Medication-Nutrient Depletion Matrix Part 2: Beyond the Top 60

Quick Answer: Dozens of commonly prescribed medications beyond the usual suspects — including fluoroquinolone antibiotics, SSRIs, antipsychotics, ACE inhibitors, amiodarone, immunosuppressants, and antiretrovirals — deplete critical nutrients your body needs. This guide covers 30+ additional medications with evidence-rated depletion data, specific nutrients affected, and practical supplementation strategies to discuss with your healthcare provider.

If you’ve read our Complete Medication-Nutrient Depletion Database, you know the major offenders: statins depleting CoQ10, metformin stripping B12, and PPIs wiping out magnesium. But that database covered the top 60 most commonly discussed medication-nutrient interactions. The reality is that the pharmaceutical landscape is far wider, and many medications that millions of people take daily have nutrient depletion profiles that rarely get discussed — even by pharmacists.

This companion guide extends the database with 30+ additional medications organized by drug class. Every entry follows the same evidence-rating system: Strong (●●●) means multiple human clinical trials or meta-analyses confirm the depletion; Moderate (●●) means observational data or smaller trials support it; Weak (●) means case reports, mechanistic data, or animal studies suggest it but human confirmation is limited.

This article is educational information, not medical advice. Never start or stop any supplement without discussing it with your prescribing physician or pharmacist. Some supplements can interact with the very medications discussed here.

How to Read the Evidence Ratings

Before diving into the tables, here’s what each rating means in practical terms:

• Strong ●●● — Multiple randomized controlled trials (RCTs), meta-analyses, or large prospective cohort studies confirm the depletion. Supplementation is well-supported. Your doctor should be aware.
• Moderate ●● — Observational studies, smaller clinical trials, or pharmacokinetic data strongly suggest depletion. Monitoring levels is reasonable. Supplementation is likely beneficial.
• Weak ● — Case reports, animal data, or mechanistic reasoning suggest depletion but human confirmation is limited. Worth awareness, but don’t supplement based on weak evidence alone without medical guidance.

Fluoroquinolone Antibiotics

Fluoroquinolones — ciprofloxacin, levofloxacin, moxifloxacin — are among the most commonly prescribed antibiotics worldwide. Their nutrient depletion profile is more significant than most patients realize, and the mechanism is built into how the drug works.

Fluoroquinolones chelate divalent and trivalent metal cations (Mg²⁺, Ca²⁺, Zn²⁺, Fe²⁺/Fe³⁺) in the gastrointestinal tract, forming insoluble complexes that prevent absorption of both the mineral and the antibiotic. This isn’t a side effect — it’s a direct chemical property of the fluoroquinolone molecular structure. The FDA-mandated prescribing information for ciprofloxacin explicitly warns against concurrent administration with calcium, magnesium, aluminum, and iron supplements for this reason [1].

Beyond chelation, fluoroquinolones have been linked to magnesium wasting at the renal level. Stahlmann and Lode’s comprehensive review of quinolone toxicity documented that fluoroquinolones can impair magnesium reabsorption in the renal tubules, contributing to hypomagnesemia that persists beyond the chelation effect [1]. This magnesium depletion has been implicated in the tendon damage (including Achilles tendon rupture) that prompted the FDA’s black box warning on fluoroquinolones.

Medication	Nutrient Depleted	Evidence	Mechanism	Recommended Supplement
Ciprofloxacin	Magnesium	Strong ●●●	GI chelation + renal wasting	Magnesium glycinate 200–400 mg/day (take 2+ hrs apart from antibiotic)
Ciprofloxacin	Calcium	Strong ●●●	GI chelation	Calcium citrate 500–600 mg/day (take 2+ hrs apart)
Ciprofloxacin	Zinc	Moderate ●●	GI chelation	Zinc picolinate 15–30 mg/day (take 2+ hrs apart)
Ciprofloxacin	Iron	Strong ●●●	GI chelation	Iron bisglycinate 18–25 mg/day (take 2+ hrs apart)
Levofloxacin	Magnesium	Strong ●●●	GI chelation + renal wasting	Magnesium glycinate 200–400 mg/day (take 2+ hrs apart)
Moxifloxacin	Magnesium	Moderate ●●	GI chelation	Magnesium glycinate 200–400 mg/day (take 2+ hrs apart)

Practical note: The timing separation is critical. Minerals taken at the same time as fluoroquinolones will reduce antibiotic absorption by 25–50%, potentially causing treatment failure. Always separate by at least 2 hours before or 6 hours after the antibiotic dose.

