Is atenolol a diuretic?


Blood Pressure Responses and Metabolic Effects of Hydrochlorothiazide and Atenolol


Thiazides and β-blockers cause adverse metabolic effects (AMEs), but whether these effects share predictors with blood pressure (BP) response is unknown. We aimed to determine whether AMEs are correlated with BP response in uncomplicated hypertensives.


In a multicenter, open-label, parallel-group trial, we enrolled 569 persons, aged 17–65, with random assignment to 9 weeks of daily hydrochlorothiazide (HCTZ) or atenolol monotherapy, followed by 9 weeks of add-on therapy with the alternate agent. Measurements included home BP, averaged over 1 week, weight and fasting levels of serum glucose, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides, and uric acid (UA) before and after monotherapy and after add-on therapy.

Results: Conclusions:

BP response correlated with changes in UA following HCTZ therapy and HDL following atenolol therapy. No other significant correlations were observed between BP response and AMEs, suggesting that these effects generally do not share predictors. Patients should be monitored for AMEs, regardless of BP response.

Hypertension is estimated to affect 1 billion of the world’s adult population and generally requires life-long treatment with one or more classes of antihypertensive therapy.1 Two antihypertensive classes, thiazide diuretics and β-blockers, are recommended as first-line therapies by current United States guidelines and are frequently used as initial therapy in newly diagnosed patients or as part of combination antihypertensive therapy.2 However, derangements in multiple metabolic parameters are common and well-known adverse effects of these antihypertensive classes. Both thiazide diuretics and β-blockers have been associated with increased glucose levels and an increased risk of diabetes.3,,–6 Additionally, adverse lipid effects, including increased low-density lipoprotein (LDL) and triglycerides, and decreased high-density lipoprotein (HDL) have been observed following thiazide diuretic and β-blockers therapy.7 Such effects may mitigate some of the cardiovascular benefits afforded by the blood pressure (BP)-lowering effects of these drugs. Finally, elevated serum uric acid (UA) during treatment with thiazide diuretics may increase the risk of developing gout.

Little is known of the mechanisms behind these common adverse effects, despite being extensively studied.8 Furthermore, relatively few variables are shown to consistently predict the occurrence or magnitude of these drug-induced adverse metabolic effects (AMEs).2,3 However, an important clinical question is whether those individuals with the greatest BP response to these agents are also the most likely to develop drug-induced AMEs during therapy. If these effects are correlated, AMEs may share predictors of BP response.

We aimed to determine whether BP response was associated with adverse effects on serum glucose, UA, LDL, HDL, triglycerides, and weight in a population of patients treated with hydrochlorothiazide (HCTZ) or atenolol.


Design. The Pharmacogenomic Evaluation of Antihypertensive Response (PEAR) study (NIH U0I GM074492; #NCT00246519) is a prospective, multicenter, randomized, open-label, parallel-group study with a primary focus of identifying genetic determinants of BP and adverse metabolic responses to a thiazide diuretic and β-blockers. Details of the PEAR trial design and purpose have been published previously.9 Participants included in this analysis were enrolled in PEAR from November 2005 through November 2009. PEAR is a multisite project that enrolled participants from the University of Florida (Gainesville, FL), Emory University (Atlanta, GA) and the Mayo Clinic (Rochester, MN). The study was conducted in accordance with the provisions of the Declaration of Helsinki. All participants provided voluntary, written informed consent and the institutional review boards of the participating study centers approved the study protocol.

Study population. Males or females with mild-to-moderate essential hypertension, of any race or ethnicity, between the ages of 17 and 65 were eligible for participation. Study participants were those with newly diagnosed hypertension, untreated hypertension or known hypertension previously treated with fewer than three antihypertensive drugs. Patients were excluded from participation if they had any secondary form of hypertension, a clinic systolic BP (SBP) >170 mm Hg during treatment with an antihypertensive, isolated systolic hypertension, other diseases requiring treatment with BP-lowering medications, a heart rate <55 beats/min, known cardiovascular disease, diabetes mellitus (type 1 or 2), renal insufficiency (defined as serum creatinine >1.5 mg/dl in males and 1.4 mg/dl in females), pregnancy or lactation, a history of Raynaud’s syndrome, chronic treatment with drugs known to elevate BP (nonsteroidal anti-inflammatory drugs, oral contraceptives), active alcoholism, or elevated liver enzymes.

Randomization and interventions. Participants with no exclusion criteria were further screened for inclusion based on untreated (for 3–6 weeks) home BP (average over 1 week seated diastolic BP (DBP) >85 mm Hg and ≤110 mm Hg and seated SBP <180 mm Hg) and clinic BP (seated DBP >90 mm Hg and ≤110 mm Hg and seated SBP <180 mm Hg). No lower cutoff was defined for home or office seated SBP. After this screening and before initiation of study medications, baseline studies included collection of home BP data, along with fasting blood, serum and urine samples. Following baseline studies, participants were randomly assigned to receive HCTZ 12.5 mg daily, titrated to 25 mg daily after 3 weeks if BP remained elevated (defined as SBP >120 or DBP >70 mm Hg) or atenolol 50 mg, titrated to 100 mg daily after 3 weeks if BP remained elevated. After 9 weeks, participants entered an add-on phase in which they received the alternate agent (i.e., those initially assigned HCTZ then received HCTZ-atenolol combination therapy and vice-versa) if their BP remained elevated. Following both the monotherapy (~9 weeks from initiation of the first study medication) and add-on phase (~18 weeks from initiation of first study medication), subjects were reassessed for home BP response and fasting blood sample collection was repeated.

Follow-up. Home BP was assessed daily using a Microlife model 3AC1-PC monitor (Microlife, Minneapolis, MN), measured in triplicate, then averaged, morning and evening over a 1-week period immediately preceding the 9-week visit. BP data were stored electronically and downloaded at prescribed clinic visits. At least five morning and five evening determinations were required during the 1-week period for inclusion in the analysis.

Fasting serum levels of glucose, lipids (LDL, HDL, and triglycerides) and UA were determined using an Hitachi 911 Chemistry Analyzer (Roche Diagnostics, Indianapolis, IN). All laboratory parameters were determined at a central laboratory at the Mayo Clinic.

Statistical analysis. Descriptive statistics were used to represent demographic information. Mean ± s.d. of BP measurements were determined at the end of the monotherapy and add-on phases and the average change in BP was calculated within each treatment group. For all analyses, changes were coded as post-treatment minus baseline, such that a reduction in BP was coded as a negative value and an increase in laboratory parameters was coded as a positive value. We compared changes from baseline to on-treatment for BP, weight and laboratory parameters within each treatment arm using paired t-tests. For nonparametric data, we used the Wilcoxon signed-rank test.

