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Food effects on absorption metabolism of alcohol
Abstract
The concomitant ingestion of various foods with alcohol resulted in a decreased area under the blood alcohol concentration curve, a lower peak concentration and an increased time to reach peak. Michaelis-Menten kinetics indicated a decreased alcohol metabolism rate after the ingestion of carbohydrates or fats.
... Alcohol and food absorption are affected by multiple factors including: concurrent consumption, sex, hormones, pregnancy, and/or disease status. While food intake can, in the short term, exert a protective effect from the toxic effects of alcohol consumption [20][21][22], alcohol consumption over time can adversely affect the quality and quantity of proper nutrient supply and energy intake, particularly for women [23,24]. Dietary intake among heavy drinkers is generally considered poor [25]. ...
... These apparent deficiencies persist even after separation into the maternal groups. Using less stringent nutrient requirements (EARs for non-pregnant females, aged [19][20][21][22][23][24][25][26][27][28][29][30], more than half of all women are still likely inadequate for seven (vitamin A, D, E, C, folate, calcium, and magnesium) of the 15 micronutrients with EARs (data not shown). Vitamin K, potassium, choline, and fiber still have observed means below AI for non-pregnant females, aged 19-30. ...
Objective:
Compare nutritional status of 57 South African mothers of children with fetal alcohol spectrum disorders (FASD) with 148 mothers of controls.
Methods:
Dietary data were analyzed for macronutrients, micronutrients, and fats via Estimated Average Requirements (EAR) and Adequate Intakes (AI) for pregnant women.
Results:
Virtually all mothers were likely deficient on most micronutrients by either EAR (<50%) or AI values. Mothers of FASD children consumed more of 13 of 25 micronutrients. For percentage below EAR, only vitamin D was significantly higher for FASD mothers. Despite no difference in total food intake, control mothers had a higher mean body mass index (BMI) than FASD mothers. Maternal BMI is more significant for positive child outcomes than any individual nutrient.
Conclusions:
Most mothers have inadequate dietary intake. Minor advantages in nutrient intake are overpowered by teratogenic effects of alcohol. Further study is needed of the interaction of alcohol, maternal nutrition, and metabolism.
... (Rose, 1979;Vantrappen, 1994;Jonderko et al., 1997;Madsen, 1992). Perhaps the most important variable in this connection is the presence of liquid or solid food in the stomach before alcohol is consumed (Sedman et al., 1976b;Wilkinson et al., 1977a;Jones and Jönsson, 1994b;Watkins and Adler, 1993;Singh, 1999). The effect of food is complicated depending on the amounts ingested and the time of eating the meal in relation to consumption of the alcohol. ...
... He proposed that alcohol might be chemically bound to amino acids in the diet such as glycine and thus prevented from being absorbed into the bloodstream. The effect of food in lowering the bioavailability of ethanol has been confirmed many times by different investigators (Goldberg, 1943;Sedman et al., 1976b, Lin et al., 1976Jones and Jönsson, 1994b;Wilkinson, 1977b), although the mechanism of this effect was more difficult to explain. ...
... Alcohol and food absorption are affected by multiple factors including: concurrent consumption, sex, hormones, pregnancy, and/or disease status. While food intake can, in the short term, exert a protective effect from the toxic effects of alcohol consumption [20][21][22], alcohol consumption over time can adversely affect the quality and quantity of proper nutrient supply and energy intake, particularly for women [23,24]. Dietary intake among heavy drinkers is generally considered poor [25]. ...
... These apparent deficiencies persist even after separation into the maternal groups. Using less stringent nutrient requirements (EARs for non-pregnant females, aged [19][20][21][22][23][24][25][26][27][28][29][30], more than half of all women are still likely inadequate for seven (vitamin A, D, E, C, folate, calcium, and magnesium) of the 15 micronutrients with EARs (data not shown). Vitamin K, potassium, choline, and fiber still have observed means below AI for non-pregnant females, aged 19-30. ...