Tetracycline Antibiotics

Tetracyclines — doxycycline, minocycline, tetracycline — share the same chelation problem as fluoroquinolones but with even broader mineral binding. The tetracycline molecule has four ring structures with multiple oxygen-containing functional groups that aggressively bind metal cations.

The clinical significance is twofold: the antibiotic becomes less effective (reduced bioavailability), and the mineral isn’t absorbed. For patients on long-term doxycycline (common for acne, rosacea, or Lyme disease prophylaxis), the cumulative mineral loss over months of treatment can be meaningful.

Medication	Nutrient Depleted	Evidence	Mechanism	Recommended Supplement
Doxycycline	Calcium	Strong ●●●	GI chelation	Calcium citrate 500–600 mg/day (take 2+ hrs apart)
Doxycycline	Magnesium	Strong ●●●	GI chelation	Magnesium glycinate 200–400 mg/day (take 2+ hrs apart)
Doxycycline	Iron	Strong ●●●	GI chelation	Iron bisglycinate 18–25 mg/day (take 2+ hrs apart)
Doxycycline	Zinc	Moderate ●●	GI chelation	Zinc picolinate 15–30 mg/day (take 2+ hrs apart)
Minocycline	Calcium	Strong ●●●	GI chelation	Calcium citrate 500–600 mg/day (take 2+ hrs apart)
Minocycline	Iron	Strong ●●●	GI chelation	Iron bisglycinate 18–25 mg/day (take 2+ hrs apart)
Tetracycline	Calcium, Magnesium, Iron, Zinc	Strong ●●●	GI chelation (broadest binding)	Full mineral complex (take 2+ hrs apart)

SSRIs and SNRIs (Antidepressants)

Selective serotonin reuptake inhibitors (SSRIs) — fluoxetine, sertraline, escitalopram, paroxetine, citalopram — and serotonin-norepinephrine reuptake inhibitors (SNRIs) — venlafaxine, duloxetine — are prescribed to tens of millions of people. Their nutrient depletion profile is underappreciated.

Sodium Depletion (Hyponatremia)

The most clinically significant nutrient impact of SSRIs is hyponatremia — low sodium levels. SSRIs stimulate inappropriate secretion of antidiuretic hormone (SIADH), causing the kidneys to retain excess water, which dilutes blood sodium. A 2025 analysis from the All of Us Research Program found that SSRI-associated hyponatremia is more common than previously recognized, with certain SSRIs carrying higher risk than others [2]. Mannheimer et al. (2021) demonstrated a time-dependent relationship, with peak risk occurring in the first 2–4 weeks of SSRI initiation [3].

Folate and B-Vitamin Status

SSRIs depend on adequate folate and B12 for proper serotonin synthesis. While SSRIs don’t directly deplete folate, patients with low folate status respond poorly to SSRI therapy. Methylfolate (5-MTHF) supplementation has been shown in multiple trials to augment SSRI efficacy in treatment-resistant depression — suggesting that functional folate insufficiency is common in SSRI-treated populations.