We performed two identical primary analyses, one in each treatment group, focused on the correlation of treatment-related SBP and DBP reductions with adverse metabolic responses, using Pearson’s correlation coefficients. For all analyses, we estimated the partial correlations among these parameters with covariate adjustments for age, race, gender, and body mass index (BMI). As secondary analyses, we determined correlation coefficients stratified by race (blacks and whites only), gender and the presence/absence of abdominal obesity (defined as waist circumference >35 in females or > 40 in males). Fisher’s z transformation was used to test for differences in correlation coefficients between subgroups. Covariate adjustment for baseline serum potassium levels or the change in serum potassium levels was not performed in the final analyses because a previous analysis revealed no relationship between potassium and the aforementioned metabolic variables, including glucose.10

Finally, we performed replication analyses using data from the add-on phase to determine whether any significant correlations in the monotherapy analyses were also found when these drugs were used as add-on therapy. For example, for the replication analyses in HCTZ-treated patients, we determined correlation coefficients between the changes in SBP/DBP and metabolic parameters from the end of atenolol monotherapy to the end of the HCTZ add-on phase. Similar analyses were repeated for patients receiving atenolol as add-on therapy.

We defined statistical significance a priori as a P value <0.0042 to account for multiple comparisons. Based on the total sample size available for analysis and assuming a two-sided test using Fisher’s z transformation and an α-level of 0.05, we had ≥95% power to detect significant correlation coefficients of at least 0.10. All statistical analyses were performed with SAS 9.2 or 9.3 (SAS Institute, Cary, NC) or R 2.12.0 (R Development Core Team, statistical software.


Complete data were available for 286 subjects in the atenolol treatment group and 283 subjects in the HCTZ treatment group. Baseline demographics for both treatment groups are presented in Table 1. Overall, the mean age of study subjects was 49.1 years with a mean BMI of 30.7 kg/m2. Approximately 54% of study subjects were female and the majority of subjects self-identified as white (57.8%) or black (37.9%). Of those treated with atenolol, 251 (87.8%) were titrated to the maximum dose of 100 mg once daily, and 280 (98.9%) of those treated with HCTZ were titrated to the maximum dose of 25 mg once daily.

Table 1

Baseline demographics according to treatment group

Table 1

Baseline demographics according to treatment group

Following 9 weeks of HCTZ monotherapy, SBP and DBP decreased by a mean of 9 and 5 mm Hg, respectively, whereas all other reported values, except HDL and weight, increased significantly (Table 2). After 9 weeks of atenolol monotherapy, SBP and DBP each decreased by a mean of 8 mm Hg. Likewise, HDL decreased significantly following 9 weeks of monotherapy, whereas serum glucose, UA, triglycerides, and weight increased significantly. LDL levels in atenolol-treated subjects were reduced slightly, but this change was not statistically significant.

Table 2

Mean changes in study parameters after treatment with HCTZ and atenolol as monotherapy or add-on therapy

Table 2

Mean changes in study parameters after treatment with HCTZ and atenolol as monotherapy or add-on therapy

Response correlations in the HCTZ treatment arms

In the unadjusted analysis of subjects treated with HCTZ as monotherapy, greater elevations in serum UA levels were significantly correlated with greater reductions in SBP (r = −0.18; P = 0.003) and DBP (r = −0.20; P = 0.001) (Figure 1). These correlations remained significant after adjusting for age, race, gender, and baseline BMI (Table 3). No other adverse metabolic responses were correlated with either BP response following HCTZ monotherapy. In stratified analyses of the correlations between UA and SBP or DBP, correlation coefficients did not differ significantly between race, gender, or the presence/absence of abdominal obesity at baseline (data not shown). Table 3

Correlation analyses during 9 weeks of monotherapy and 9 weeks of add-on therapy with HCTZ and atenolol

Table 3

Correlation analyses during 9 weeks of monotherapy and 9 weeks of add-on therapy with HCTZ and atenolol

Figure 1. Figure 1.

Similar results were obtained in the unadjusted analysis using data from participants receiving HCTZ as add-on therapy. However, elevations in serum UA levels were more strongly correlated with reductions in SBP (r = −0.27; P < 0.0001) and DBP (r = −0.21; P = 0.0007) with HCTZ add-on therapy compared with HCTZ monotherapy. After controlling for age, race, gender, and baseline BMI, only the relationship between UA and SBP remained significant (Table 3).

Response correlations in the atenolol treatment arms

In the unadjusted analysis of subjects receiving atenolol monotherapy, a greater reduction in HDL was significantly correlated with a greater SBP response (r = 0.18; P = 0.002), but not DBP response (r = 0.13; P = 0.03) (Figure 2). After controlling for age, race, gender, and BMI, a greater SBP response (r = 0.22; P = 0.0002) and a greater DBP response (r = 0.18; P = 0.002) were significantly correlated with greater reductions in HDL (Table 3). In stratified analyses, these correlations did not differ significantly between races, genders, or the presence/absence of abdominal obesity at baseline (data not shown). Stronger correlations (r = 0.29; P < 0.0001 for SBP response, and r = 0.22; P = 0.0003 for DBP response) were observed between each of these parameters and HDL during treatment with atenolol as add-on therapy (Table 3). We also observed significant correlations between reductions in HDL and SBP response (r = 0.18; P = 0.003) and DBP response (r = 0.20; P = 0.001) during atenolol + HCTZ add-on therapy. A sensitivity analysis excluding subjects who started a statin during the trial (n = 3 per treatment group) did not appreciably alter any of the aforementioned results (data not shown). Otherwise, no significant correlations were found between BP response and changes in reported parameters following atenolol treatment as monotherapy or add-on therapy. Figure 2. Figure 2.


Following 9 weeks of monotherapy with HCTZ, SBP and DBP were reduced significantly, whereas serum glucose, UA, LDL, and triglycerides levels increased. In the HCTZ monotherapy and add-on groups, reductions in SBP and DBP were correlated with changes in serum UA. These significant correlation coefficients did not differ significantly among subgroups in analyses stratified by race, gender, and the presence/absence of abdominal obesity. A significant correlation between changes in serum UA and BP response in HCTZ-treated patients may be attributable to thiazide-induced volume depletion which contributes significantly to initial BP response and increases serum UA by increasing net reabsorption of urate at the renal tubule, either through enhanced reabsorption or reduced secretion.11 This effect on urate is mitigated in diuretic-treated patients receiving volume replacement.12 Consequently, the shared predictor between BP response and changes in serum UA may be the degree of volume depletion incurred following HCTZ treatment. In support of this hypothesis, a follow-up analysis found that treatment-induced changes in plasma renin activity were correlated with changes in serum UA during HCTZ monotherapy (r = 0.26; P < 0.0001), HCTZ add-on therapy (r = 0.31; P < 0.0001), and during atenolol add-on therapy (e.g., HCTZ + atenolol therapy; r = 0.22; P = 0.0002), but not during atenolol monotherapy (r = 0.09; P = 0.12). These data support the hypothesis that volume depletion may be a shared predictor during HCTZ therapy because as plasma renin activity increases (and, ostensibly, volume decreases), serum UA also increases.

