Medications That Deplete Nutrients: Chart and Safety Guide

Almost every prescription comes with a list of side effects. Very few come with a list of nutrients it might quietly change.

That gap is why this article exists. Drug-induced nutrient depletion is real, it is documented in the peer-reviewed literature, and it is also one of the sloppiest topics in consumer health writing. Most articles hand you a chart with no sources, skip the safety warnings, and never tell you which findings are strong and which are guesses.

So let's fix that. Below you will find a sourced nutrient depletion chart, honest evidence grades for each drug and nutrient pair, a clear separation of three problems that usually get muddled together, and a section on what you should not add without checking with your prescriber first.

This is education, not medical advice, and not a reason to stop or change a medication you have been prescribed.

Table of contents

• Three different problems wearing one name
• The nutrient depletion chart
• Metformin and vitamin B12
• Acid-suppressing drugs: PPIs, H2 blockers, B12 and magnesium
• Statins and CoQ10: the honest answer
• Corticosteroids and bone nutrients
• Diuretics, potassium and magnesium
• Oral contraceptives, antibiotics, NSAIDs and blood pressure drugs
• What not to add without asking first
• Timing rules: when the fix is just spacing doses apart
• Questions to ask your prescriber or pharmacist
• What We Recommend
• Frequently asked questions
• References

Three different problems wearing one name

Search for "medications that deplete nutrients" and you find one big pile. Metformin, statins, antacids and diuretics all get thrown in together as if they do the same thing. They do not.

There are three separate mechanisms, and the fix differs for each. Getting this straight is the whole ballgame, because the advice you need depends on which one you face.

1. Absorption interference. The drug blocks a nutrient while the drug is on board. Stop the drug, or move it away from the nutrient, and the problem usually resolves. The classic version runs in reverse: a calcium or iron supplement binds levothyroxine in the gut and reduces how much of the drug your body takes up. Timing is the entire fix. Nothing has been drained from your body.

2. True depletion. The drug genuinely drains body stores over months or years. It is slower, it can be silent, and it may need supplementation to correct rather than a schedule change. Metformin and vitamin B12 is one of the best-documented examples.

3. Altered synthesis. The drug changes how your body makes something, rather than how it absorbs something. Statins block the mevalonate pathway, the same assembly line that makes both cholesterol and coenzyme Q10. The drug works as designed; the CoQ10 drop is a downstream consequence.

A chart that treats all three as one thing tells you to supplement for problems that timing would solve, and to space doses for problems that need a conversation about nutrient status. Absorption interference is a scheduling problem, true depletion is a nutrient-status problem, and altered synthesis is a biology problem.

A warm, natural-light still life of unbranded bottles on a cream surface.

The nutrient depletion chart

Here is the chart the top-ranking pages keep promising and not delivering. Every row comes from the peer-reviewed sources listed at the end of this article, not from a supplement company's marketing sheet. There is one disclosed exception, and it is disclosed rather than buried: the antibiotics row is a mechanism-based extrapolation with thin direct human evidence, and it is labeled that way.

Medication class	Nutrient affected	Mechanism	Evidence strength
Metformin	Vitamin B12	Impairs calcium-dependent B12 absorption	Well documented
Proton pump inhibitors	Vitamin B12, magnesium, iron, calcium	Raises stomach pH (magnesium route unclear)	Well documented
H2 blockers	Vitamin B12	Reduced acid release	Well documented
Statins	Coenzyme Q10	Shared mevalonate pathway	Well documented
Thiazide and loop diuretics	Potassium, magnesium	Increased urinary loss	Well documented
Corticosteroids	Calcium, vitamin D	Lower absorption, higher loss	Well documented
Oral contraceptives	Vitamin B6, magnesium	Altered metabolism	Mixed evidence
Antibiotics	B vitamins, vitamin K	Gut flora disruption	Limited evidence
Aspirin and NSAIDs	Vitamin C, iron	Impaired absorption, GI blood loss	Limited evidence
ACE inhibitors	Zinc	Thiol chelation (captopril)	Limited evidence

Read the evidence label honestly, because it means what it says.

