Several RCTs have reported the magnitude of effect of alcohol on blood pressure, but because those trials are small, their findings are not sufficient to justify a strong conclusion. In 2005, McFadden and colleagues conducted a systematic review of RCTs, which investigated the haemodynamic effects of daily consumption of alcohol (McFadden 2005). Based on nine RCTs in which participants consumed alcohol repeatedly over days, these review authors reported that alcohol increases SBP by 2.7 mmHg and DBP by 1.4 mmHg. However, they excluded studies for which the duration of BP observation was less than 24 hours and articles published in non‐English languages.

Bleich 2001 published data only

The RAAS is responsible for maintaining the balance of fluid and electrolytes. An increase in plasma renin results in increased production of angiotensin I (AI), which is converted to angiotensin II (AII) by angiotensin‐converting enzyme (ACE). The hormone AII is a potent vasoconstrictor that stimulates aldosterone and vasopressin secretion from the adrenal gland, promoting sodium and water retention (Schrier 1999). As a result, peripheral resistance and blood volume are increased, leading to elevated arterial blood.

Kaul 2010 published data only

Swapping some of your usual alcoholic drinks for a tasty non-alcoholic option is an easy way to cut back. Or making a permanent switch to lower alcohol alternatives can be a sustainable approach to cutting down in the longer term, if you’re not ready to give up alcohol. Dr. Cho also warns that if you have liver dysfunction or take other medicines that are processed through the liver, your risks might be different. Talk to your healthcare provider about how alcohol might interact with your prescription medicines.

Contributions of authors

High levels of triglycerides in the blood have therefore been linked to atherosclerosis, heart disease, and stroke. Ethanol-induced changes may be related to oxidative or nonoxidative pathways of ethanol metabolism. More than one mechanism may be activated and may lead to the multitude of ethanol-induced changes in cellular proteins and cell function. As reviewed in the text, data from pharmacologic and transgenic approaches revealed an important role for oxidative stress and the hormone angiotensin II. Each study had to meet strict eligibility criteria, allowing researchers to focus on participants with no previous history of cardiovascular disease.

Petrone 2014 published data only

  1. Those who drink regularly and consume more than the lower risk guidelines are likely to be advised to cut down or stop drinking completely.
  2. Even though Dumont 2010 mentioned blinding of outcome assessors, it is not clear whether blinding of outcome assessment was maintained in the case of blood pressure and heart rate measurements.
  3. After 13 hours, high doses of alcohol increased SBP by 3.7 mmHg compared to placebo.
  4. This review did not find any eligible RCTs that reported the effects of alcohol on women separately.
  5. In the case of detection bias, we classified nine studies as having low risk of performance bias (Agewall 2000; Bau 2005; Bau 2011; Cheyne 2004; Dai 2002; Karatzi 2013; Narkiewicz 2000; Rosito 1999; Van De Borne 1997).
  6. INTERHEART results also suggested that the protective effect of any alcohol use against MI was greater in women and those over age 45.

We created three SoF tables to show the certainty of evidence and the summary of effects on outcomes of interest (SBP, DBP, and HR) for high (Table 1), medium (Table 2), and low doses (Table 3) of alcohol. We identified Stott 1987 and Barden 2013 from Analysis 3.1 and Analysis 3.2 as having a considerably lower standard error (SE) of the mean difference (MD) compared to the other included studies. Assuming that the low SEs of MDs reported in Stott 1987 and Barden 12 step programs for addiction recovery 2013 are errors and are not reliable, we replaced these measures with the average SE of MD from the rest of the included studies. It is recommended that there should be at least 10 studies reporting each of the subgroups in question. Among the 32 included studies, only four studies included hypertensive participants (Kawano 1992; Kawano 2000; Kojima 1993; Foppa 2002). So, it was not appropriate to conduct a separate meta‐analysis based on that population.

In addition, we included illustrative risks to present findings for the most important outcome (change in systolic blood pressure). For the other domains, we grouped outcomes together and provided only one judgement. We contacted study authors for missing or unclear information required for the risk of bias assessment dilaudid hydromorphone injection side effects and then reassessed the domains once the information was available. The molecular mechanisms through which alcohol raises blood pressure are unclear. Previous research suggests that acute alcohol consumption affects the renin–angiotensin–aldosterone system (RAAS) by increasing plasma renin activity (Puddey 1985).

A 2022 study found that people with severe hypertension who drank 2 or more cups of coffee per day had a higher risk of death from cardiovascular disease. Additionally, 6 ways to lower high blood pressure without using medication doses of over 240 mL were also able to reduce diastolic blood pressure. Diastolic blood pressure is the pressure in the arteries between heartbeats.

We classified six studies as having low risk of performance bias (Dai 2002; Narkiewicz 2000; Nishiwaki 2017; Potter 1986; Rosito 1999; Van De Borne 1997). In this study, all test drinks were poured into paper cups to achieve blinding of participants. We contacted the author of Rosito 1999 to request additional information regarding the method of blinding used. The study author explained the blinding method in detail in an email, so we classified this study as having low risk of bias. Heavy alcohol users who cut back to moderate drinking can lower their top number in a blood pressure reading (systolic pressure) by about 5.5 millimeters of mercury (mm Hg) and their bottom number (diastolic pressure) by about 4 mm Hg.

Opaque sealed randomised envelopes were used in Cheyne 2004 and Foppa 2002, and random number allocator was used in Rosito 1999. It is important to note that information regarding the method of allocation concealment used in Foppa 2002 and Rosito 1999 was provided by the study author via email. We also contacted Hering 2011, but the study author did not explicitly mention in the email the method of allocation concealment used. We used GRADEpro software to construct a ‘Summary of findings’ table to compare outcomes including change in SBP and DBP and HR (GRADEpro 2014).

Among the 34 included studies, only four studies included hypertensive participants. So, it was not possible to conduct a subgroup analysis based on blood pressure. For the planned subgroup analysis based on sex, no study reported male and female participant data separately. Thus alcohol decreases blood pressure initially (up to 12 hours after ingestion) and increases blood pressure after that. Alcohol consistently increases heart rate at all times within 24 hours of consumption.

Because of space limitations, not all of the excellent scientific work on alcohol and the cardiovascular system could be assessed in this review. Alcohol may affect various mechanisms implicated in ischemic preconditioning. Among these is the activation of mitogen-activated protein kinases (MAPK) signaling cascades. MAPKs are activated in response to stressful stimuli and help regulate apoptosis.

We conducted meta‐analysis for the three dose groups (low dose, medium dose, and high dose of alcohol) separately. We considered statistical, clinical, and methodological heterogeneity between study populations and proceeded with the meta‐analysis if only we considered interventions, comparisons, and outcome measures similar enough to pool. When trials compared more than one dose of alcohol, we handled each comparison separately. Because all of our outcomes of interest provided continuous data, we used the inverse variance approach and a fixed‐effect model to combine effect sizes across studies. The carry‐over effect in a cross‐over trial can confound the effects of subsequent treatment.

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