Medication	Nutrient Affected	Evidence	Mechanism	Recommended Action
All SSRIs	Sodium	Strong ●●●	SIADH → dilutional hyponatremia	Monitor sodium levels; highest risk in first month and in elderly patients
Fluoxetine	Sodium	Strong ●●●	SIADH (higher risk vs other SSRIs)	Baseline and 2-week sodium check; watch for confusion, headaches, nausea
Paroxetine	Sodium	Strong ●●●	SIADH (higher risk in elderly)	Baseline and 2-week sodium check
All SSRIs	Folate (functional)	Moderate ●●	Increased demand for serotonin synthesis	Methylfolate (L-5-MTHF) 1–15 mg/day as augmentation
Venlafaxine (SNRI)	Sodium	Strong ●●●	SIADH	Monitor sodium; risk comparable to SSRIs
Duloxetine (SNRI)	Sodium	Moderate ●●	SIADH (lower incidence than venlafaxine)	Monitor sodium in at-risk patients

Antipsychotic Medications

Second-generation antipsychotics (SGAs) — olanzapine, clozapine, risperidone, quetiapine, aripiprazole — are used for schizophrenia, bipolar disorder, and increasingly for treatment-resistant depression and off-label uses. Their metabolic effects are well-known (weight gain, insulin resistance), but their nutrient depletion profiles receive far less attention.

Vitamin D Deficiency

Vitamin D deficiency is strikingly prevalent in patients taking antipsychotics. A 2025 systematic review by Mosiołek et al. found that vitamin D deficiency is both a risk factor for and a consequence of schizophrenia treatment, with antipsychotic-treated patients consistently showing lower 25(OH)D levels than matched controls [4]. Krivoy et al.’s RCT (2017) demonstrated that vitamin D supplementation in clozapine-treated schizophrenia patients improved metabolic parameters, suggesting the deficiency has functional consequences beyond bone health [5].

The mechanisms are multiple: antipsychotics promote weight gain and indoor sedentary behavior (reducing sun exposure), alter hepatic metabolism of vitamin D, and may directly impair vitamin D receptor expression.

Medication	Nutrient Depleted	Evidence	Mechanism	Recommended Supplement
Olanzapine	Vitamin D	Strong ●●●	Weight gain → reduced sun exposure; altered hepatic metabolism	Vitamin D3 2,000–5,000 IU/day; check 25(OH)D levels
Clozapine	Vitamin D	Strong ●●●	Weight gain + metabolic syndrome + hepatic effects	Vitamin D3 2,000–5,000 IU/day; check 25(OH)D levels
Risperidone	Vitamin D	Moderate ●●	Weight gain + sedation-related inactivity	Vitamin D3 2,000–4,000 IU/day
Quetiapine	Vitamin D	Moderate ●●	Weight gain; sedation	Vitamin D3 2,000–4,000 IU/day
All SGAs	B Vitamins (B12, folate)	Moderate ●●	Metabolic syndrome → increased homocysteine; dietary changes	Methylated B-complex
All SGAs	Chromium	Weak ●	Insulin resistance → increased chromium demand	Chromium picolinate 200–400 mcg/day

Cardiovascular Drugs: Digoxin, Amiodarone, and ACE Inhibitors

Digoxin

Digoxin has an extremely narrow therapeutic index, and its toxicity is directly worsened by electrolyte imbalances — specifically low potassium, low magnesium, and low calcium. While digoxin itself doesn’t always directly deplete these minerals, it is almost always prescribed alongside diuretics that do, creating a dangerous synergy. Hypokalemia and hypomagnesemia increase myocardial sensitivity to digoxin, dramatically raising the risk of fatal arrhythmias.

Amiodarone

Amiodarone is the most iodine-dense medication in common clinical use. Each 200 mg tablet contains approximately 75 mg of organic iodine, of which about 6 mg is released as free iodide daily — roughly 20–40 times the recommended daily iodine intake. This massive iodine load disrupts thyroid function in 15–20% of patients, causing either amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH) [6][7].

ACE Inhibitors and Zinc

ACE inhibitors — captopril, enalapril, lisinopril, ramipril — work by inhibiting angiotensin-converting enzyme, which is a zinc-dependent metalloprotease. The drug binds to the zinc atom in ACE’s active site. This zinc-binding property extends beyond ACE, and multiple studies have documented increased urinary zinc excretion in patients on ACE inhibitors. Golik et al. (1990) found that captopril significantly increased urinary zinc loss compared to controls [8]. Koren-Michowitz et al. (2005) documented similar zinc and magnesium effects with losartan, particularly when combined with hydrochlorothiazide [9].

