Blood Pressure Medications and Vitamin Depletion

Apr 13, 2020 | Nutrient Deficiency, Wellness

Blood pressure drugs deplete a wide variety of vitamins and minerals, some of which are required for optimal immune system and cardiac health.

In this article, we’ll cover the most common blood pressure drug-induced vitamin and nutrient depletions. The information in this article was sourced from independent literature reviews of published scientific literature, books by practicing pharmacists, and the definitive book on the subject: The Drug-Induced Nutrient Depletion Handbook.

The following blood pressure medication classes and their effects on vitamin, mineral, and other nutrient levels will be discussed in this order:

  • Ace Inhibitors
  • Chlorthalidone
  • Clonidine
  • Hydralazine
  • Loop diuretics
  • Potassium-Sparing Diuretics
  • Thiazide Diuretics

ACE Inhibitors

Example ACE inhibitors that deplete nutrients1

Captopril, enalapril, lisin opril, quinapril, ramipril, tranopril, fosinopril

Nutrients depleted by ACE Inhibitors


ACE Inhibitor-Induced Zinc Depletion

ACE inhibitors relax and widen blood vessels to allow blood to flow through, and lowers your body’s water retention. Some research indicates that they can deplete zinc, and that different ACE inhibitor blood pressure medications have varying effects on zinc levels.

“Two separate studies that compared the effects of captopril and enalapril on markers of zinc status found that, although both ACE inhibitors decreased zinc status compared to untreated hypertensive patients or healthy controls, chronic captopril use had a larger effect on zinc status than enalapril. In a different randomized, double-blind study, both captopril and benazepril lowered serum zinc and increased urinary zinc in patients with essential hypertension after four weeks. However, after eight weeks, serum zinc decreased more significantly with captopril use,” write the authors of a literature review.2 


Nutrients depleted by Clonidine


Clonidine-Induced CoQ10 Depletion

The evidence is extremely limited on this interaction, but one study from 1975 indicates that clonidine “inhibited CoQ10-NADH-oxidase.”3


Nutrients depleted by Hydralazine

CoQ10, B6

Hydralazine-induced nutrient depletion

The same 1975 study that found clonidine depleted CoQ10 indicated that hydralazine had a similar effect3. B6 depletion has more scientific corroboration4, 5, 6, 7. According to the PeaceHealth healthcare network in the Pacific Northwest, “Vitamin B6 can bind to hydralazine to form a complex that is excreted in the urine, increasing vitamin B6 loss.” 

Loop diuretics

Example loop diuretics that deplete nutrients1

Bumetanide, ethacrynic acid, furosemide, torsemide

Nutrients depleted by loop diuretics

Calcium, magnesium, potassium, B1, B6, Vitamin C, zinc

Loop diuretic-induced nutrient depletion

Diuretics increase urine production, which causes increased excretion of water-soluble nutrients that your body cannot store. The authors of Drug-Induced Nutrient Depletion8 cite ten studies that confirm that loop diuretics deplete magnesium9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19. This depletion can be particularly problematic as high blood pressure is a symptom of magnesium deficiency. 

Potassium depletion by loop diuretics is also well researched18, 20, 21, 22, 23, 24. Thiamine depletion has been the subject of numerous studies in humans and rats, and particularly affects medication users with heart failure25, 26, 27, 28. A limited number of studies show that loop diuretics deplete vitamins B629, 30 and C29 while a single study of 26 subjects indicates a relationship between this drug class and zinc depletion24.

Potassium-Sparing Diuretics

Example potassium-sparing diuretics that deplete nutrients1


Nutrients depleted by potassium-sparing diuretics

Calcium, folate

Potassium-sparing diuretic-induced nutrient depletion

Two studies suggest a relationship between potassium-sparing diuretics and increased calcium excretion causing depletion of the mineral31, 32. Two studies dating back to the 1970s indicate that the potassium-sparing diuretic triamterene interferes with folate absorption in humans. In a fourth study about a single elderly woman who presented with folate deficiency, researchers theorized that this was caused by triamterene34.

Thiazide Diuretics

Example thiazide diuretics that deplete nutrients1

HCTZ, hydrochlorothiazide, chlorothiazide, chlorthalidone, methylclothiazide, metolazone

Nutrients depleted by thiazide diuretics

Magnesium, potassium, sodium, zinc, CoQ10

Thiazide diuretic-induced nutrient depletion

In the aforementioned 1975 study examining various hypertension drugs on CoQ10 levels, researchers found that the thiazide diuretic hydrochlorothiazide had a similar inhibiting effect as clonidine and hydralazine3. 