In this study, we describe the nutritional status of women from a South African community with very high rates of fetal alcohol spectrum disorders (FASD). Nutrient intake (24-hours recall) of mothers of children with FASD was compared to mothers of normal controls. Nutrient adequacy was assessed using Dietary Reference Intakes (DRIs). More than 50 percent of all mothers were below the Estimated Average Requirement (EAR) for vitamins A, D, E, and C, thiamin, riboflavin, vitamin B6, folate, calcium, magnesium, iron, and zinc. Mean intakes were below the Adequate Intake (AI) for vitamin K, potassium, and choline. Mothers of children with FASD reported significantly lower intake of calcium, docosapentaenoic acid (DPA), riboflavin, and choline than controls. Lower intake of multiple key nutrients correlates significantly with heavy drinking. Poor diet quality and multiple nutritional inadequacies coupled with prenatal alcohol exposure may increase the risk for FASD in this population.
... Because of this, it is considered a minor polar substance [13,14]. The absorption rate differences fluctuate in accordance with the genetic and environmental situation as the type of consumption of food and nutrients [15][16][17]. Also, gender is other significant factor for ethanol metabolism [18,19]. ...
The natural active compounds in Oregano essential oils are extremely beneficial for human health and when used as a drug for treatment. In this study, we have examined the two main Oregano essential oils Thymol and Carvacrol. These oils have many functions; predominantly, in biochemical reactions in metabolism. In our research, we theoretically investigated the chemical activities of Carvacrol and Thymol by using B3LYP/6-31G(d,p) method in the gas, water, and blood phases. The point at which ethanol was used as a solvent was important to the study outcome; hence, in this study; the researchers determined the effective rate of Carvacrol with ethanol to explain the interaction mechanism.
... genetics, gender , and previous drinking history) and the drinking occasion( e.g. speed of consumption, beverage consumed and whether food has been consumed)(101, 115,[117][118][119][120]. In a sample of 412 twins from the general population usual drinking history was found to affect both peak blood alcohol concentration and the rate of decline in blood alcohol concentration for the same dose of alcohol (118). ...
Male life expectancy in Russia is extremely low for an industrialised country. Alcohol is an important contributory factor to low life expectancy and an important health determinant in Russian men. Conventional methods of measuring alcohol consumption may not fully capture distinctive aspects of Russian drinking. The aim of this PhD was to identify latent dimensions of alcohol use and to investigate their socio-demographic correlates and their effects on health and employment among working-age men (aged 25-60) in Izhevsk, Russia. The data used were from the Izhevsk Family Studies (IFS -1 and IFS-2). IFS-1 included a cross-sectional survey of 1941 working-age men resident in Izhevsk (2003-6). Controls were followed up at IFS-2 (2008-10).Three latent dimensions of beverage alcohol intake (beer, wine and spirit intake) were constructed from questionnaire responses on frequency, usual volume and maximum volume of each beverage and one latent dimension of acute alcohol-related dysfunction from responses on frequency of hangover, excessive drunkenness, sleeping in clothes because of drunkenness and failing family or personal obligations because of drinking. The relationship between these latent dimensions of alcohol use, socio-demographic factors, employment and cardiovascular risk factors were investigated using structural equation modelling. The latent factors of beverage alcohol intake were strong predictors of alcohol-related dysfunction, with spirit intake being the most influential. Alcohol-related dysfunction showed a strong association with education which was only partly explained by beverage alcohol intake and other observed aspects of alcohol consumption. Alcohol-related dysfunction was a strong predictor of employment status and an important mediator of the relationship between alcohol intake and employment. All four latent variables showed similar associations with serum lipids. Beer intake, spirit intake and alcohol-related dysfunction were strongly associated with hypertension. Hazardous alcohol consumption in Russian men strongly influenced employment status and cardiovascular risk factors. A latent variable approach to measuring alcohol use particularly acute alcohol-related dysfunction provided information of the relationship between alcohol, health and socio-economic circumstances in Russian men beyond that obtained using more conventional observed measures such as total volume of ethanol.
... While beer is consumed like regular drinks, soy sauce, vinegar and tapai are only consumed in a miniature manner along together with solid foods. Thus, even though soy sauce, Tapai, and vinegar have a significantly higher percentage of ethanol than other dietary product, due to the nature of human consumption of these products, it will induce higher threshold of intoxication (Lin, Garg, & Wagner, 1976;Sedman, Wilkinson, Sakmar, Weidler, & Wagner, 1976), making the comparison of soy sauce and tapai against beer is somewhat arguable. One way to ensure a justified comparison is by studying the relationship between the threshold of intoxication against the consumption of dietary in daily life particularly products that within the confine of halal research. ...