• Well documented means the depletion itself has been shown in controlled trials or large studies, not just theorized from a mechanism.
• Mixed evidence means the finding shows up mostly in observational work, the effect size is debated, and reasonable researchers disagree about how much it matters.
• Limited evidence means the mechanism is plausible and the data is thin. Treat those rows as a reason to ask a question, not a reason to act.
• One gap worth naming: for PPIs and magnesium the association is fairly consistent across studies, but the underlying mechanism is not established. That is why the chart says the route is unclear instead of pretending to know.

One caveat on the statin row: the depletion of CoQ10 is well documented. Whether supplementing CoQ10 changes how you feel is a genuinely open question, covered below.

Nutrient-dense whole foods arranged with an unbranded supplement bottle.

Metformin and vitamin B12

If you take metformin for blood sugar support, this is the pair worth knowing about. It has the strongest evidence base of anything in this article.

A randomized placebo-controlled trial published in the BMJ followed 390 people over 4.3 years. Metformin lowered vitamin B12 by a mean of about 19 percent compared with placebo. Absolute risk of B12 deficiency was 7.2 percentage points higher, a number needed to harm of 13.8 over those 4.3 years. [2]

The Diabetes Prevention Program Outcomes Study added a second data point. At five years, low B12 was more common on metformin than off it, at 4.3 percent versus 2.3 percent, and low B12 in the metformin group was linked to a higher prevalence of peripheral neuropathy. By thirteen years the gap had narrowed to 7.4 percent versus 5.4 percent and was no longer statistically significant, a useful reminder that this signal is real but not inevitable. The authors concluded that routine B12 testing for long-term metformin users should be considered. [3]

Why does it happen? B12 absorption depends on a calcium-dependent step in the gut. Metformin appears to interfere with that step, so less B12 reaches your bloodstream. The mechanism is well described even though the exact molecular detail is still being worked out. [1]

What that means in practice: the effect is slow and shows up over years rather than weeks, it is measurable with a serum B12 test plus methylmalonic acid or homocysteine, and it is a conversation, not a decision. Ask your prescriber whether testing makes sense for you, and never stop metformin on your own.

For background on how B12 status and methylation are assessed, the Agape Nutrition guide to B12, folate and methylation support is a useful next read. For the wider metabolic picture, see the weight and metabolism resource page.

Acid-suppressing drugs: PPIs, H2 blockers, B12 and magnesium

Acid-suppressing medication is one of the most widely prescribed categories of medicine. It comes with two well-documented nutrient questions.

PPIs and vitamin B12

Stomach acid is not an inconvenience. It is a tool. Your body uses it to pry vitamin B12 loose from the proteins in food. Less acid means less B12 gets released to be absorbed.

A large case-control study in JAMA looked at 25,956 people with B12 deficiency and 184,199 controls. [4] Two or more years of proton pump inhibitor use carried an odds ratio of 1.65 for B12 deficiency. H2 blockers, a weaker acid suppressant, carried an odds ratio of 1.25. The study found a clear dose response: more suppression, more deficiency.

Two things follow from that. The duration and the degree of acid suppression both matter, which is why this was not a two-week course and why the PPI signal was stronger. And an odds ratio is a population statistic, so it does not predict what happens to any one person.

PPIs and magnesium

Magnesium is the second PPI concern. Several meta-analyzes of observational studies point the same way, toward an association with long-term use, though the authors of one analysis noted significant heterogeneity across studies and stopped short of a definitive conclusion. The mechanism is not established either. [5][6][7]

Low magnesium is easy to miss because the symptoms are vague and gradual. That is a reason to ask your prescriber about monitoring if you have been on a PPI for years, not a reason to panic or self-prescribe.

H2 blockers

H2 blockers work on the same acid pathway through a different door, which is why they land in the chart with a smaller but real signal.