Atenolol was associated with significant reductions in SBP, DBP, and HDL and a significant increase in serum glucose, UA, and triglyceride levels. Following atenolol therapy, whether as monotherapy or in combination with HCTZ, reductions in HDL were correlated with reductions in SBP and DBP, with the strongest correlations observed following add-on atenolol therapy to HCTZ. A reduction in HDL levels following β-blockers therapy has been consistently demonstrated, particularly with atenolol.13,,–16 However, the mechanism behind this AME has not been fully elucidated. Given that the correlations were replicated in both the atenolol monotherapy and add-on therapy groups as well as the HCTZ add-on group (e.g., HCTZ added on to atenolol therapy), this consistent finding suggests that BP response and adverse effects on HDL in atenolol-treated patients may share common predictors. As with the significant correlations observed between UA and BP response during HCTZ treatment, the correlation coefficients in these analyses were relatively low, suggesting that only a small portion of the variation in changes in HDL levels is related to BP response following atenolol treatment.

We found no evidence of a relationship between BP response and changes in glucose, LDL, triglycerides, or weight during treatment with either drug. These findings suggest that treatment-related BP response does not share similar predictors with these AMEs during HCTZ or atenolol therapy. These findings are important since we found no evidence that persons most likely to have a greater BP response to thiazide or β-blocker therapy will likewise experience the greatest adverse effects on these metabolic parameters. From a clinical standpoint, measurement of BP response during therapy is unlikely to provide additional insight into potential effects on glucose, LDL, triglycerides, and weight. Consequently, monitoring for these AMEs during therapy is essential, regardless of BP response to these drugs. The present findings also highlight the need for future research to identify determinants of these antihypertensive-associated AMEs that, according to our results, should differ substantially from determinants of BP response to these agents. These determinants, whether clinical or genetic, will allow clinicians to identify persons most likely to benefit from the BP-lowering effects of these drugs while minimizing most AMEs.

Three limitations of this analysis are noteworthy. First, the maximum allowed dose of HCTZ was 25 mg/day. Higher doses may cause greater AMEs and greater BP response. However, this dose reflects current prescribing patterns and current guideline recommendations. Whether higher doses alter the relationship (or lack of relationship) between treatment-induced BP response and AMEs is unknown. Second, we did not objectively measure volume depletion during diuretic therapy and thus were unable to fully answer whether volume depletion may be link between treatment-induced changes in UA and BP response. Finally, this analysis included a low number of participants that were not white or black which precluded conducting correlation analyses in other racial subgroups.

In conclusion, we found that BP response and increases in serum UA were correlated during HCTZ therapy, while BP response and reductions in HDL were correlated during atenolol therapy. While the effects of these drugs on UA and HDL has long been recognized, our study is the first to our knowledge to describe a relationship between BP response and these metabolic parameters. Additionally, we found no significant evidence that other AMEs were correlated with BP response during therapy with either HCTZ or atenolol. Excepting UA and HDL, BP response and AMEs are unlikely to share significant predictors and thus clinicians should remain vigilant in assessing potential antihypertensive-induced AMEs regardless of a patient’s BP response to these medications. Future research, including the forthcoming results from the PEAR study, should help to identify genetic predictors of antihypertensive-induced AMEs. Combined with clinical and laboratory predictors, these findings will be useful in maximizing the benefit-to-risk ratio for patients with indications for thiazide or β-blocker therapy.


We acknowledge and thank the valuable contributions of the study participants, support staff, and study physicians: Drs George Baramidze, Carmen Bray, R. Whit Curry, Karen Hall, Frederic Rabari-Oskoui, Dan Rubin, and Seigfried Schmidt. This work is supported by a grant from the National Institutes of Health (Bethesda, MD), grant # U01 GM074492, funded as part of the Pharmacogenetics Research Network. Additional support for this work includes: K23 grants HL091120 (A.L.B.) and HL086558 (R.M.C.-D); CTSA grants UL1-RR029890 (University of Florida), UL1-RR025008 (Emory University), and UL1-RR024150 (Mayo Clinic); and funds from the Mayo Foundation. The authors are solely responsible for the design and conduct of the study, all study analyses, the drafting and editing of the manuscript, its final contents, and the decision to submit for publication.


The authors declared no conflict of interest.