... [47][48][49] In addition, the ingestion of food with alcohol slows the rate of alcohol absorption and decreases blood alcohol concentrations. [50] Therefore, food may modify the risk of bleeding associated with alcohol through systemic mechanisms. For example, alcohol has a number of deleterious effects on hemostasis, and bleeding time and blood loss are increased following acute ethanol administration in animal models. ...
Background and Aims
Data regarding smoking and alcohol consumption and risk of gastrointestinal bleeding (GIB) are sparse and conflicting. We assessed the risk of major GIB associated with smoking and alcohol consumption in a large, prospective cohort.
Methods
We prospectively studied 48,000 men in the Health Professional follow-up Study (HPFS) who were aged 40–75 years at baseline in 1986. We identified men with major GIB requiring hospitalization and/or blood transfusion via biennial questionnaires and chart review.
Results
We documented 305 episodes of major GIB during 26 years of follow-up. Men who consumed >30 g/day of alcohol had a multivariable relative risk (RR) of 1.43 (95% confidence interval (CI), 0.88–2.35; P for trend 0.006) for major GIB when compared with nondrinkers. Alcohol consumption appeared to be primarily related to upper GIB (multivariable RR for >30 g/day vs. nondrinkers was 1.35; 95% CI, 0.66–2.77; P for trend 0.02). Men who consumed ≥ 5 drinks/week vs. < 1 drink/month of liquor had a multivariable RR of 1.72 (95% CI, 1.26–2.35, P for trend <0.001). Wine and beer were not significantly associated with major GIB. The risk of GIB associated with NSAIDs/aspirin use increased with greater alcohol consumption (multivariable RR 1.37; 95% CI, 0.85–2.19 for 1-14g/day of alcohol, RR 1.75; 95% CI, 1.07–2.88 for ≥ 15g/day compared to nondrinkers). Smoking was not significantly associated with GIB.
Conclusions
Alcohol consumption, but not smoking, was associated with an increased risk of major GIB. Associations were most notable for upper GIB associated with liquor intake. Alcohol appeared to potentiate the risk of NSAID-associated GIB.
... Following ingestion, alcohol is absorbed slowly in the stomach and rapidly in the small intestines. The rate of alcohol absorption is affected by the rate of gastric emptying, which in turn is influenced by various factors such as food ingestion (Holt, 1981;Holt et al., 1980;Sedman et al., 1976;Lin et al., 1976). ...
Alcohol concentrations in biological matrices offer information regarding an individual's level of intoxication level at a given time. In forensic cases, the alcohol concentration in the blood (BAC) at the time of death is sometimes used interchangeably with the BAC measured post-mortem, without consideration for alcohol concentration changes in the body after death. However, post-mortem factors must be taken into account for accurate forensic determination of BAC prior to death to avoid incorrect conclusions. The main objective of this work was to describe best practices for relating ante-mortem and post-mortem alcohol concentrations, using a combination of modeling, empirical data and other qualitative considerations. The Widmark modeling approach is a best practices method for superimposing multiple alcohol doses ingested at various times with alcohol elimination rate adjustments based on individual body factors. We combined the selected ante-mortem model with a suggestion for an approach used to roughly estimate changes in BAC post-mortem, and then analyzed the available data on post-mortem alcohol production in human bodies and potential markers for alcohol production through decomposition and putrefaction. Hypothetical case provide best practice approaches as an example for determining alcohol concentration in biological matrices ante-mortem, as well as potential issues encountered with quantitative post-mortem approaches. This study provides information for standardizing BAC determination in forensic toxicology, while minimizing real world case uncertainties.
... Solid food intake can reduce the ethanol absorption rate by 30% and it has been suggested that this effect is due to the need for food digestion prior to absorption process. As such, if food is taken in as a liquid then it would not produce this effect [49,54]. Moreover, a small amount of ethanol can be oxidized to acetaldehyde by alcohol dehydrogenase (ADH) classes I and IV [52,55] in the stomach and intestine. ...