The effects of these drugs on magnesium13, 36, 37, 38, 39, 40, 41 and potassium39, 41, 42, 43 levels have far more validation. While researchers have found in numerous studies correlations between thiazide diuretic use and low levels of both nutrients, they are not sure of the exact reasons why. One theory is that the lack of magnesium, which regulates other electrolytes, leads to potassium depletion.

High blood pressure is also a symptom of magnesium deficiency, which may confound the relationship. 

Thiazide diuretics may also deplete sodium levels44, 45, 46, 47, 48. While we’ve been told for decades to monitor sodium intake, that sweeping statement refers to table salt, not the critical electrolyte needed to maintain ideal fluid levels in your cells. You may follow a low-sodium diet, but you don’t want depleted sodium in your cells. In multiple studies conducted on elderly subjects, researchers found relationships between thiazide diuretic use and low sodium. 

The mechanism behind zinc depletion are more clear: numerous studies have confirm that thiazide diuretics increase zinc excretion49, 50, 51, 52.

Do you have blood pressure drug vitamin or mineral depletion?

Simple blood tests, ordered by a doctor and administered by a professional phlebotomist or phlebotomy technician, are often enough to measure deficiency of some nutrients. Others, like magnesium, are more difficult to assess. Doctors should be able to tell you if you have a deficiency.

Why replenish vitamins and minerals depleted by blood pressure drugs?

Zinc is a critical nutrient for your immune system, and even mild deficiency depresses immune response. CoQ10 is beneficial for optimal heart health and acts as a powerful antioxidant. 

Magnesium, potassium, calcium, and sodium are electrolytes, which regulate fluid levels in your cells. They also have other important roles, with magnesium performing 300+ essential functions in your body. And, without the B vitamins, your cells can’t produce the energy they need to survive. 

How to replenish nutrients depleted by blood pressure drugs

While some foods are high in specific nutrients, the most effective way to ensure you are getting all the nutrients you need is to eat a varied whole food diet that does not exclude major food groups. 

Zinc, for example, is at its most bioavailable in animal foods. Phytates in plant sources of zinc, like seeds and legumes, interfere with zinc absorption, leading the National Institutes of Health to recommend vegetarians and vegans consume up to 50% more zinc than the recommended daily allowance. 

Many experts recommend supplementing with magnesium as the recommended daily allowance is difficult to consume in food alone due to lower levels of magnesium in traditional plant sources. Just look for a bioavailable magnesium supplement. 

B vitamins are easy to find in supplements. A B Complex is your best bet because it will include optimal ratios of all the vitamins in the B family. Look for one, like our Lypo-Spheric® B Complex Plus, that includes absorbable forms of the vitamins (like methylated folate and benfotiamine). 

1 Cohen, Suzy, RPh. Drug Muggers: Which Medications Are Robbing Your Body of Essential Nutrients—and Natural Ways to Restore Them. Rodale, 2011.

2 Mohn, Emily S et al. “Evidence of Drug-Nutrient Interactions with Chronic Use of Commonly Prescribed Medications: An Update.” Pharmaceutics vol. 10,1 36. 20 Mar. 2018, doi:10.3390/pharmaceutics10010036

3 Kishi H, Kishi T, Folkers K. “Bioenergetics in Clinical Medicine. III. Inhibition of Coenzyme Q10-Enzymes by Clinically Used Antihypertensive Drugs.” Res Commun Chem Pathol Pharmacol, 1975, 12(3):533-40.

4 Vidrio H. “Interaction of Pryidoxal as a Possible Mechanism of Hydralazine Hypotension.” J Cardiocas Pharmacol, 1990, 15(1):150-6.

5 Shigetomi S, Kuchel O. “Defective 3,4-Dihydroxyphenylaline Decarboxylation to Dopamine in Hydralize-Treated Hypertensive Patients May Be Pyridoxine Remediable.” Am J Hypertens, 1993, 6(1):33-40.

6 Rosen F, et al. “Selective Metabolic and Chemotherapeutic Effects of Vitamin B6 Antimetabolites.” Vitamins and Hormones, Harris RS, Wool IG, and Loraine JA, eds, New York, NY: Academic Press, 1964, 609-41.