1. Kearney PM , Whelton M , Reynolds K , Muntner P , Whelton PK , He J . Global burden of hypertension: analysis of worldwide data. Lancet 2005;365:217–223. 2. Chobanian AV , Bakris GL , Black HR , Cushman WC , Green LA , Izzo JLJr, Jones DW , Materson BJ , Oparil S , Wright JTJr, Roccella EJ National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003;289:2560–2572. 3. Barzilay JI , Davis BR , Cutler JA , Pressel SL , Whelton PK , Basile J , Margolis KL , Ong ST , Sadler LS , Summerson J ALLHAT Collaborative Research Group. Fasting glucose levels and incident diabetes mellitus in older nondiabetic adults randomized to receive 3 different classes of antihypertensive treatment: a report from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). Arch Intern Med 2006;166:2191–2201. 4. Sowers JR , Bakris GL . Antihypertensive therapy and the risk of type 2 diabetes mellitus. N Engl J Med 2000;342:969–970. 5. Cooper-DeHoff RM , Pacanowski MA , Pepine CJ . Cardiovascular therapies and associated glucose homeostasis: implications across the dysglycemia continuum. J Am Coll Cardiol 2009;53:S28–S34. 6. Zillich AJ , Garg J , Basu S , Bakris GL , Carter BL . Thiazide diuretics, potassium, and the development of diabetes: a quantitative review. Hypertension 2006;48:219–224. 7. Lithell HO . Effect of antihypertensive drugs on insulin, glucose, and lipid metabolism. Diabetes Care 1991;14:203–209. 8. Carter BL , Einhorn PT , Brands M , He J , Cutler JA , Whelton PK , Bakris GL , Brancati FL , Cushman WC , Oparil S , Wright JTJr; Working Group from the National Heart, Lung, and Blood Institute. Thiazide-induced dysglycemia: call for research from a working group from the national heart, lung, and blood institute. Hypertension 2008;52:30–36. 9. Johnson JA , Boerwinkle E , Zineh I , Chapman AB , Bailey K , Cooper-DeHoff RM , Gums J , Curry RW , Gong Y , Beitelshees AL , Schwartz G , Turner ST . Pharmacogenomics of antihypertensive drugs: rationale and design of the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) study. Am Heart J 2009;157:442–449. 10. Smith SM , Anderson SD , Wen S , Gong Y , Turner ST , Cooper-Dehoff RM , Schwartz GL , Bailey K , Chapman A , Hall KL , Feng H , Boerwinkle E , Johnson JA , Gums JG . Lack of correlation between thiazide-induced hyperglycemia and hypokalemia: subgroup analysis of results from the pharmacogenomic evaluation of antihypertensive responses (PEAR) study. Pharmacotherapy 2009;29:1157–1165. 11. Kahn AM . Effect of diuretics on the renal handling of urate. Semin Nephrol 1988;8:305–314. 12. Steele TH , Oppenheimer S . Factors affecting urate excretion following diuretic administration in man. Am J Med 1969;47:564–574. 13. Fogari R , Zoppi A , Corradi L , Preti P , Mugellini A , Lusardi P : β-blocker effects on plasma lipids during prolonged treatment of hypertensive patients with hypercholesterolemia. J Cardiovasc Pharmacol 1999;33:534–539. 14. Bell DS , Bakris GL , McGill JB . Comparison of carvedilol and metoprolol on serum lipid concentration in diabetic hypertensive patients. Diabetes Obes Metab 2009;11:234–238. 15. Giugliano D , Acampora R , Marfella R , De Rosa N , Ziccardi P , Ragone R , De Angelis L , D’Onofrio F . Metabolic and cardiovascular effects of carvedilol and atenolol in non-insulin-dependent diabetes mellitus and hypertension. A randomized, controlled trial. Ann Intern Med 1997;126:955–959. 16. Maitland-van der Zee AH , Klungel OH , Kloosterman JM , Seidell JC , Leufkens HG , de Boer A . The association between antihypertensive drug therapies and plasma lipid levels in the general population. J Hum Hypertens 2001;15:701–705. © 2012 by the American Journal of Hypertension, Ltd. American Journal of Hypertension, Ltd.

What is Atenolol / Chlorthalidone?

Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive.

Using this medicine with any of the following medicines is usually not recommended, but may be required in some cases. If both medicines are prescribed together, your doctor may change the dose or how often you use one or both of the medicines.

  • Aceclofenac
  • Acemetacin
  • Acetyldigoxin
  • Amtolmetin Guacil
  • Arsenic Trioxide
  • Aspirin
  • Bepridil
  • Bromfenac
  • Bufexamac
  • Celecoxib
  • Ceritinib
  • Choline Salicylate
  • Clonidine
  • Clonixin
  • Crizotinib
  • Deslanoside
  • Desmopressin
  • Dexibuprofen
  • Dexketoprofen
  • Diclofenac
  • Diflunisal
  • Digitalis
  • Digitoxin
  • Digoxin
  • Diltiazem
  • Dipyrone
  • Dofetilide
  • Dronedarone
  • Droperidol
  • Droxicam
  • Etodolac
  • Etofenamate
  • Etoricoxib
  • Felbinac
  • Fenoldopam
  • Fenoprofen
  • Fepradinol
  • Feprazone
  • Fingolimod
  • Flecainide
  • Floctafenine
  • Flufenamic Acid
  • Flurbiprofen
  • Ibuprofen
  • Indomethacin
  • Iohexol
  • Ketanserin
  • Ketoprofen
  • Ketorolac
  • Lacosamide
  • Levomethadyl
  • Lithium
  • Lornoxicam
  • Loxoprofen
  • Lumiracoxib
  • Meclofenamate
  • Mefenamic Acid
  • Meloxicam
  • Metildigoxin
  • Morniflumate
  • Nabumetone
  • Naproxen
  • Nepafenac
  • Niflumic Acid
  • Nimesulide
  • Nimesulide Beta Cyclodextrin
  • Oxaprozin
  • Oxyphenbutazone
  • Parecoxib
  • Phenylbutazone
  • Piketoprofen
  • Piroxicam
  • Proglumetacin
  • Propyphenazone
  • Proquazone
  • Rivastigmine
  • Rofecoxib
  • Salicylic Acid
  • Salsalate
  • Siponimod
  • Sodium Salicylate
  • Sotalol
  • Sulindac
  • Tenoxicam
  • Tiaprofenic Acid
  • Tolfenamic Acid
  • Tolmetin
  • Valdecoxib
  • Verapamil

Using this medicine with any of the following medicines may cause an increased risk of certain side effects, but using both drugs may be the best treatment for you. If both medicines are prescribed together, your doctor may change the dose or how often you use one or both of the medicines.

  • Acarbose
  • Aceclofenac
  • Acemetacin
  • Acetyldigoxin
  • Albiglutide
  • Alfuzosin
  • Alogliptin
  • Aminolevulinic Acid
  • Amtolmetin Guacil
  • Arbutamine
  • Aspirin
  • Bromfenac
  • Bufexamac
  • Bunazosin
  • Canagliflozin
  • Celecoxib
  • Chlorpropamide
  • Choline Salicylate
  • Clonixin
  • Dapagliflozin
  • Deslanoside
  • Dexibuprofen
  • Dexketoprofen
  • Diclofenac
  • Diflunisal
  • Digitoxin
  • Digoxin
  • Dipyrone
  • Disopyramide
  • Doxazosin
  • Droxicam
  • Dulaglutide
  • Empagliflozin
  • Ertugliflozin
  • Etodolac
  • Etofenamate
  • Etoricoxib
  • Exenatide
  • Felbinac
  • Fenoprofen
  • Fepradinol
  • Feprazone
  • Floctafenine
  • Flufenamic Acid
  • Flurbiprofen
  • Glimepiride
  • Glipizide
  • Glyburide
  • Gossypol
  • Ibuprofen
  • Indomethacin
  • Insulin Aspart, Recombinant
  • Insulin Degludec
  • Insulin Detemir
  • Insulin Glargine, Recombinant
  • Insulin Glulisine
  • Insulin Human Inhaled
  • Insulin Human Isophane (NPH)
  • Insulin Human Regular
  • Insulin Lispro, Recombinant
  • Ketoprofen
  • Ketorolac
  • Licorice
  • Linagliptin
  • Liraglutide
  • Lixisenatide
  • Lornoxicam
  • Loxoprofen
  • Lumiracoxib
  • Meclofenamate
  • Mefenamic Acid
  • Meloxicam
  • Metformin
  • Metildigoxin
  • Mibefradil
  • Miglitol
  • Morniflumate
  • Moxisylyte
  • Nabumetone
  • Naproxen
  • Nateglinide
  • Nepafenac
  • Niflumic Acid
  • Nimesulide
  • Nimesulide Beta Cyclodextrin
  • Oxaprozin
  • Oxyphenbutazone
  • Parecoxib
  • Phenoxybenzamine
  • Phentolamine
  • Phenylbutazone
  • Piketoprofen
  • Pioglitazone
  • Piroxicam
  • Pramlintide
  • Pranoprofen
  • Prazosin
  • Proglumetacin
  • Propyphenazone
  • Proquazone
  • Quinidine
  • Repaglinide
  • Rofecoxib
  • Rosiglitazone
  • Salicylic Acid
  • Salsalate
  • Saxagliptin
  • Sitagliptin
  • Sodium Salicylate
  • St John’s Wort
  • Sulindac
  • Tamsulosin
  • Tenoxicam
  • Terazosin
  • Tiaprofenic Acid
  • Tolazamide
  • Tolbutamide
  • Tolfenamic Acid
  • Tolmetin
  • Trimazosin
  • Urapidil
  • Valdecoxib
  • Vildagliptin
  • Warfarin