If you take acid-suppressing medication daily, the heartburn and reflux category is the relevant aisle, and the questions further down are the right ones to bring to your pharmacist.

A capsule and a glass of citrus water, showing two paths a nutrient can take.

Statins and CoQ10: the honest answer

This is where most articles either lie to you or sell you something. Let's do neither.

First, the part that is not disputed. Statins lower circulating coenzyme Q10. Statins work by blocking the mevalonate pathway, and CoQ10 is made on that same pathway. Lower the pathway's output and you lower CoQ10 alongside cholesterol. That is a predictable consequence of how the drug works, and it is well documented. [1]

Second, the part that is genuinely contested. Does supplementing CoQ10 relieve the muscle aches some people get on statins? Three meta-analyzes of randomized controlled trials have asked this, and they do not agree.

• Banach 2015 (Mayo Clinic Proceedings) pooled 6 randomized trials with 302 patients and found no significant benefit for muscle pain or for creatine kinase, a muscle enzyme used as a marker of muscle stress. [8]
• Kennedy 2020 (Atherosclerosis) pooled 7 randomized trials with 321 patients and found no benefit for muscle aches, and no improvement in whether people stayed on their statin. [9]
• Qu 2018 (Journal of the American Heart Association) pooled 12 randomized trials with 575 patients and did find improvement in muscle symptoms, including pain, weakness, cramp and tiredness. It found no improvement in creatine kinase. [10]

Two of the three say no benefit. The third says benefit for symptoms but not for the objective marker. Note that the third analysis covered more trials and more patients than the other two, which cuts both ways: more data, and the disagreement did not disappear.

The conclusion, stated plainly: the depletion is real, the clinical benefit of supplementing is unproven, and the meta-analyzes disagree.

If you take a statin and you have muscle symptoms, talk to your prescriber about the symptom. Do not add a supplement to fix a problem that has not been assessed. If your clinician wants to trial CoQ10, that is their call to make and to monitor. This article will not sell you on it, because the evidence does not support a sales pitch. For the basics of what CoQ10 does in the body, see the CoQ10 benefits guide, and for the wider cardiovascular picture, the heart and circulation resource page.

Corticosteroids and bone nutrients

Corticosteroids are effective, widely used, and hard on bone over time. This is the one section where the guidance comes from a formal clinical guideline, the strongest evidence type in this article.

The 2022 American College of Rheumatology guideline on glucocorticoid-induced osteoporosis recommends that adults who take at least 2.5 mg per day of glucocorticoids for more than 3 months receive a fracture-risk assessment and bone mineral density testing. Clinical guidelines include calcium and vitamin D as part of standard bone-supportive care in that situation; your clinician decides whether that applies to you. [11]

A 2018 review in Endocrine describes the mechanism: glucocorticoids reduce calcium absorption from the gut, increase calcium loss through the kidneys, and shift the balance of bone building and bone breakdown in the wrong direction. [12]

So duration and dose both count, the monitoring is defined by a guideline threshold, and calcium plus vitamin D sit inside standard care rather than outside it. The bone, joint and pain resource page covers the broader nutrient picture for bone health.

Diuretics, potassium and magnesium

Diuretics make you urinate more, which is the point. The side effect is that you also lose electrolytes and minerals with the extra fluid.

The Mohn 2018 review in Pharmaceutics reports that thiazide and loop diuretics are associated with lower potassium and lower magnesium. [1] The same review reports higher odds of hip fracture with long-term diuretic use, including an odds ratio of 3.9 for furosemide users in one reported analysis, while a thiazide analysis showed a reduction. Report that exactly as the review does: mixed fracture findings, not a clean signal against one drug class.

Two practical notes. Potassium is checked on a standard blood panel, so that one is easy to follow. Magnesium usually is not included, so if you are on a long-term diuretic it is worth asking whether it should be added. And potassium is the nutrient where self-supplementing is genuinely risky, which is why it appears again below.

Oral contraceptives, antibiotics, NSAIDs and blood pressure drugs

Everything in this section carries a softer evidence label. That is deliberate: these findings are real enough to mention and too thin to act on without a conversation.