7 Raskin NH and Fishman RA. “Pyridoxine-Deficiency Neuropathy Due to Hydralazine,” N Engl J Med, 1965, 273(22):1182-5.

8 Pelton, Ross, RPh, PhD, CCN, LaValle, James, RPh, DHM, NMD, CCN, Hawkins, Ernest, RPh, MS, Krinsky, Daniel, RPh, MS. Drug-Induced Nutrient Depletion Handbook Volume 2. Lexi-Comp, 2001.

9 Rolla G, Bucca C, Bugiani M, et al. “Hypomagnesemia in Chronic Obstructive Lung Disease: Effect of Therapy,” Magnes Trace Elem, 1990, 9(3):132-6.

10 Quamme, GA. “Renal Magnesium Handling: New Insights in Understanding Old Problems,” Kidney Int, 1997, 52(5):1180-95.

11 Schwinger, RH and Erdmann E. “Heart Failure and Electrolyte Disturbances,” Methods Find Exp Clin Pharmacol, 1992, 14(4):315-25.

12 Ryan, MP. “Magnesium and Potassium-Sparing Diuretics.” Magnesium, 1986, 5(5-6):282-92.

13 al-Ghamdi SM, Cameron EC, Suttom RA. “Magnesium Deficiency: Pathophysiologic and Clinical Overview.” Am J Kidney Dis, 1994, 24(5):737-52.

14 Wong NL, Sutton RA, Dirks JH. “Is Lymphocyte Magnesium Concentration a Relfection of Intracellular Magnesium Concentration?” J Lab Clin Med, 198, 112(6):721-6.

15 Iseri LT, Freed J, Bures AR. “Magnesium Deficiency and Cardiac Disorders.” Am J Med, 1975, 58(6)837-46.

16 Lucker PW, Witzman HK. “Influence of Magnesium and Potassium Deficiency on Renal Elimination and Cardiovascular Function Demonstrated by Impedance Cardiography.” Magnesium, 1984, 3(6):265-73.

17 Ryan MP, Devane J, Ryan MF, et al. “Effects of Diuretics on the Renal Handling of Magnesium.” Drugs, 1984, 28 (Suppl 1):167-81.

18 Cohen N, Golik A, Dishi V, et al. “Effect of Furosemide Oral Solution Versus Furosemide Tablets on Diuresis and Electrolytes in Patients with Moderate Congestive Heart Failure,” Miner Electrolyte Metab, 1996, 22(4):248-52.

19 Lindeman RD. “Hypokalemia: Causes, Consequences, and Correction.” Am J Med Sci, 1976, 272(1):5-17.

20 Schwinger RH and Erdmann E. “Heart Failure and Electrolyte Disturbances.” Methods Find Exp Coin Pharmacol, 1992, 14(4):315-25.

21 Physicians Desk Reference, 49th ed, Montvale, NJ: Medical Economics Co, 1995, 1133, 2547, 2032.

22 Rastogi S, Bayliss JM, Nascimento L, et al. “Hyperkalemic Renal Tubular Acidosis: Effect of Furosemide in Humans and in Rats.” Kidney Int, 1985, 28(5):801-7.

23 Nuutinen LS. “The Effect of Furosemide on Potassium Balance in Open Heart Surgery.” Ann Chir Gynaecol, 1976, 65(4):277-81.

24 Valmin K, Hansen T, Ronsted P. “Treatment of Benign Essential Hypertension with Furoseide in Different Doses.” Pharmatherapeutica, 1980, 2(5):296-304.

25 Brady JA, Rock CL, and Horneffer MR. “Thiamine Status, Diuretic Medications, and the Management of Congestive Heart Failure.” J Am Diet Assoc, 1995, 95(5):541-4.

26 Yui Y, Itokawa Y, and Kawai C. “Furosemide-Induced Thiamine Deficiency,” Cardiovasc Res, 1980, 14(9):537-40.

27 Shimon I, Almog S, Vered Z, et al. “Improved Left Ventricular Function After Thiamine Supplementation in Patients with Congestive Heart Failure Receiving Long-Term Furosemide Therapy.” Am J Med, 1995, 98(5):485-90.

28 Seligman H, Halkin H, Rauchfleisch S, et al. “Thiamine Deficiency in Patience with Congestive Heart Failure Receiving Long-Term Furosemide Therapy: A Pilot Study.” Am J Med, 1991, 91(2):151-5.

29 Mydlik M, Derzsiova K, Zemberova E, et al. “The Effect of Furosemide on Urinary Excretion of Oxalic Acid, Vitamin C and Vitamin B6 in Chronic Kidney Failure.” Vanity Lek, 1998, 44(3):127-31.