Atenolol; Chlorthalidone tablets

What is this medicine?

ATENOLOL; CHLORTHALIDONE (a TEN oh lole; klor THAL i done) is a combination of a beta-blocker and a diuretic. It is used to treat high blood pressure.

This medicine may be used for other purposes; ask your health care provider or pharmacist if you have questions.


What should I tell my health care provider before I take this medicine?

They need to know if you have any of these conditions:

  • chest pain or angina

  • decreased urine

  • diabetes

  • gout

  • heart or vessel disease like slow heart rate, worsening heart failure, heart block, sick sinus syndrome or Raynaud’s disease

  • kidney or liver disease

  • lung or breathing disease

  • pheochromocytoma

  • thyroid disease

  • an unusual or allergic reaction to chlorthalidone, atenolol, other beta-blockers, sulfa drugs, other medicines, foods, dyes, or preservatives

  • pregnant or trying to get pregnant

  • breast-feeding

How should I use this medicine?

Take this medicine by mouth with a glass of water. Follow the directions on the prescription label. You can take this medicine with or without food. Take your doses at regular intervals. Do not take your medicine more often than directed. Do not stop taking this medicine suddenly. This could lead to serious heart-related effects.

Talk to your pediatrician regarding the use of this medicine in children. Special care may be needed.

Overdosage: If you think you have taken too much of this medicine contact a poison control center or emergency room at once.

NOTE: This medicine is only for you. Do not share this medicine with others.

What if I miss a dose?

If you miss a dose, take it as soon as you can. If it is almost time for your next dose, take only that dose. Do not take double or extra doses.

What may interact with this medicine?

This medicine may interact with the following medications:

  • certain medicines for blood pressure, heart disease, irregular heart beat

  • clonidine

  • diuretics

  • lithium

  • NSAIDs, medicines for pain or inflammation, like ibuprofen or naproxen

This list may not describe all possible interactions. Give your health care provider a list of all the medicines, herbs, non-prescription drugs, or dietary supplements you use. Also tell them if you smoke, drink alcohol, or use illegal drugs. Some items may interact with your medicine.

What should I watch for while using this medicine?

Visit your doctor or health care professional for regular check ups. Check your heart rate and blood pressure regularly. Ask your doctor or health care professional what your blood pressure should be and when you should contact him or her.

Check with your doctor or health care professional if you get an attack of severe diarrhea, nausea and vomiting, or if you sweat a lot. The loss of too much body fluid can make it dangerous for you to take this medicine.

You may get drowsy or dizzy. Do not drive, use machinery, or do anything that needs mental alertness until you know how this drug affects you. Do not stand or sit up quickly, especially if you are an older patient. This reduces the risk of dizzy or fainting spells. Alcohol can make you more drowsy and dizzy. Avoid alcoholic drinks.

This medicine can affect blood sugar levels. If you have diabetes, check with your doctor or health care professional before you change your diet or the dose of your diabetic medicine.

This medicine can make you more sensitive to the sun. Keep out of the sun. If you cannot avoid being in the sun, wear protective clothing and use sunscreen. Do not use sun lamps or tanning beds/booths.

Do not treat yourself for coughs, colds, or pain while you are taking this medicine without asking your doctor or health care professional for advice. Some ingredients may increase your blood pressure.

What side effects may I notice from receiving this medicine?

Side effects that you should report to your doctor or health care professional as soon as possible:

  • allergic reactions like skin rash, itching or hives, swelling of the face, lips, or tongue

  • breathing problems

  • chest pain

  • cold, tingling, or numb hands or feet

  • irregular heartbeat

  • muscle cramps

  • redness, blistering, peeling or loosening of the skin, including inside the mouth

  • swollen ankles, legs

  • trouble passing urine or change in the amount of urine

  • unusual bruising

  • unusually weak or tired

  • vomiting

  • worsened gout pain

  • yellowing of the eyes or skin

Side effects that usually do not require medical attention (report to your doctor or health care professional if they continue or are bothersome):

  • change in sex drive or performance

  • depression

  • diarrhea

  • dry eyes or mouth

  • headache

  • nausea

This list may not describe all possible side effects. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.

Where should I keep my medicine?

Keep out of the reach of children.

Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F). Protect from light. Keep container tightly closed. Throw away any unused medicine after the expiration date.

NOTE: This sheet is a summary. It may not cover all possible information. If you have questions about this medicine, talk to your doctor, pharmacist, or health care provider.

Share Facebook Twitter LinkedIn Email Get useful, helpful and relevant health + wellness information enews

Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy

Atenolol / chlorthalidone and Alcohol / Food Interactions

  1. Samuel P, Chin B, Schoenfeld BH, et al “Comparison of the effect of pindolol versus propranolol on the lipid profile in patients treated for hypertension.” Br J Clin Pharmacol 24 (1987): s63-4
  2. Rossner S, Weiner L “Atenolol and metoprolol: comparison of effects on blood pressure and serum lipoproteins, and side effects.” Eur J Clin Pharmacol 24 (1983): 573-7
  3. Gordon NF, Scott CB, Duncan JJ “Effects of atenolol versus enalapril on cardiovascular fitness and serum lipids in physically active hypertensive men.” Am J Cardiol 79 (1997): 1065-9
  4. Rossner S, Weiner L “Atenolol and metoprolol: comparison of effects on blood pressure and serum lipoproteins, and side effects.” Eur J Clin Pharmacol 24 (1983): 573-7
  5. Lithell H, Andersson PE “Metabolic effects of carvedilol in hypertensive patients.” Eur J Clin Pharmacol 52 (1997): 13-7
  6. “Product Information. Zebeta (bisoprolol).” Lederle Laboratories, Wayne, NJ.
  7. “Product Information. Blocadren (timolol).” Merck & Co, Inc, West Point, PA.
  8. “Product Information. Levatol (penbutolol).” Reed and Carnrick, Jersey City, NJ.
  9. Darga LL, Hakim MJ, Lucas CP, Franklin BA “Comparison of the effects of guanadrel sulfate and propranolol on blood pressure, functional capacity, serum lipoproteins and glucose in systemic hypertension.” Am J Cardiol 67 (1991): 590-6
  10. Ferrara LA, Marotta T, Scilla A, et al “Effect of oxprenolol and metoprolol on serum lipid concentration.” Eur J Clin Pharmacol 26 (1984): 331-4
  11. Terent A, Ribacke M, Carlson LA “Long-term effect of pindolol on lipids and lipoproteins in men with newly diagnosed hypertension.” Eur J Clin Pharmacol 36 (1989): 347-50
  12. Northcote RJ, Packard CJ, Ballantyne D “The effect of sotalol on plasma lipoproteins and apolipoproteins.” Clin Chim Acta 158 (1986): 187-91
  13. Lind L, Pollare T, Berne C, Lithell H “Long-term metabolic effects of antihypertensive drugs.” Am Heart J 128 (1994): 1177-83
  14. Sasaki J, Saku K, Ideishi M, et al “Effects of pindolol on serum lipids, apolipoproteins, and lipoproteins in patients with mild to moderate essential hypertension.” Clin Ther 11 (1989): 219-24
  15. Valimaki M, Maass L, Harno K, Nikkila EA “Lipoprotein lipids and apoproteins during beta-blocker administration: comparison of penbutolol and atenolol.” Eur J Clin Pharmacol 30 (1986): 17-20
  16. Clucas A, Miller N “Effects of acebutolol on the serum lipid profile.” Drugs 36 Suppl 2 (1988): 41-50
  17. “Product Information. Normodyne (labetalol).” Schering Laboratories, Kenilworth, NJ.
  18. Sasaki J, Kajiyama G, Kusukawa R, Mori H, Koga S, Takagi R, Tanaka N, Ogawa N, Arakawa K “Effect of bevantolol and propranolol on serum lipids in patients with essential hypertension.” Int J Clin Pharmacol Ther 32 (1994): 660-4
  19. “Product Information. Cartrol (carteolol).” Abbott Pharmaceutical, Abbott Park, IL.
  20. Leren P, Foss PO, Nordvik B, Fossbakk B “The effect of enalapril and timolol on blood lipids.” Acta Med Scand 223 (1988): 321-6
  21. “Product Information. Coreg (carvedilol).” SmithKline Beecham, Philadelphia, PA.
  22. Kasiske BL, Ma JZ, Kalil RS, Louis TA “Effects of antihypertensive therapy on serum lipids.” Ann Intern Med 122 (1995): 133-41
  23. “Product Information. Tenormin (atenolol).” ICN Pharmaceuticals Inc, Cost Mesa, CA.
  24. “Product Information. Corgard (nadolol).” Bristol-Myers Squibb, Princeton, NJ.
  25. Disler LJ, Joffe BI, Seftel HC “Massive hypertriglyceridemia associated with atenolol.” Am J Med 85 (1988): 586-7
  26. Weiner L, Rossner S “Atenolol 50 mg or metoprolol 200 mg: a comparison of antihypertensive efficacy, side effects and lipoprotein changes.” Acta Med Scand 677 (1983): 153-7
  27. Lehtonen A, Hietanen E, Marniemi J, Peltonen P, Nikkila EA “Effect of sotalol withdrawal on serum lipids and lipoprotein lipase activity.” Int J Clin Pharmacol Ther Toxicol 21 (1983): 73-6
  28. “Product Information. Kerlone (betaxolol).” Searle, Skokie, IL.
  29. Szollar LG, Meszaros I, Tornoci L, et al “Effect of metoprolol and pindolol monotherapy on plasma lipid- and lipoprotein-cholesterol levels (including the HDL subclasses) in mild hypertensive males and females.” J Cardiovasc Pharmacol 15 (1990): 911-7
  30. “Product Information. Trandate (labetalol).” Glaxo Wellcome, Research Triangle Park, NC.
  31. “Product Information. Sectral (acebutolol).” Wyeth-Ayerst Laboratories, Philadelphia, PA.
  32. Carlson LA, Ribacke M, Terent A “A long-term study on the effect of pindolol on serum lipoproteins: a preliminary report.” Br J Clin Pharmacol 24 (1987): s61-2
  33. “Product Information. Visken (pindolol).” Sandoz Pharmaceuticals Corporation, East Hanover, NJ.
  34. “Product Information. Betapace (sotalol).” Berlex, Richmond, CA.
  35. Safran AB, Simona F, Sansonetti A, Pometta D, James R “Effects of ocular carteolol and timolol on plasma high-density lipoprotein cholesterol level.” Am J Ophthalmol 117 (1994): 683
  36. Pasotti C, Capra A, Fiorella G, et al “Effects of pindolol and metoprolol on plasma lipids and lipoproteins.” Br J Clin Pharmacol 13 (1982): s435-9
  37. “Product Information. Inderal (propranolol).” Wyeth-Ayerst Laboratories, Philadelphia, PA.
  38. Harvengt C, Heller FR, Martiat P, Nieuwenhuyze YV “Short-term effects of beta blockers atenolol, nadolol, pindolol, and propranolol on lipoprotein metabolism in normolipemic subjects.” J Clin Pharmacol 27 (1987): 475-80
  39. “Product Information. Lopressor (metoprolol).” Novartis Pharmaceuticals, East Hanover, NJ.

View all 39 references

244 Medications That Should Never Be Mixed with Alcohol

Could your drinking be interfering with your prescription medications?

According to a 2015 study by the National Institutes of Health, more than 4 out of 10 adults in the United States take medications that interact with alcohol. That figure goes up among for people over 65, where 78% of those who drink use alcohol-interactive prescription medications.

Improperly or carelessly mixing alcohol and the drugs you take can have significant effects on your health, ranging from relatively minor (headaches, nausea, dizziness, etc.) to so severe as to be life-threatening (breathing difficulties, internal bleeding, organ damage, etc.).