• Oral contraceptives. A 2011 review in Nutrition Reviews looked at folate, vitamin B6 and vitamin B12. It concluded that current low-dose oral contraceptives do not appear to lower folate status and do not significantly affect functional B12 measures, but that they may lower vitamin B6 status. The B6 finding is the one with real support, and its clinical importance is still debated. [14]
• Antibiotics. This is the one row in the chart that is not backed by a source in our reference list, and we are labeling it rather than hiding it. The proposed mechanism is disruption of gut bacteria that help produce certain B vitamins and vitamin K. It is plausible and it is widely repeated, but the direct human evidence is thin, so treat it as a question to raise rather than a finding to act on.
• Aspirin and NSAIDs. The Mohn review reports associations with vitamin C and iron, through impaired absorption and small ongoing blood loss. Modest findings, worth knowing, not worth self-treating over. [1]
• ACE inhibitors. These appear in the chart with zinc and a limited label, on the basis of zinc chelation by the thiol group in captopril. The honest caveat: for this drug class the bigger practical issue runs the opposite way, since these drugs raise potassium rather than depleting it. That is a safety matter, not a deficiency one. [1]

What not to add without asking first

Almost every article on this topic tells you what to add. Very few tell you what to be careful about adding, and the second list is the more important one.

None of this is a reason to be frightened of supplements. It is a reason to say the word "pharmacist" before you say the word "checkout."

Potassium supplements with ACE inhibitors, ARBs or potassium-sparing diuretics. These medications already reduce how much potassium your body excretes. Adding a potassium supplement on top can push blood potassium too high, which affects heart rhythm.

Here is the honest nuance, and it matters. A clinical trial in the American Journal of Clinical Nutrition found that potassium intake at dietary levels, from food, did not cause high blood potassium in people taking medication that blocks the renin-angiotensin-aldosterone system. [15] The concern is high-dose supplemental potassium, not potassium from food. Talk to your prescriber before adding a potassium supplement, not before eating a banana.

Vitamin K with warfarin. Warfarin works by interfering with vitamin K, so a big, sudden change in vitamin K intake in either direction can change how the drug behaves. One nuance worth knowing: a systematic review of dietary vitamin K and warfarin found the evidence on diet to be genuinely conflicting, and that a minimum intake is needed for stable anticoagulation. So the old advice to avoid every green vegetable is not well supported. Consistency is what matters, and any change in vitamin K intake or supplementation should go through the clinician managing your dose. [17]

Calcium and iron supplements with levothyroxine. Calcium measurably reduces levothyroxine absorption, cutting it by roughly 20 to 25 percent in a pharmacokinetic study, and levothyroxine adsorbs to calcium carbonate in the gut. Standard labeling and the NIH's patient guidance are to take calcium or iron at least 4 hours before or after levothyroxine. This is absorption interference, not depletion. Nothing is drained from your body; the drug simply is not getting in properly when the two are taken together. [13][16][20]

Niacin and red yeast rice with statins. In a trial of 25,673 people, adding extended-release niacin (with laropiprant) to simvastatin increased the risk of definite myopathy roughly fourfold. [18] Red yeast rice is a separate case and worth understanding on its own terms: it contains naturally occurring monacolins, compounds in the same pharmacological family as statin drugs. Because it is sold as a supplement, the dose is not standardized or monitored the way a prescription is, so raise it with your prescriber before combining it with a statin rather than assuming it is a gentler version of the same thing.

St John's Wort. This herb activates a liver receptor that speeds up the enzymes clearing a long list of medications, including statins and warfarin, which can lower drug levels in your blood. Ask your pharmacist before combining it with anything prescribed. [19]

For a broader look at combinations to be careful with, including supplement-to-supplement interactions, our guide to supplements not to take together covers the territory.

The riskiest supplement is never the one you researched, it is the one you added without mentioning.