30 Mydlik M, Derzsiova K, Zemberova E, et al. “Metabolism of Vitamin B6 and Its Requirement in Chronic Renal Failure.” Kidney Int Suppl, 1997, 62:S56-9.

31 Hanze S and Seyberth H. “Studies of the Effect of the Diuretics Furosemide, Ethacrynic Acid, and Triamterene on Renal Magnesium and Calcium Excretion.” Klin Wochenschr, 1967, 45(6):313-4.

32 D’Arcy PF and Griffin JP. Iatrogenic Diseases, New York, NY: Oxford University Press, 1972.

33 Lambie DG and Johnson RH, “Drugs and Folate Metabolism.” Drugs, 1985, 30(2):145-55.

34 Corcino J, Waxman S, and Herbert V. “Mechanism of Triamterene-Induced Megaloblastosis.” Ann Intern Med, 1970, 73(3):419-24.

35 Joosten E and Pelemans W. “Megaloblastic Anaemia in an Elderly Patient Treated with Triamterene.” Neth J Med, 1991, 38(5-6):209-11.

36 Dai LJ, Friedman PA, Quale GA. “Cellular Magnesium of Chlorothiazide and Cellular Potassium Depletion on Mg2+ Uptake in Mouse Distal Convoluted Tubule Cells.” Kidney Int, 1997, 51(4):1008-17.

37 Malini PL, Strocchi E, Valtancoli G, et al. “Angiotensin-Converting Enzyme Inhibitors, Thiazide Diuretics and Magnesium Balance. A Preliminary Study.” Magnes Res, 100-, 3(3):193-6.

38 Nicholls MG. “Interaction of Diuretics and Electrolytes in Congestive Heart Failure.” Am J Cardiol, 1990, 65(10):17E-21E; discussion 22E-23E.

39 Hollifield JW. “Potassium and Magnesium Abnormalities: Diuretics and Arrythmias in Hypertension.” Am J Med, 1984, 77(5A):28-32.

40 Duckner T and Wester PO. “Potassium/Magensium Depletion in Patients with Cardiovascular Disease.” Am J Med, 1987, 82(3A):11-7.

41 Petri M, Cumber P, Grimes L, et al. “The Metabolic Effects of Thiazide Therapy in the Elderly: A Population Study.” Age Ageing, 1986, 15(3):151-5.

42 Gettes LS. “Electrolyte Abnormalities Underlying Lethal and Ventricular Arrhythmias.” Circulation, 1992, 85(1 Suppl):I70-6.

43 Robertson JI. “Diuretics, Potassium Depletion, and Risk of Arrhythmias.” Eur Heart J, 1984, 5(Suppl A):25-8.

44 Clark BA, Shannon BP, Rosa RM, et al. “Increased Susceptibility to Thiazide-Induced Hyponatremia in the Elderly.” J Am Soc Nephrol, 1994, 5(4):1106-11.

45 Friedman E, Shadel M, Halkin H, et al. “Thiazide-Induced Hyponatremia Reproducibility by Single Dose Rechallenge and an Analysis of Pathogenesis.” Ann Intern Med, 1989, 110(1):24-30.

46 Kone B, Gimenez L, and Watson AJ. “Thiazide-Induced Hyponatremia.” South Med J, 1986, 79(11):1456-7.

47 Oles KS and Denham JW. “Hyponatremia Induced by Thiazide-Like Diuretics in the Elderly.” South Med J, 1984, 77(10):1314-15.

48 Johnson JE and Wright LF. “Thiazide-Induced Hyponatremia.” South Med J, 1983, 76(11):1363-7.

49 Reyes AL, Olhaberry JV, Leary WP, et al. “Urinary Zinc Excretion, Diuretics, Zinc Deficiency and Some Side Effects of Diuretics.” S Afr Med J, 1983, 64(24):936-41.

50 Reyes AJ, Leary WP, Locket CJ, et al. “Diuretics and Zinc.” S Afr Med J, 1982, 62(11):373-5.

51 Mountokalakis TT, Dourakis S, Karartzas N, et al. “Zinc Deficiency in Mild Hypertensive Patients Treated with Diuretics.” J Hypertens Suppl, 1984, 2(3):S571-2.

52 Cohanim M and Yendt ER. “The Effects of Thiazides on Serum and Urinary Zinc in Patients with Renal Calculi.” Johns Hopkins Med J, 1975, 136(3):137-41.

Related Posts