The implications of this study could impact the vast majority of Americans. Consider these statistics:

  • Over 86% of American adults drink alcohol at some point in their life
  • Nearly 70% of Americans use at least one prescription drug
  • Over half are prescribed two or more
  • 1 out of 5 take 5 or more prescriptions
  • Between 2007 and 2010, the percentage of people who took at least one prescription medication within the past 30 days increased by 50%

1 out of every 4 emergency room visits is because of alcohol-drug interactions.

“Abusing alcohol & medication can be a sign of a deeper issue. We accept many insurance plans, take a look.”

Let us take a closer look at some of the prescription medications that should never be mixed with alcohol.

“Combining alcohol with medications often carries the potential for serious health risks.”

~Dr. George Koob, Director of the National Institute on Alcohol Abuse and Alcoholism

Alcohol and Opioid Pain Medications – a Deadly Combination

“Mixing alcohol and other sedatives, like sleeping pills or narcotic pain medications, can cause sleepiness, problems with coordination, and potentially suppress brain stem areas tasked with controlling vital reflexes like breathing, heart rate, and gagging to clear the airway.”

~ Dr. Aaron White, NIAAA

Both alcohol and prescription opioid pain medications are central nervous system depressants. This means that each substance magnifies the effects of the other dramatically.

All prescription pain medications depress respiration to varying degrees. In fact, one of the signs of an opioid overdose is breathing that has become extremely shallow or has stopped altogether.

Now, a brand-new study published in the February 2017 issue of Anesthesiology, a medical journal put out by the American Society of Anesthesiologists, suggests that combining alcohol and opioids maybe even more dangerous than was previously thought.

Researchers at the Anesthesia and Pain Research Unit at Leiden University Medical Center in the Netherlands report that drinking even a modest amount of alcohol after taking just one dose of an opioid painkiller such as Oxycontin increases the risk of respiratory depression.

Two groups of test subjects, one group between the ages of 21 and 28, and the other group between the ages of 66 and 77, were given the equivalent of one 20 mg oxycodone tablet and 5 drinks, with the following results:

  • The oxycodone tablet depressed breathing by 28%.
  • The alcohol depressed breathing by an additional 19%.
  • Together, the two substances cause respiratory depression to reach 47%.
  • What’s more, the alcohol/opioid combinations increased the number of times that the test subjects temporarily stopped breathing.

Although both test groups experienced these effects, they were especially profound in the group of elderly subjects. The study’s lead author, Dr. Albert Dahan, M.D., Ph.D., a Professor of Anesthesiology, said, “Respiratory depression is a potentially fatal complication of opioid use. We found alcohol exacerbated the already harmful respiratory effects of opioids.”

The Centers for Disease Control and Prevention have reported that alcohol is involved in 18.5% of opioid pain reliever emergency room visits and 22.1% of pain reliever deaths.

Common opioid pain medications include:

Alcohol and Muscle Relaxants –Sedating Spasmolytics

Like opioids, muscle relaxants are usually prescribed in response to pain. However, unlike opioids, not all muscle relaxants depress the central nervous system.

Neuromuscular blockers, as their name suggests, interfere with the transmission of signals within the muscles. Spasmolytics, on the other hand, act in the spinal cord, brainstem, or cortex, so they DO depress the CNS.

Muscle relaxants are very powerful medications that can cause sedation, drowsiness, confusion, and loss of alertness. As with opioids, drinking magnifies these effects to a dangerous degree, even to the point of being fatal.

At a minimum, drinking while taking muscle relaxers will cause drowsiness, dizziness, and impairments in judgment, thinking, and concentration.

Common muscle relaxants include:

“We accept many health insurance plans. You can get your life back in order with our outpatient program today!”

Sleep medications are sedatives that can help people who have trouble falling or staying asleep. Because insomnia is a highly individual condition, not every sleep aid is beneficial to every situation.

Because they can be extremely habit-forming. With strong potential for abuse, most sleeping medications are only prescribed short-term. Another possible issue with some sleeping pills is prolonged impairment.

For example, individuals taking an extended-release formulation of Ambien would still show impairment 8 hours after taking a dose – 33% of women and 25% of men.

Because of the way that sleeping medications interact with the brain’s receptors, people with a personal history of alcohol abuse are at increased risk of physical dependency.

Like muscle relaxants and opioids, sleep aids are CNS depressants, and when combined with alcohol, can lead to extreme sedation, depressed respiration, overdose, coma, and death.

Some sleeping medications – Restoril, for example – are benzodiazepines and are even stronger depressants than the non-benzodiazepine sleep aid options. In addition to the aforementioned effects, benzo sleep aids can cause memory impairment, “drunkenness”, and numbs emotions, among others.

The interaction between benzodiazepines and alcohol is particularly strong – the CDC reports that over 27% of benzodiazepine-related emergency room visits also involve alcohol.

Common sleep medications include:

Alcohol and Antidepressants—Defeating the Purpose

People battling depression have to be especially careful with alcohol. Approximately one-third of individuals with major depression also meet the criteria for an Alcohol Use Disorder. When the two conditions cooccur, each can worsen the other.

In terms of antidepressant medications and alcohol consumption, there is a fine line. Alcohol is a depressant, and drinking actively acts against positive effects of the medication.

In fact, people who drink while taking antidepressants run the risk of achieving the OPPOSITE effect – increasing their feelings of depression and hopelessness.

It is true that most SSRI-class antidepressants such as Paxil do not react to alcohol, but that is not true for every type of medication.

Drinking while taking a tricyclic (TCA) antidepressant such as Tofranil can result in increased drowsiness and impaired cognition and motor control.

Taking monoamine-oxidase inhibitors (MAOI) medications like Nardil or Marplan. with alcohol – especially beer or red wine – can result in a dangerous spike in blood pressure.

Using alcohol with atypical antidepressants such as Remeron can cause excessive sleepiness and coordination problems.

Common antidepressant medications include:

Alcohol and Antianxiety Drugs – Double the Depressant Effect

As there is with depression, there is a strong link between anxiety and alcohol use/abuse. About 1 in 5 people with anxiety also abuse alcohol. To complicate matters, even more, approximately 85% of people with depression also suffer from Generalized Anxiety Disorder (GAD).

Benzodiazepine-class drugs such as Xanax or Klonopin are the most-frequently-prescribed pharmacological solutions to anxiety. Because alcohol and benzodiazepines are both CNS depressants their effects are greatly magnified when used together. Because the alcohol is metabolized first, the benzodiazepines stay in the person’s system longer.

Side effects of this combination can include:

  • Increased intoxication
  • Cognitive impairment
  • Loss of judgment
  • Disinhibition
  • Impulsiveness
  • Aggression/Hostility
  • Reduction in physical response time
  • Poor motor coordination
  • Inability to perform complex actions
  • Blackouts
  • Heart attack
  • Stroke
  • Suicidal ideation
  • Seizures
  • Organ damage
  • Overdose
  • Death due to respiratory depression

If one or both of these substances are abused long-term, serious psychological disorders can worsen or develop anew – psychosis, PTSD, depression, and cross-addiction.

