Not graded — disclosed evidence gap

See study details

No mechanism and no circulating claim connect digoxin to iron status. This is a genuine evidence gap, not a clean bill of health.

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: The mechanism screen found no pathway by which digoxin plausibly affects iron status, and a targeted search combining digoxin with iron, anemia, and absorption terms returned zero results. Neither consumer chart already cited in this dossier (Sources 9 and 10) lists iron against digoxin. Both conditions for an ungraded outcome are met.
  • What would fill it: A study measuring iron status, transferrin saturation, or ferritin before and after digoxin exposure, or a mechanistic study of digoxin and intestinal iron transport.

Gut Microbiome Risk

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

Gut microbiome - inactivates digoxin, not the reverse

Yellow — Low

Direction: reverse direction (as labelled in the source)

A specific gut bacterium, Eggerthella lenta, carries an enzyme that inactivates digoxin in a substantial share of people. This is the microbiome affecting the drug, not digoxin disrupting the microbiome.

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. reverse direction, human data

Limits on what this shows

  • Key negative/null findings: No study reviewed shows digoxin altering gut microbial composition or diversity in the forward direction. Confounding by indication: heart failure and atrial fibrillation, the conditions digoxin treats, are independently associated with gut-microbiome and gut-barrier changes in the broader heart-failure literature; no source reviewed here isolates digoxin, apart from the underlying cardiovascular disease, as a cause of any such change, so no forward-direction microbiome-disruption claim is made.
  • At-risk subgroups: People who carry high-Cgr2-activity Eggerthella lenta strains may under-respond to a given digoxin dose, a bioavailability question rather than a nutrient-deficiency one. The reverse has been proposed elsewhere, antibiotic suppression of E. lenta raising digoxin levels, but no source specifically confirming that direction was opened for this review.

Regulatory status

Not addressed directly in the FDA label; the label's absorption and food-interaction section, already in the PK basis above, does not mention gut bacterial metabolism.

Population evidence

Koppel N, Bisanz JE, Pandelia ME, Turnbaugh PJ, Balskus EP, "Discovery and characterization of a prevalent human gut bacterial enzyme sufficient for the inactivation of a family of plant toxins," eLife 2018;7:e33953. Full text independently retrieved and read for this review. Metagenomic analysis of 1,872 individuals across three continents plus in vitro enzyme work: the Cgr2 enzyme, encoded by Eggerthella lenta, reduces digoxin to inactive dihydrodigoxin; genes for it were detected in over 40% of individuals by metagenomic sequencing and in 74.7% of a validation cohort by targeted qPCR. Haiser HJ, Seim KL, Balskus EP, Turnbaugh PJ, "Mechanistic insight into digoxin inactivation by Eggerthella lenta," Gut Microbes 2014;5(2):233-238; Lu L, et al., "Intestinal microbiome and digoxin inactivation: meal plan for digoxin users?" World J Microbiol Biotechnol 2014; and Ganamurali N, Sabarathinam S, "Microbial modulation of digoxin bioavailability: A pharmacomicrobiome perspective," J Steroid Biochem Mol Biol 2025, are named in bibliographic records as addressing the same mechanism; full text of these three could not be opened for this review (see Sources), so no additional statistic beyond their titles is drawn from them.

Mechanism

Named and confirmed at full-text level for the lead source: Cgr2, a flavin- and iron-sulfur-cluster-dependent reductase, specifically reduces cardenolides including digoxin to an inactive metabolite. A naturally occurring amino-acid substitution (Y333N) sharply reduced enzyme activity in the source's own data, which the authors relate to individual variability in digoxin bioavailability. This is a bacterial enzyme acting on the drug; no mechanism identified anywhere in this review has digoxin acting on the bacteria.

Counter-evidence held on record

No source reviewed supports digoxin causing a measurable, forward-direction disruption of the gut microbiome; every mechanism identified runs from the microbiome toward the drug's bioavailability. Do not present this as "digoxin harms gut bacteria" or "digoxin depletes the microbiome." The consumer-relevant content, if any, is that gut bacterial variation is a recognized source of individual variability in digoxin levels, a monitoring and dosing question for a prescriber, not a supplement or probiotic recommendation.

Oxygen and ATP Output

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

Oxygen delivery/utilization - not gradeable as a nutrient finding

Not graded — disclosed evidence gap

See study details

Human data exist on digoxin changing myocardial oxygen supply and demand, but that is digoxin's own inotropic mechanism of action, not a nutrient-mediated effect, and no nutrient mechanism for altered oxygen carriage was found.