Medication	Nutrient Depleted	Evidence	Mechanism	Recommended Supplement
Digoxin (with diuretics)	Potassium	Strong ●●●	Concurrent diuretic use → renal K⁺ wasting	Potassium monitoring; KCl supplementation per physician
Digoxin (with diuretics)	Magnesium	Strong ●●●	Concurrent diuretic use → renal Mg²⁺ wasting	Magnesium glycinate 200–400 mg/day
Amiodarone	Thyroid hormone balance (iodine excess)	Strong ●●●	75 mg organic iodine per 200 mg dose	Thyroid function monitoring (TSH, free T4) every 6 months; NO iodine supplementation
Amiodarone	Vitamin A (retinol)	Weak ●	Hepatic accumulation; lipid metabolism disruption	Monitor liver function; consider vitamin A if deficiency confirmed
Captopril	Zinc	Moderate ●●	Zinc binding at ACE active site; increased urinary excretion	Zinc picolinate 15–30 mg/day
Enalapril	Zinc	Moderate ●●	Increased urinary zinc excretion	Zinc picolinate 15–30 mg/day
Lisinopril	Zinc	Moderate ●●	Increased urinary zinc excretion	Zinc picolinate 15–30 mg/day
All ACE inhibitors	Potassium (elevation risk)	Strong ●●●	Reduced aldosterone → potassium retention	AVOID potassium supplements; monitor levels

Critical safety note for ACE inhibitors: Unlike most medications on this list, ACE inhibitors can cause potassium to rise, not fall. Adding potassium supplements to ACE inhibitor therapy risks dangerous hyperkalemia. Monitor, don’t supplement.

Immunosuppressants: Cyclosporine and Tacrolimus

Organ transplant recipients and patients with severe autoimmune conditions take calcineurin inhibitors — cyclosporine and tacrolimus — which have well-documented effects on mineral metabolism. The magnesium depletion caused by these drugs is one of the most clinically significant drug-nutrient interactions in transplant medicine.

Barton et al. (1987) first documented that cyclosporine causes renal magnesium wasting in transplant recipients, with hypomagnesemia occurring in the majority of patients [10]. De Waele et al. (2019) confirmed that electrolyte disturbances — particularly hypomagnesemia and hypophosphatemia — remain common complications of calcineurin inhibitor therapy in kidney transplant recipients [11].

The mechanism involves cyclosporine’s direct toxic effect on the renal tubular cells responsible for magnesium reabsorption. Unlike dietary-intake-related deficiency, this is active renal wasting — the kidneys are being forced to excrete magnesium regardless of dietary intake.

Medication	Nutrient Depleted	Evidence	Mechanism	Recommended Supplement
Cyclosporine	Magnesium	Strong ●●●	Renal tubular magnesium wasting	Magnesium glycinate 400–600 mg/day; monitor serum Mg²⁺
Cyclosporine	Potassium	Strong ●●●	Hyperkalemia (impaired renal excretion)	AVOID potassium supplements; monitor levels
Cyclosporine	Phosphorus	Moderate ●●	Renal phosphate wasting	Monitor phosphate levels; supplement if low
Cyclosporine	Vitamin D	Moderate ●●	Impaired 1α-hydroxylation	Vitamin D3 2,000–4,000 IU/day; check 25(OH)D
Tacrolimus	Magnesium	Strong ●●●	Renal tubular magnesium wasting (same mechanism as cyclosporine)	Magnesium glycinate 400–600 mg/day; monitor serum Mg²⁺
Tacrolimus	Phosphorus	Moderate ●●	Renal phosphate wasting	Monitor phosphate levels
Tacrolimus	Potassium	Moderate ●●	Hyperkalemia (less common than cyclosporine)	AVOID potassium supplements; monitor levels

Transplant patients: Do not add ANY supplement without explicit approval from your transplant team. Many supplements interact with immunosuppressant drug levels — St. John’s wort, for example, can drop cyclosporine levels dangerously and trigger organ rejection.

Antiretroviral Medications

Combination antiretroviral therapy (cART) has transformed HIV from a terminal diagnosis to a manageable chronic condition. But long-term antiretroviral use comes with nutrient depletion patterns that matter over decades of treatment.