Timing rules: when the fix is just spacing doses apart

Some drug and nutrient clashes are not deficiencies at all. They are scheduling problems, and they can often be solved without changing anything you take.

• Levothyroxine and calcium or iron. Separate them by about 4 hours.
• Iron and calcium supplements. Take them at different times of day, since they compete for the same absorption pathways.
• Acid-suppressing medication. Take it as directed relative to meals, since it works best when acid production is about to ramp up.
• Magnesium supplements. Many people tolerate them better in the evening, and separating them from other minerals avoids competition.
• Any new supplement. Add one thing at a time so you can tell what is doing what.

The general principle is simple. If the problem is interference, fix the schedule. If the problem is depletion, fix the nutrient status. Scheduling your way out of a true depletion will not work, and supplementing your way out of a timing clash is unnecessary.

A quiet moment at the table, with a notebook for the questions worth bringing to your prescriber.

Questions to ask your prescriber or pharmacist

You will not find this list on most of the pages competing for this topic. Bring it to your next appointment or to the pharmacy counter.

1. How long do you expect me to be on this medication? Duration changes the risk profile for almost every pair in the chart.
2. Should any of my nutrient levels be tested, and how often? B12 for metformin, magnesium for long-term acid suppression, and bone density for corticosteroids all have reasonable cases.
3. Is there a timing change that would help here? Sometimes the answer is a 4-hour gap, not a new bottle.
4. Are there supplements I should avoid entirely while taking this? Ask specifically about potassium, vitamin K, niacin and St John's Wort.
5. If I do supplement, what dose and what form do you want me on? Dose and form are clinical decisions, not marketing claims.
6. What symptoms would tell us this is becoming a problem? Knowing what to watch for turns a vague worry into an early signal.

Write the answers down. A ten-minute conversation with a pharmacist covers most of this and costs nothing.

What We Recommend

If you and your prescriber decide that one of the well-documented nutrients above is worth testing or supporting, these are the Agape products that match. Each one maps to a nutrient pair this article graded as well documented, not to a symptom, and none of them treats or prevents the condition a medication is prescribed for. Nothing here replaces the conversation you are supposed to have first, and nothing here is a reason to change a prescription on your own.

XYMOGEN, OptiMag Neuro 90 Capsules

A magnesium formula for readers whose clinician has flagged magnesium status on long-term acid suppression or a thiazide or loop diuretic.

Price: $64.99

XYMOGEN, Methyl Protect 120 Capsules

Active B12 and folate in their methylated forms, for the metformin and long-term PPI readers whose B12 status this article graded as well documented.

Price: $74.99

Nordic Naturals, Vitamin D3 5000 - 120 Softgels

Vitamin D3 for readers whose clinician has flagged vitamin D status alongside long-term corticosteroid use.

Price: $24.95

Researched Nutritionals, CoQ10 Power™ 60 Softgels

A CoQ10 option for readers whose prescriber has raised CoQ10 status. It supports CoQ10 levels, and this article is clear that the muscle symptom question is unresolved.

Price: $66.98

Frequently asked questions

Does metformin deplete vitamin B12?

Yes, and this is one of the better-established findings in the field. The BMJ trial showed a mean 19 percent drop in B12 over 4.3 years and a 7.2 percentage point higher absolute risk of deficiency. The Diabetes Prevention Program Outcomes Study found low B12 more common at five years, linked to a higher prevalence of peripheral neuropathy in the metformin group, and concluded that routine testing should be considered. Ask your prescriber about a B12 test if you have been on metformin for years. [2][3]

Do statins deplete CoQ10, and should I supplement?

Statins do lower circulating CoQ10 through the mevalonate pathway, and that is not disputed. Whether supplementing helps with muscle symptoms is a different question, and the meta-analyzes disagree: Banach 2015 and Kennedy 2020 found no benefit, while Qu 2018 found improvement in symptoms but not in creatine kinase. The depletion is real, the clinical benefit of supplementing is unproven.

Can I take magnesium with my blood pressure medication?