... Traditionally, it has been assumed that the kinetics of elimination of ethanol from the blood of animals and human subjects can be described as zero order, i.e., independent of ) the blood concentration (above about 2 to 3 mM or 0.09 to 0.14 mg/ml). This concept (zero order elimination), first postulated by Widmark,28 still persists 10,19 despite several studies 8 , 14,17,21,29 that suggest nonzero order elimination kinetics. Wagner and associates 27 reported substantial evidence that the elimination of ethanol from the blood of man obeys Michaelis-Menten kinetics and not zero order kinetics. ...
Blood ethanol concentrations were determined in 7 subjects during and subsequent to a 2-hr constant-rate intravenous infusion of ethyl alcohol (8% V/V). Eight to 10 capillary blood samples were collected during the infusion and 10 to 21 samples were obtained after the infusion ceased. Thus, the total time course of blood ethanol concentrations in man was defined, both during and postirifusion. Blood ethanol concentration data from each of 6 subjects were fitted simultaneously to the two equations for the one-compartment open model with zero order input and Michaelis-Menten elimination kinetics. The average Vm [0.232 mg/(ml × hr)] and Km [0.0821 mg/ml] obtained from these fittings correspond very closely with corresponding values estimated by the fitting of all the mean concentration-time data obtained following oral administration of 4 different doses of ethanol to 8 other fasting subjects in another study. A disproportionate increase in area under the concentration-time curve with increase in dose (gmlkg) was observed in a single subject who was infused with equal volumes of a 4% and an 8% (V/V) ethanol solution at the same constant rate.
... Solid food intake can reduce the ethanol absorption rate by 30% and it has been suggested that this effect is due to the need for food digestion prior to absorption process. As such, if food is taken in as a liquid then it would not produce this effect [49,54]. Moreover, a small amount of ethanol can be oxidized to acetaldehyde by alcohol dehydrogenase (ADH) classes I and IV [52,55] in the stomach and intestine. ...
The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms.
... A more useful Third, although the subjects were asked to arrive to the laboratory in a fasted state, there was no independent way of determining whether that was the case. There is overwhelming evidence that ingesting alcohol with a full stomach reduces the bioavailability of the dose, resulting in lower peak BACs, increased times to peak BAC, and smaller areas under the curve [23,24]. There is also evidence that food increases the elimination rate of alcohol [25,26]. ...
... Professor of pharmaceutics at the College of Pharmacy at the University of Michigan, U.S. Wagner wrote several books on the subject of biopharmacy and pharmacokinetics and was a strong proponent for use of the Michaelis-Menten equation or saturation kinetics to describe the C-T profiles of ethanol [251,253]. Wagner and his collaborators published several articles on the pharmacokinetics of ethanol including the effect of dose, eating solid or liquid meals [168,227], and oral vs intravenous administration in the fasting state [267][268][269]. Wagner verified that the area under the blood-alcohol curve increased more than proportionally with increasing dose, which is characteristic of drugs metabolized by non-linear kinetics. ...
A reliable method for the quantitative analysis of ethanol in microvolumes (50-100 μL) of blood became available in 1922, making it possible to investigate the absorption, distribution, metabolism, and excretion (ADME) of ethanol in healthy volunteers. The basic principles of ethanol pharmacokinetics were established in the 1930s, including the notion of zero-order elimination kinetics from blood and distribution of the absorbed dose into the total body water. The hepatic enzyme alcohol dehydrogenase (ADH) is primarily responsible for the oxidative metabolism of ethanol. This enzyme was purified and characterized in the early 1950s and shown to have a low Michaelis constant (km), being about ~0.1 g/L. Liver ADH is therefore saturated with substrate after the first couple of drinks and for all practical purposes the concentration-time (C-T) profiles of ethanol are a good approximation to zero-order kinetics. However, because of dose-dependent saturation kinetics, the entire postabsorptive declining part of the blood-alcohol concentration (BAC) curve looks more like a hockey stick rather than a straight line. A faster rate of ethanol elimination from blood in habituated individuals (alcoholics) is explained by participation of a high km microsomal enzyme (CYP2E1), which is inducible after a period of chronic heavy drinking. Owing to the combined influences of genetic and environmental factors, one expects a roughly threefold difference in elimination rates of ethanol from blood (0.1-0.3 g/L/h) between individuals. The volume of distribution (Vd) of ethanol, which depends on a person's age, gender, and proportion of fat to lean body mass, shows a twofold variation between individuals (0.4-0.8 L/kg). This forensic science review traces the development of forensic pharmacokinetics of ethanol from a historical perspective, followed by a discussion of important issues related to the disposition and fate of ethanol in the body, including (a) quantitative evaluation of blood-alcohol curves and the factors influencing the peak concentration in blood (Cmax) and the time of its occurrence (tmax), (b) biological variations in the ADME of ethanol, including the apparent volume of distribution (Vd or rho), the disappearance rate from blood (β or k0), and the disposal rate by the entire body in 1 h (B60), and (c) questions about ADME of ethanol often arising during the prosecuting of accused drunken drivers.