Tenofovir Disoproxil Fumarate (TDF)

Tenofovir (the older formulation, TDF) is one of the most thoroughly documented nutrient-depleting antiretrovirals. Casado (2016) reviewed the renal and bone toxicity of tenofovir, documenting proximal renal tubular dysfunction that causes phosphate wasting, leading to hypophosphatemia and bone demineralization [12]. Childs et al. (2012) found that vitamin D deficiency compounds tenofovir’s bone effects, with combination antiretroviral therapy patients showing significantly lower bone mineral density when vitamin D levels were insufficient [13].

The newer formulation, tenofovir alafenamide (TAF), has significantly less renal and bone toxicity — switching from TDF to TAF is one of the most impactful interventions for tenofovir-related mineral depletion.

Other Antiretrovirals

Protease inhibitors (ritonavir, atazanavir, darunavir) affect vitamin D metabolism through CYP3A4 interactions and have been associated with vitamin D deficiency, insulin resistance, and dyslipidemia. Eckard and McComsey (2014) reviewed the multifactorial nature of vitamin D deficiency in HIV-infected individuals, noting that both the virus and its treatment contribute to deficiency [14].

Medication	Nutrient Depleted	Evidence	Mechanism	Recommended Supplement
Tenofovir (TDF)	Phosphorus	Strong ●●●	Proximal renal tubular dysfunction → phosphate wasting	Monitor serum phosphate; supplement if low
Tenofovir (TDF)	Vitamin D	Strong ●●●	Renal tubular effects + impaired 1α-hydroxylation	Vitamin D3 2,000–4,000 IU/day; check 25(OH)D
Tenofovir (TDF)	Calcium (bone)	Strong ●●●	Phosphate wasting → secondary hyperparathyroidism → bone calcium loss	Calcium citrate 500–1,000 mg/day + vitamin D
Protease inhibitors (ritonavir, etc.)	Vitamin D	Moderate ●●	CYP3A4 induction → accelerated vitamin D catabolism	Vitamin D3 2,000–4,000 IU/day
Zidovudine (AZT)	Folate	Moderate ●●	Impaired folate metabolism	Methylfolate 800 mcg–1 mg/day
Zidovudine (AZT)	B12	Moderate ●●	Altered absorption and utilization	Methylcobalamin 1,000 mcg/day
All cART regimens	Zinc	Moderate ●●	HIV-related increased demand + drug effects	Zinc picolinate 15–30 mg/day

Additional Psychiatric Medications

Lithium

Lithium, the gold-standard mood stabilizer for bipolar disorder, concentrates in the thyroid gland and inhibits thyroid hormone synthesis and release. Lithium-induced hypothyroidism affects 20–30% of patients, particularly women. It also affects calcium metabolism through its effects on parathyroid hormone, occasionally causing hyperparathyroidism and hypercalcemia.

Valproic Acid

Valproic acid (Depakote) depletes carnitine by inhibiting its biosynthesis and increasing its renal excretion. Stadler et al. (1999) documented impaired carnitine reabsorption efficiency in humans receiving long-term valproic acid [15]. This carnitine depletion contributes to the hepatotoxicity and hyperammonemia that are serious adverse effects of valproate therapy.

Medication	Nutrient Depleted	Evidence	Mechanism	Recommended Supplement
Lithium	Thyroid hormones (T3, T4)	Strong ●●●	Inhibits thyroid hormone synthesis/release	TSH monitoring every 6 months; levothyroxine if hypothyroid
Lithium	Calcium (regulation)	Moderate ●●	Hyperparathyroidism → calcium dysregulation	Monitor PTH and calcium; do not supplement without testing
Valproic acid	Carnitine	Strong ●●●	Inhibits biosynthesis + increases renal excretion	L-carnitine 500–1,000 mg/day (especially in children)
Valproic acid	Folate	Moderate ●●	Impairs folate metabolism	Methylfolate 800 mcg–1 mg/day
Valproic acid	Vitamin D	Moderate ●●	Hepatic enzyme induction → accelerated vitamin D catabolism	Vitamin D3 2,000–4,000 IU/day
Carbamazepine	Vitamin D	Strong ●●●	CYP3A4 induction → accelerated 25(OH)D catabolism	Vitamin D3 2,000–5,000 IU/day; check 25(OH)D
Carbamazepine	Folate	Strong ●●●	Impairs folate absorption and metabolism	Methylfolate 1 mg/day
Carbamazepine	Calcium	Moderate ●●	Secondary to vitamin D depletion	Calcium citrate 500–1,000 mg/day + vitamin D