It depends which one. Magnesium is generally well tolerated, but if you take an ACE inhibitor, an ARB or a potassium-sparing diuretic, the concern is potassium rather than magnesium, and that is a conversation to have first. If you take a thiazide or loop diuretic, magnesium and potassium are both worth monitoring.

Should I take a multivitamin while on medication?

A multivitamin is usually a low-dose, broad-spectrum product, so it is rarely the highest-risk item on the shelf. The bigger issue is that it is a blunt instrument: it will not correct a specific depletion that needs a targeted, monitored dose.

What supplements should I avoid with statins?

The ones to raise with your prescriber are niacin at higher doses, red yeast rice (which contains monacolins, compounds in the same pharmacological family as statin drugs), and St John's Wort, which speeds up the liver enzymes that clear many medications. CoQ10 is not in the "avoid" category, but it is also not a proven fix for muscle symptoms.

How long do you have to take a PPI before B12 or magnesium becomes a concern?

The B12 signal in the JAMA study was for two or more years of proton pump inhibitor use, and it was stronger with more complete acid suppression. The magnesium meta-analyzes point the same way, toward long-term use. Short courses are a different situation from years of daily use.

Should I get tested before supplementing?

If a deficiency is suspected, testing first is the better sequence. It tells you whether there is a real gap, how large it is, and gives you a baseline to measure against later. Supplementing blind means you never learn whether the problem existed or whether anything you did changed it.

