Elevated Red Blood Cell Count And Alcohol – Validity of absolute intake and nutrient density of protein, potassium and sodium estimated by different dietary assessment methods: an exploratory study

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Elevated Red Blood Cell Count And Alcohol

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ICCC Cardiovascular Program; Institut de Recerca Hospital Santa Creu i Sant Pau—IIB Sant Pau, Sant Antoni Maria Claret, 167, 08025 Barcelona, ​​Spain

Received: 25 November 2019 / Revised: 23 December 2019 / Accepted: 25 December 2019 / Published: 30 December 2019

Alcohol has a hormetic physiological behavior that results in either increased or decreased cardiovascular risk depending on the amount consumed, the frequency of drinking, the pattern of consumption and the outcome being studied, or even the type of alcoholic beverage consumed. However, the vast majority of studies elucidating the role of alcohol in cardiovascular and global disease burden rely on epidemiologic studies of an associative nature that carry several limitations. Therefore, the cardiovascular benefits of low to moderate alcohol consumption are questionable and may be overestimated. Therefore, the aim of this review was to critically discuss the current knowledge about the connection between alcohol consumption and cardiovascular diseases. In addition to emerging evidence linking low and moderate alcohol consumption with reduced risk of cardiovascular disease, several questions remain unanswered regarding the specific amount of safe consumption, type of alcoholic beverage, and differences in age, gender, and genetics/ethnicity. in alcohol consumption.

Cardiovascular diseases (CVD) are the leading cause of death in Europe (47% of all deaths) and one of the main causes of death worldwide (31% of all deaths worldwide) [1]. The influence of modifiable risk factors, such as smoking, high blood pressure, dyslipidemia or poor diet, has been the subject of research since the 1950s, and studies such as the Framingham Heart Study [2] or the INTERHEART study [3] have shown that 90 % of acute myocardial infarctions (AMIs) are attributable to potentially reversible risk factors, making reduction of CV risk factors a high priority nationally and globally. For health systems, alcohol consumption has been a subject of strong debate, as the findings of different studies on the effects of alcohol on CVD have been contradictory. While most studies have found that low-moderate alcohol consumption may be beneficial [4] — or at least not harmful [5] — to the CV system by reducing the risk of major adverse CV events (MACE), excessive alcohol consumption increases the risk of CVD [6] and is associated with an increased risk of more than 50 diseases [7]. In fact, alcohol use, in addition to related mental disorders caused by addiction [8], was the seventh leading risk factor for both death and disability-adjusted life-years in 2016, accounting for 2.2% and 6.8% of total age. standardized mortality among women and men, respectively [9], and has been identified as a major contributor to the burden of disease worldwide [7, 10].

Population Level Risks Of Alcohol Consumption By Amount, Geography, Age, Sex, And Year: A Systematic Analysis For The Global Burden Of Disease Study 2020

According to the Dietary Guidelines Advisory Committee (USA) [11], if alcohol is consumed, it should be consumed in moderation (≤1 and 2 drinks per day for women and men, respectively) and only by adults of drinking age . However, guidelines for alcohol consumption vary considerably around the world: low-risk guidelines range from 10-42 g/day or 98-140 g/week for women and 10-56 g/day or 150-280 g/week for men [ 12]. ]. In 2016, 32.5% (25% of women and 39% of men) currently consumed alcohol, and the median amount of alcohol consumed was 0.73 standard drinks per day for women and 1.7 standard drinks per day for men [9] .

Although moderate alcohol intake may have long-term CV benefits, even low consumption may have some risk. Alcohol has a hormetic physiological behavior that results in either increased or decreased CV risk depending on the amount consumed, the frequency of drinking, the pattern of consumption (irregular or heavy/binge drinking, which is not uniformly defined) and the outcome being studied [13, 14], and even and the type of alcoholic beverage consumed [15, 16]. In addition to this, some factors are critical in interpreting the health effects of alcohol consumption in the available studies, such as measurement of alcohol consumption (and its misreporting) or drink size (and corresponding alcohol concentration). Additionally, many individuals do not follow a habitual drinking pattern, and low to moderate consumption combined with episodes of heavy/binge drinking may not be beneficial for CVD. Moreover, alcohol intake in most epidemiologic studies is measured only once through food frequency questionnaires or quantity-frequency measures that may underestimate alcohol consumption, as the validity of self-reported alcohol intake has been questioned due to fear of stigmatization [10]. . These questions need to be further addressed by epidemiologic trials, and alcohol exposure requires international standardization, as cutoff points for alcohol intake categories vary significantly among studies.

Considering all these limitations, the CV benefits of low to moderate alcohol consumption are questioned, and it is thought that they may have been overestimated. Therefore, the aim of this review was to critically discuss the current knowledge on the relationship between alcohol consumption and CVD.

In order to analyze the effects of alcohol consumption on CVD and/or overall health, levels of alcohol consumption must be defined. As summarized in Table 1, the US National Institute on Alcohol Abuse and Alcoholism defines drinking levels as low-risk drinking, moderate drinking, binge drinking, and heavy alcohol use [17], although some studies have their own classification. Moderate alcohol consumption is called regular daily consumption, while low intake, at the same maximum amount of alcohol intake as moderate consumption, is called occasional and alternates with some days without alcohol consumption. This classification will be used in this review, and low-risk consumption will be referred to as low consumption.

Haematological Changes In Alcohol And Substance Use Disorders An Overview

As will be discussed further, the relationship between CVD and alcohol intake is complex and responsive to hormetic behavior reflected in U- or J-shaped relationships, with low-moderate intake being more protective than abstinence or abusive drinking. However, in addition to the category of alcohol consumption, it is extremely important to consider that subjects in the category of non-drinkers (ie, teetotalers) generally include both never-drinkers and former drinkers (ie, non-drinkers). Former drinkers may have stopped drinking because of serious or chronic illness, previous alcohol abuse, prodromal symptoms before clinical manifestations of major events, and/or because of taking prescription medications that are incompatible with alcohol consumption. It has been reported that sober individuals have significantly more prevalent CV risk factors than light to moderate drinkers, which would overestimate the health benefits of alcohol consumption [18, 19, 20] and bias or underestimate recent alcohol intake which could explain, in turn, cross-examining the heterogeneity found in meta-analyses.

In addition, the majority of studies on the effect of alcohol on CVD rely on groups over 35 years of age, which may affect the effect of alcohol consumption over the course of a lifetime. Drinking patterns have been shown to vary across the lifespan, with heavy drinking peaking in the 20s and followed by episodes of binge drinking (in which, incidentally, CVD controls are rare [21]) and falling to a minimum in the 40s. im years. . In fact, heavy and irregular drinking (>60 g of alcohol) is associated with increased arterial stiffness [22], even at an early age [23], and with a 45% increased risk of ischemic heart disease compared to moderate drinking [24]. . Therefore, subjects who drink alcohol regularly in their 20s are more likely to be abstainers over the age of 35; therefore, CV risk among these subjects—considered sober in several studies—may be high compared to lifelong moderate drinkers due to underestimated drinking patterns in adolescence and early adulthood [21, 25] rather than potential protective effects. moderate alcohol consumption.

A cross-sectional study showed that people who drink lightly, moderately and heavily have significantly lower results of allostatic load, which

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