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: Sethna D, Moffitt E, Gray R, et al., "Effects of digoxin on myocardial oxygen supply and demand in patients following coronary artery bypass surgery," Anesthesiology 1982; Kotter V, Schuren K, Schroder R, "Effect of digoxin on coronary blood flow and myocardial oxygen consumption in patients with chronic coronary artery disease," Am J Cardiol 1978; and Tauchert M, et al., "Effect of digoxin on myocardial oxygen consumption in coronary heart disease," Verh Dtsch Ges Inn Med 1977, are named in bibliographic records as human studies measuring digoxin's hemodynamic effect on myocardial oxygen supply and demand. Full text of none of these could be opened for this review (see Sources), so no statistic is cited from them; their titles alone are enough to establish that this is digoxin's known pharmacodynamic action as a positive inotrope, not a nutrient-status finding, and it is excluded from grading on that basis. Separately, no mechanism or study was found linking digoxin to a nutrient, iron, copper, or vitamin B12, that governs blood oxygen-carrying capacity; iron and copper are already ungraded above for that same absence of evidence.
  • What would fill it: A study measuring a nutrient specifically implicated in oxygen delivery (for example, iron status or hemoglobin synthesis) before and after digoxin exposure, independent of digoxin's own hemodynamic action.

ATP production - already addressed under Thiamine, no independent new evidence

Not graded — disclosed evidence gap

See study details

The only nutrient-ATP mechanism with any evidence for digoxin, thiamine, is already graded above. No additional evidence was found for any other ATP-relevant nutrient specific to digoxin.

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: Grading this category a second time on the same thiamine/Zangen 1998 evidence already graded above would double count a single finding under two headings (see the overlap map below). Beyond thiamine, a targeted search for digoxin's effect on mitochondrial ATP synthesis found no additional Tier B or Tier C evidence for any other ATP-relevant nutrient (riboflavin, niacin, CoQ10, L-carnitine), and neither consumer chart reviewed lists any ATP-related nutrient other than the already-addressed thiamine/B1 against digoxin.
  • What would fill it: A study measuring a distinct, non-thiamine ATP-relevant nutrient before and after digoxin exposure, or a mechanism beyond the one already captured in the Thiamine entry.

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.

  • Potassium, magnesium, calcium ("depleted by digoxin")

    Where it comes from: Consumer medication-nutrient-depletion charts (e.g., a widely circulated clinic chart listing digoxin/Lanoxin against calcium, magnesium, and potassium with no citation)

    Why it fails: Direction is reversed. Digoxin's own label describes these nutrients as modifiers of digoxin's toxicity and action, not as nutrients digoxin depletes. The correctly-framed, opposite-direction relationship is graded yellow above; this backward framing is not supported at any tier.

  • Phosphorus

    Where it comes from: Same consumer chart, uncited

    Why it fails: No mechanism, and no Tier B or Tier C evidence of any kind linking digoxin to phosphorus status was found in this review.

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

    Serum digoxin level

    Draw at trough, at least 6-8 hours after the last dose (or immediately before the next). Target 0.8-2.0 ng/mL; about a third of clinically toxic patients still fall under 2.0 ng/mL, so a "normal" level does not rule out toxicity.

  • Lab · Electrolyte

    Serum potassium

    Monitor especially during diuretic co-therapy. Hypokalemia sensitizes the myocardium to digoxin and can produce toxicity even at subtherapeutic digoxin levels.

  • Lab · Electrolyte

    Serum magnesium

    Often checked less consistently than potassium. Check it if arrhythmia or toxicity signs appear despite a normal potassium and a normal digoxin level.

  • Lab · Electrolyte

    Serum calcium

    Avoid unsupervised high-dose calcium or vitamin D supplementation in a digoxin-treated patient; hypercalcemia predisposes to toxicity. Correct hypocalcemia only under medical supervision.

  • Lab · Renal

    Renal function (eGFR/creatinine)

    Digoxin clearance is proportional to GFR. Declining renal function is the most common cause of chronic digoxin toxicity and requires dose reduction, not just electrolyte correction.

  • Timing · Absorption

    Fiber, antacids, kaolin-pectin

    Separate digoxin dosing from antacids, kaolin-pectin, cholestyramine, sulfasalazine, and neomycin by at least 2 hours; avoid taking with high-bran-fiber meals, which can reduce the amount absorbed.

  • Drug interaction

    P-glycoprotein inhibitors

    Amiodarone, quinidine, verapamil, itraconazole, ritonavir, and cyclosporine raise digoxin levels via P-gp inhibition. A 30-50% digoxin dose reduction with level monitoring is typically advised when starting these.