References

1. Mohn ES, Kern HJ, Saltzman E, Mitmesser SH, McKay DL. Evidence of Drug-Nutrient Interactions with Chronic Use of Commonly Prescribed Medications: An Update. Pharmaceutics. 2018;10(1):E36. https://pubmed.ncbi.nlm.nih.gov/29558445/ doi:10.3390/pharmaceutics10010036
2. de Jager J, Kooy A, Lehert P, et al. Long term treatment with metformin in patients with type 2 diabetes and risk of vitamin B-12 deficiency: randomised placebo controlled trial. BMJ (Clinical research ed.). 2010;340:c2181. https://pubmed.ncbi.nlm.nih.gov/20488910/ doi:10.1136/bmj.c2181
3. Aroda VR, Edelstein SL, Goldberg RB, et al. Long-term Metformin Use and Vitamin B12 Deficiency in the Diabetes Prevention Program Outcomes Study. The Journal of clinical endocrinology and metabolism. 2016;101(4):1754-1761. https://pubmed.ncbi.nlm.nih.gov/26900641/ doi:10.1210/jc.2015-3754
4. Lam JR, Schneider JL, Zhao W, Corley DA. Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA. 2013;310(22):2435-2442. https://pubmed.ncbi.nlm.nih.gov/24327038/ doi:10.1001/jama.2013.280490
5. Srinutta T, Chewcharat A, Takkavatakarn K, et al. Proton pump inhibitors and hypomagnesemia: A meta-analysis of observational studies. Medicine. 2019;98(44):e17788. https://pubmed.ncbi.nlm.nih.gov/31689852/ doi:10.1097/md.0000000000017788
6. Cheungpasitporn W, Thongprayoon C, Kittanamongkolchai W, et al. Proton pump inhibitors linked to hypomagnesemia: a systematic review and meta-analysis of observational studies. Renal failure. 2015;37(7):1237-1241. https://pubmed.ncbi.nlm.nih.gov/26108134/ doi:10.3109/0886022x.2015.1057800
7. Park CH, Kim EH, Roh YH, Kim HY, Lee SK. The association between the use of proton pump inhibitors and the risk of hypomagnesemia: a systematic review and meta-analysis. PloS one. 2014;9(11):e112558. https://pubmed.ncbi.nlm.nih.gov/25394217/ doi:10.1371/journal.pone.0112558
8. Banach M, Serban C, Sahebkar A, et al. Effects of coenzyme Q10 on statin-induced myopathy: a meta-analysis of randomized controlled trials. Mayo Clinic proceedings. 2015;90(1):24-34. https://pubmed.ncbi.nlm.nih.gov/25440725/ doi:10.1016/j.mayocp.2014.08.021
9. Kennedy C, Köller Y, Surkova E. Effect of Coenzyme Q10 on statin-associated myalgia and adherence to statin therapy: A systematic review and meta-analysis. Atherosclerosis. 2020;299:1-8. https://pubmed.ncbi.nlm.nih.gov/32179207/ doi:10.1016/j.atherosclerosis.2020.03.006
10. Qu H, Guo M, Chai H, et al. Effects of Coenzyme Q10 on Statin-Induced Myopathy: An Updated Meta-Analysis of Randomized Controlled Trials. Journal of the American Heart Association. 2018;7(19):e009835. https://pubmed.ncbi.nlm.nih.gov/30371340/ doi:10.1161/jaha.118.009835
11. Humphrey MB, Russell L, Danila MI, et al. 2022 American College of Rheumatology Guideline for the Prevention and Treatment of Glucocorticoid-Induced Osteoporosis. Arthritis & rheumatology (Hoboken, N.J.). 2023;75(12):2088-2102. https://pubmed.ncbi.nlm.nih.gov/37845798/ doi:10.1002/art.42646
12. Compston J. Glucocorticoid-induced osteoporosis: an update. Endocrine. 2018;61(1):7-16. https://pubmed.ncbi.nlm.nih.gov/29691807/ doi:10.1007/s12020-018-1588-2
13. Singh N, Singh PN, Hershman JM. Effect of calcium carbonate on the absorption of levothyroxine. JAMA. 2000;283(21):2822-2825. https://pubmed.ncbi.nlm.nih.gov/10838651/ doi:10.1001/jama.283.21.2822
14. Wilson SM, Bivins BN, Russell KA, Bailey LB. Oral contraceptive use: impact on folate, vitamin B₆, and vitamin B₁₂ status. Nutrition reviews. 2011;69(10):572-583. https://pubmed.ncbi.nlm.nih.gov/21967158/ doi:10.1111/j.1753-4887.2011.00419.x
15. Malta D, Arcand J, Ravindran A, et al. Adequate intake of potassium does not cause hyperkalemia in hypertensive individuals taking medications that antagonize the renin angiotensin aldosterone system. The American journal of clinical nutrition. 2016;104(4):990-994. https://pubmed.ncbi.nlm.nih.gov/27581475/ doi:10.3945/ajcn.115.129635
16. Zamfirescu I, Carlson HE. Absorption of levothyroxine when coadministered with various calcium formulations. Thyroid : official journal of the American Thyroid Association. 2011;21(5):483-486. https://pubmed.ncbi.nlm.nih.gov/21595516/ doi:10.1089/thy.2010.0296
17. Violi F, Lip GY, Pignatelli P, Pastori D. Interaction Between Dietary Vitamin K Intake and Anticoagulation by Vitamin K Antagonists: Is It Really True?: A Systematic Review. Medicine. 2016;95(10):e2895. https://pubmed.ncbi.nlm.nih.gov/26962786/ doi:10.1097/md.0000000000002895
18. HPS2-THRIVE Collaborative Group. HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment. European heart journal. 2013;34(17):1279-1291. https://pubmed.ncbi.nlm.nih.gov/23444397/ doi:10.1093/eurheartj/eht055
19. Nicolussi S, Drewe J, Butterweck V, Meyer Zu Schwabedissen HE. Clinical relevance of St. John's wort drug interactions revisited. British journal of pharmacology. 2020;177(6):1212-1226. https://pubmed.ncbi.nlm.nih.gov/31742659/ doi:10.1111/bph.14936
20. MedlinePlus (U.S. National Library of Medicine, National Institutes of Health). Levothyroxine. MedlinePlus Drug Information. https://medlineplus.gov/druginfo/meds/a682461.html

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

This article is education, not medical advice. It is not a substitute for a conversation with your own prescriber or pharmacist, and no one should stop or change a prescribed medication without their prescriber.