The Combination Problem: Polypharmacy and Nutrient Depletion

The tables above present individual medications, but the clinical reality for most patients is polypharmacy — multiple medications at once. A typical cardiac patient might take a statin (depletes CoQ10), an ACE inhibitor (depletes zinc), a diuretic (depletes magnesium, potassium, and B vitamins), and aspirin simultaneously. The cumulative nutrient burden is never assessed because each medication’s nutrient impact is evaluated in isolation.

A psychiatric patient on an SSRI, an antipsychotic, and valproic acid faces simultaneous depletion of sodium, vitamin D, folate, and carnitine. None of these depletions may be severe enough to flag individually, but collectively they can contribute to fatigue, cognitive impairment, and metabolic dysfunction that gets attributed to the underlying condition rather than the treatment.

This is why a comprehensive medication-nutrient review — ideally with a clinical pharmacist — matters. Not to create fear about medications (which are prescribed for important reasons), but to identify and correct preventable nutritional deficiencies that may be undermining both health and treatment efficacy.

Frequently Asked Questions

Should I stop my medication if it depletes nutrients?

No. Never stop a prescribed medication because of nutrient depletion concerns. Medications are prescribed because the benefit outweighs the risk. The correct approach is to supplement the depleted nutrient while continuing the medication, under the guidance of your healthcare provider. The goal is optimization, not avoidance.

How soon after starting a medication should I worry about nutrient depletion?

It varies by mechanism. Chelation-based depletions (fluoroquinolones, tetracyclines) begin immediately with the first dose. SIADH-related sodium depletion from SSRIs peaks in the first 2–4 weeks. Renal wasting from cyclosporine develops over weeks to months. Vitamin D depletion from antipsychotics is typically a slow-onset, cumulative effect over months to years. If you’re starting a medication known to deplete nutrients, discuss testing timelines with your doctor.

Can I take a general multivitamin to cover all potential depletions?

A multivitamin can provide a baseline, but it typically won’t contain therapeutic doses of specifically depleted nutrients. For example, most multivitamins contain 50–100 mg of magnesium, while cyclosporine-induced magnesium wasting may require 400–600 mg daily. Targeted supplementation based on your specific medications is more effective than a shotgun multivitamin approach. That said, a quality multivitamin as a foundation plus targeted additions for known depletions is a reasonable strategy.

My pharmacist didn’t mention nutrient depletion when filling my prescription. Should I be concerned?

Pharmacists are trained in drug-drug interactions and contraindications, which take priority. Drug-nutrient interactions are real but typically develop over longer timeframes and are less immediately dangerous than drug-drug interactions. Most pharmacy systems don’t flag nutrient depletions automatically. This doesn’t mean the depletions aren’t real — it means the system isn’t designed to catch them. Bringing a list of your medications to a clinical pharmacist or integrative medicine practitioner specifically for a nutrient depletion review is a proactive approach.

Are the “recommended supplement” doses in this article safe to start on my own?

The doses listed are generally within standard supplemental ranges, but individual safety depends on your complete medication list, kidney function, and other health conditions. Potassium supplementation with ACE inhibitors can be dangerous. Calcium supplementation with certain heart conditions requires monitoring. Mineral supplementation with chelating antibiotics requires careful timing. Always confirm with your prescriber before starting any supplement, especially if you take multiple medications or have kidney or liver disease.

Where can I find the full depletion data for the top 60 most common medications?