  • Clinical · Safety

    Toxicity symptom awareness

    Blurred or yellow-green tinged vision, anorexia, nausea, and new arrhythmia are classic toxicity signs, not nutrient-deficiency signs. Report promptly to a prescriber; do not attempt to self-treat with supplements.

All references used above
  1. FDA. LANOXIN (digoxin) tablets, USP - prescribing information, NDA 020405/S-006. — Used for absorption/bioavailability, protein binding, metabolism and CYP450 status, elimination and half-life, dialysis, renal impairment dosing, and the electrolyte-toxicity statements (potassium, magnesium, calcium). Revised 2011.
  2. FDA. LANOXIN (digoxin) tablets, USP - prescribing information, NDA 020405/S-013. — Used for P-glycoprotein substrate status (sections 7.1, 12.3) and interaction magnitudes with quinidine, amiodarone, verapamil, itraconazole, ritonavir, and cyclosporine (section 7.2). Revised 2016.
  3. WHO Collaborating Centre for Drug Statistics Methodology. ATC/DDD Index, C01AA05 (digoxin). — Used for ATC classification and defined daily dose.
  4. StatPearls. "Cardiac Glycoside Toxicity." NCBI Bookshelf, NBK459165. — Used for the electrolyte-toxicity mechanism (hypokalemia, hypomagnesemia, hypercalcemia), classic toxicity symptoms, and monitoring guidance. Tier B established pharmacology reference.
  5. StatPearls. "Digoxin." NCBI Bookshelf, NBK556025. — Used for drug class, indications, mechanism of action, and renal-impairment dosing context. Tier B established pharmacology reference.
  6. Zangen A, Botzer D, Zangen R, Shainberg A. "Furosemide and digoxin inhibit thiamine uptake in cardiac cells." Eur J Pharmacol. 1998 Nov 13;361(1):151-155. PMID 9851552. — In vitro cultured-cardiac-cell study; digoxin tested directly alongside furosemide, additive effect on thiamine uptake reported. Tier B mechanistic evidence for the thiamine entry.Primary ScienceDirect record blocked by robots.txt for this review; detail taken from an institutional abstract mirror (Ben-Gurion University research portal), not the publisher's full text.
  7. Wang LH, et al. "Risk of digoxin intoxication in heart failure patients exposed to digoxin-diuretic interactions: a population-based study." Br J Clin Pharmacol. 2010;70(2):258-266. PMID 20653679. — Population-based study of digoxin-diuretic co-prescription and intoxication risk, named in the potassium entry above for context.Full text and abstract could not be retrieved for this review (access blocked). Named here only to document that the study exists; no statistic, effect estimate, or sample size from it is cited anywhere in this dossier.
  8. Young IS, et al. "Magnesium status and digoxin toxicity." Br J Clin Pharmacol. 1991;32(6):717-721. — Named in the secondary literature as a human study of magnesium status in digoxin-toxic patients, referenced in the magnesium entry above for context.Abstract could not be retrieved for this review (access blocked). Named here only; no statistic from it is cited anywhere in this dossier.
  9. Riordan Clinic. "Medication-Induced Nutrient Depletion" chart. — Consumer reference listing digoxin/Lanoxin against calcium, magnesium, thiamine (B1), phosphorus, and potassium with no citation. Tier D circulating-claim source, cited only to document that the claim circulates, not as evidence.
  10. "Prescription Drug Depletion Chart" (consumer clinic reference, hosted file). — Tier D circulating-claim source, notable because it correctly states that digoxin does not deplete potassium while still flagging the toxicity-risk relationship - cited to document that some circulating material already gets the direction right.
  11. Ovey IS, Oncel CR. "The effect of melatonin on digoxin-induced cardiac damage in cardiomyocytes." Bratisl Lek Listy. 2019;120(2):83-89. PMID 30685997. — Cell-based (cardiomyocyte) study; digoxin tested directly, with and without melatonin co-treatment. Tier B mechanistic evidence for the oxidative-stress entry.Full text and rendered abstract could not be retrieved for this review (PubMed abstract page returned no readable content on repeated attempts). Named here only to document title, journal, and year; no statistic, marker value, or sample size from it is cited anywhere in this dossier.
  12. Revis N, Marusic N. "Sequestration of 45Ca2+ by mitochondria from rabbit heart, liver, and kidney after doxorubicin or digoxin/doxorubicin treatment." Exp Mol Pathol. 1979;31(1):46-56. PMID 228971. — Animal (rabbit) study; digoxin tested directly, alone and with doxorubicin. Tier B mechanistic evidence for the mitochondrial burden entry.Full text and abstract could not be retrieved for this review (access blocked). Named here only to document that the study exists; no statistic from it is cited anywhere in this dossier.