Even with a “safer” non-benzodiazepine medication like Atarax, alcohol should be avoided. While Atarax does not present the same risk of dependence or addiction as benzo drugs, it is still a hypnotic sedative and CNS depressant.

Mixing alcohol and Atarax causes dizziness, severe sedation, and confusion.

Common anti-anxiety medications include:

Alcohol and Antipsychotics – Self-Medication That Makes It Worse

Anti-psychotic medications are major tranquilizers typically prescribed for the management of psychotic disorders such as schizophrenia or bipolar disorder.

The rate of alcohol use and abuse among schizophrenics is much higher than the general population, making a medication interaction exceedingly probable. According to the NIH, 33% of schizophrenics meet the lifetime criteria for an AUD.

Likewise, the rate of alcohol dependence among people struggling with a bipolar disorder is over 31%. To put those numbers in perspective, in 2015, just over 6% of the general population had an AUD.

The biggest danger of “self-medicating” with alcohol to ease the symptoms of a psychotic disorder is that alcohol abuse actually worsens the condition and reduces the positive effects of the prescribed medication.

Individual antipsychotics interact with alcohol in several ways. For example, drinking while taking Abilify, Risperidal, or Seroquel can result in extremely low blood pressure and dizziness, while at the same time, magnifying the CNS-depressing effects of the alcohol.

Common antipsychotic medications include:

Alcohol and Blood Pressure Medications – Dehydration and Dizziness

“Alcohol can increase blood pressure, which could be counterproductive if one is taking medications to control blood pressure. Mixing diuretic medications with alcohol, which is also a diuretic, could contribute to dehydration.”

~ Dr. Aaron White, NIAAA

The first thing to consider about alcohol and hypertension medications is that often, drinking is a major contributor to high blood pressure. Not only does having 3 or more drinks in one sitting temporarily raise your blood pressure, regular heavy or binge drinking can lead to long-term unhealthy increases.

There are several types of high blood pressure medications, and drinking has a different interaction with each.

Because alcohol is a diuretic, when you drink while taking diuretic medications like Lasix or Diuril, it is easy to become dehydrated.

The interaction of alcohol and ACE inhibitors such as Lisinopril or Vasotec, especially when the person is new to antihypertensive medication, can result in a drastic drop in blood pressure, causing dizziness and fainting.

This is similar to the effects that are felt when beta blockers and alcohol are combined. Alcohol is a depressant, and beta blockers like Tenormin or Sectral slow the heart rate and significantly lower blood pressure, resulting in extreme dizziness, lethargy, and increased risk of fainting.

Individual calcium channel blockers (CCBs) interact with alcohol in different ways. For example, the effect that drinking has on Norvasc is negligible, while Verapamil increases the concentration of alcohol in the blood, thereby enhancing drinking’s effects.

Common blood pressure medications include:

Alcohol and Diabetes Medications –Alarming Acidosis

“Alcohol increases insulin levels and lowers blood glucose, so combining alcohol with antidiabetic agents that regulate glucose levels could cause an undesirable drop in blood sugar. And, over time, alcohol can contribute to insulin insensitivity.”

~ Dr. Aaron White, NIAAA

For someone with diabetes, drinking is always risky. Moderate drinking causes blood sugar to rise, but heavy drinking can cause it to drop dangerously low – especially for individuals with Type I Diabetes.

Diabetics who take Diabinese and drink can experience a harsh Disulfiram-like reaction to the alcohol:

  • Severe headache
  • Copious vomiting
  • Excessive sweating
  • Chest pain
  • Heart palpitations
  • Hyperventilation
  • Dizziness
  • Blurred vision
  • Confusion
  • Respiratory depression
  • Cardiac arrhythmia
  • Myocardial infarction
  • Convulsions
  • Unconsciousness
  • Death

When heavy drinking has lowered your blood sugar, and you take insulin or an oral medication such as Victoza that that lowers it even further, you run the risk of diabetic ketoacidosis – a potentially-fatal condition.

Taking metformin after you have been drinking can result in lactic acidosis – a serious medical condition characterized by reaction an excessive buildup of lactic acid in the blood. Symptoms include:

  • Nausea
  • Vomiting
  • Muscle weakness
  • Hyperventilation
  • Death – the mortality rate for lactic acidosis due to an alcohol/metformin interaction is 25%.

Common diabetes medications include:

Alcohol and Cholesterol Medications

Although some studies say that alcohol increases a person’s “good cholesterol “levels, that information is not a license to drink without consideration, especially when taken any of the medications prescribed for high cholesterol. For every “positive” health benefit provided by alcohol, at least one “negative” comes along.

Both statin drugs such as Lipitor, Crestor, or Zocor and heavy drinking can damage the liver. Obviously, when they are done at the same time, the damage can be more serious. But consuming alcohol and cholesterol medications together also involves your liver in a different way.

Your liver breaks down and processes the alcohol FIRST, before the drug. This means that the medication stays in your body longer and side effects are strengthened:

  • Muscle pain and cramps
  • Fatigue
  • Diarrhea
  • Lowered immunity
  • Dizziness
  • Irregular or accelerated heartbeat
  • Joint pain
  • Frequent urination
  • Dark, pink, or cloudy urine

This last side effect could be a symptom of rhabdomyolysis, a breakdown of skeletal muscle tissue. This breakdown causes excessive protein into your blood, and too much of this protein can seriously damage your kidneys – to the point of renal failure and a need for dialysis.

Common cholesterol medications include:

“Get the help you need today. We offer outpatient assistance, so you can maintain your work, family, and life commitments while getting the help you deserve!”

Prescription medications are given for specific conditions or illnesses in your body. Alcohol changes how those medications act on your body, just as those medications change how your body responds to alcohol. The results of these changes can be uncomfortable, serious, or even deadly.

The first thing you should do when you are prescribed medication as having a frank and open talk with your doctor and with your pharmacist about your alcohol use. Follow their advice about drinking while using your medication to the letter.

Next, ALWAYS read the instructions and contraindications for any medications you are taking. Sometimes, you may need to make lifestyle changes when taking certain medications.

Finally, on the lookout for any adverse reactions that you may be experiencing. If you suffer any serious side effects, contact your doctor IMMEDIATELY.

Because the list of prescribed medications is constantly changing, this list is by no means comprehensive. Your best resource for questions about drinking alcohol with your prescription medications is your personal physician.


5 / 5 ( 1 vote )

About the author

Leave a Reply

Your email address will not be published. Required fields are marked *