Our companion article, The Complete Medication-Nutrient Depletion Database, covers the 60 most commonly discussed medication-nutrient interactions, including statins, metformin, PPIs, diuretics, corticosteroids, and more. Together, these two resources cover the vast majority of prescription medications that meaningfully affect nutritional status.

Sources

1. Stahlmann R, Lode H. Toxicity of quinolones. Drugs. 1999;58 Suppl 2:37-42. PMID: 10553703
2. Mo H, Channa Y, Ferrara TM, et al. Hyponatremia Associated with the Use of Common Antidepressants in the All of Us Research Program. Clinical Pharmacology and Therapeutics. 2025. PMID: 39540435
3. Mannheimer B, Falhammar H, Calissendorff J, Skov J, Lindh JD. Time-dependent association between selective serotonin reuptake inhibitors and hospitalization due to hyponatremia. Journal of Psychopharmacology. 2021;35(6):657-662. PMID: 33860708
4. Mosiołek J, Mosiołek B, Szulc A. Vitamin D as a Modifiable Risk Factor in Schizophrenia: A Systematic Review. Biomolecules. 2025;15(5):610. PMID: 40867540
5. Krivoy A, Onn R, Vilner Y, et al. Vitamin D Supplementation in Chronic Schizophrenia Patients Treated with Clozapine: A Randomized, Double-Blind, Placebo-controlled Clinical Trial. EBioMedicine. 2017;26:138-145. PMID: 29226809
6. Medić F, Bakula M, Alfirević M, et al. Amiodarone and Thyroid Dysfunction. Acta Clinica Croatica. 2022;61(2):327-341. PMID: 36818930
7. Ylli D, Wartofsky L, Burman KD. Evaluation and Treatment of Amiodarone-Induced Thyroid Disorders. The Journal of Clinical Endocrinology and Metabolism. 2021;106(1):226-236. PMID: 33159436
8. Golik A, Modai D, Averbukh Z, et al. Zinc metabolism in patients treated with captopril versus enalapril. Metabolism. 1990;39(7):665-667. PMID: 2195291
9. Koren-Michowitz M, Dishy V, Zaidenstein R, et al. The effect of losartan and losartan/hydrochlorothiazide fixed-combination on magnesium, zinc, and nitric oxide metabolism in hypertensive patients. American Journal of Hypertension. 2005;18(3):358-363. PMID: 15797654
10. Barton CH, Vaziri ND, Martin DC, Choi S, Alikhani S. Hypomagnesemia and renal magnesium wasting in renal transplant recipients receiving cyclosporine. The American Journal of Medicine. 1987;83(4):693-699. PMID: 3314493
11. De Waele L, Van Gaal PJ, Abramowicz D. Electrolytes disturbances after kidney transplantation. Acta Clinica Belgica. 2019;74(1):48-55. PMID: 30482110
12. Casado JL. Renal and Bone Toxicity with the Use of Tenofovir: Understanding at the End. AIDS Reviews. 2016;18(2):59-68. PMID: 27230467
13. Childs K, Welz T, Samarawickrama A, Post FA. Effects of vitamin D deficiency and combination antiretroviral therapy on bone in HIV-positive patients. AIDS. 2012;26(3):253-262. PMID: 22112601
14. Eckard AR, McComsey GA. Vitamin D deficiency and altered bone mineral metabolism in HIV-infected individuals. Current HIV/AIDS Reports. 2014;11(3):263-270. PMID: 24962286
15. Stadler DD, Bale JF Jr, Chenard CA, Rebouche CJ. Effect of long-term valproic acid administration on the efficiency of carnitine reabsorption in humans. Metabolism. 1999;48(1):74-79. PMID: 9920148

Related Articles

• The Complete Medication-Nutrient Depletion Database — The original database covering the top 60 medications
• Dangerous Supplement Interactions You Need to Know — Critical supplement-drug interaction warnings

This article is for educational and informational purposes only. It is not intended as medical advice and should not be used to diagnose, treat, cure, or prevent any disease. Always consult your physician, pharmacist, or qualified healthcare provider before starting, stopping, or changing any supplement or medication regimen. Individual responses to medications and supplements vary, and what works for one person may not be appropriate for another.