  13. Itagaki S, et al. "Interaction of coenzyme Q10 with the intestinal drug transporter P-glycoprotein." J Agric Food Chem. 2008;56(16):6923-6927. PMID 18656939. — Named in bibliographic records as examining coenzyme Q10 at the P-glycoprotein transporter, the same transporter digoxin depends on for absorption and clearance. Tier B mechanistic evidence for the mitochondrial burden entry.Full text and abstract could not be retrieved for this review (PubMed abstract page returned no readable content on repeated attempts). Named here only; no statistic from it is cited anywhere in this dossier.
  14. Haiser HJ, Seim KL, Balskus EP, Turnbaugh PJ. "Mechanistic insight into digoxin inactivation by Eggerthella lenta." Gut Microbes. 2014;5(2):233-238. PMID 24637603. — Mechanistic groundwork for gut bacterial digoxin inactivation, extended by the Koppel 2018 source below. Tier B evidence for the gut microbiome risk entry.Full text could not be retrieved for this review (publisher site returned a 403 error, PubMed abstract page blocked by a CAPTCHA challenge). Named here only to document title, journal, and year; no statistic from it is cited anywhere in this dossier.
  15. Koppel N, Bisanz JE, Pandelia ME, Turnbaugh PJ, Balskus EP. "Discovery and characterization of a prevalent human gut bacterial enzyme sufficient for the inactivation of a family of plant toxins." eLife. 2018;7:e33953. PMID 29761785. — Human metagenomic analysis of 1,872 individuals across three continents, plus comparative genomics and in vitro enzyme characterization (Cgr2). Digoxin tested directly as the model cardenolide substrate. Lead source for the gut microbiome risk entry; full text independently retrieved and read for this review via the publisher (eLife).
  16. Lu L, Wu Y, Zuo L, et al. "Intestinal microbiome and digoxin inactivation: meal plan for digoxin users?" World J Microbiol Biotechnol. 2014;30(11):2957-2962. PMID 24105082. — Named in bibliographic records as addressing dietary influence on gut bacterial digoxin inactivation. Tier B/C context for the gut microbiome risk entry.Full text could not be retrieved for this review (publisher page returned a 404 error on the DOI route attempted). Named here only; no statistic from it is cited anywhere in this dossier.
  17. Ganamurali N, Sabarathinam S. "Microbial modulation of digoxin bioavailability: A pharmacomicrobiome perspective." J Steroid Biochem Mol Biol. 2025. PMID 40425055. — Recent narrative review named in bibliographic records as covering the same gut bacterial digoxin-inactivation mechanism. Tier C context for the gut microbiome risk entry.Full text and abstract could not be retrieved for this review (access blocked). Named here only to document title, journal, and year; no statistic from it is cited anywhere in this dossier.
  18. Sethna D, Moffitt E, Gray R, et al. "Effects of digoxin on myocardial oxygen supply and demand in patients following coronary artery bypass surgery." Anesthesiology. 1982;57(3):A9. PMID 6978623. — Human (Tier A) study of digoxin's hemodynamic effect on myocardial oxygen supply and demand. Cited only to document that this evidence exists and is digoxin's own pharmacodynamic action, not a nutrient finding; excluded from grading in the oxygen delivery/utilization entry.Full text and abstract could not be retrieved for this review (access blocked). Named here only; no statistic from it is cited anywhere in this dossier.
  19. Kotter V, Schuren K, Schroder R. "Effect of digoxin on coronary blood flow and myocardial oxygen consumption in patients with chronic coronary artery disease." Am J Cardiol. 1978;42(4):568-575. PMID 696638. — Human (Tier A) study of digoxin's hemodynamic effect. Same purpose as the Sethna 1982 entry above: documents that this evidence exists and is out of scope for a nutrient grade.Full text and abstract could not be retrieved for this review (access blocked). Named here only; no statistic from it is cited anywhere in this dossier.
  20. Tauchert M, Behrenbeck DW, Hotzel J, et al. "Effect of digoxin on myocardial oxygen consumption in coronary heart disease." Verh Dtsch Ges Inn Med. 1977;83:1145-1147. PMID 611899. — Human (Tier A) study, German language. Same purpose as the two entries above: documents that this evidence exists and is out of scope for a nutrient grade.Full text and abstract could not be retrieved for this review (access blocked; German-language original not opened). Named here only; no statistic from it is cited anywhere in this dossier.