Copyright © 2011 Central Police University.
... The form in which the alcohol is consumed is also likely to have an effect on alcohol absorption (Holt, 1981). For example, the presence of glucose in sweet drinks is known to reduce absorption rates, (Holt, 1981;Sedman et al., 1976). Alternatively, carbonated mixers have been found to increase alcohol absorption (Roberts & Robinson, 2007). ...
... Previous studies reported variable results depending on the concentration of alcohol in the beverage. Some studies reported that higher concentration of alcohol in a beverage delays the rate of gastric emptying particularly after a meal (Haggard et al., 1941;Roine et al., 1991;Sedman et al., 1976). Many of these studies utilized 95% EtOH diluted to different concentrations in orange juice or water, although some used beer, wine, and spirits (both diluted and neat) during or after a standard meal. ...
Background
Both the amount and the rate of absorption of ethanol (EtOH) from alcoholic beverages are key determinants of the peak blood alcohol concentration (BAC) and exposure of organs other than gut and liver. Previous studies suggest EtOH is absorbed more rapidly in the fasting than in the postprandial state. The concentration of EtOH and the type of beverage may determine gastric emptying/absorption of EtOH.Methods
The pharmacokinetics of EtOH were measured in 15 healthy men after consumption of 0.5 g of EtOH/kg body weight. During this 3-session crossover study, subjects consumed in separate sessions, beer (5.1% v/v), white wine (12.5% v/v), or vodka/tonic (20% v/v) over 20 minutes following an overnight fast. BAC was measured by gas chromatography at multiple points after consumption.ResultsPeak BAC (Cmax) was significantly higher (p < 0.001) after vodka/tonic (77.4 ± 17.0 mg/dl) than after wine (61.7 ± 10.8 mg/dl) or beer (50.3 ± 9.8 mg/dl) and was significantly higher (p < 0.001) after wine than beer. The time to Cmax occurred significantly earlier (p < 0.01) after vodka/tonic (36 ± 10 minutes) compared to wine (54 ± 14 minutes) or beer (62 ± 23 minutes). Six subjects exceeded a Cmax of 80 mg/dl after vodka/tonic, but none exceeded this limit after beer or wine. The area under the concentration–time curve (AUC) was significantly greater after drinking vodka/tonic (p < 0.001) than after wine or beer. Comparison of AUCs indicated the relative bioavailability of EtOH was lower after drinking beer.Conclusions
Findings indicate that BAC is higher after drinking vodka/tonic than beer or wine after fasting. A binge pattern is significantly more likely to result in BAC above 80 mg/dl after drinking vodka/tonic than beer or wine. Men drinking on an empty stomach should know BAC will vary depending on beverage type and the rate and amount of EtOH.
... A more useful Third, although the subjects were asked to arrive to the laboratory in a fasted state, there was no independent way of determining whether that was the case. There is overwhelming evidence that ingesting alcohol with a full stomach reduces the bioavailability of the dose, resulting in lower peak BACs, increased times to peak BAC, and smaller areas under the curve [23,24]. There is also evidence that food increases the elimination rate of alcohol [25,26]. ...
The objective of this study was to determine whether breath alcohol elimination rate varies as a function of age, gender, and drinking practice, factorially combined. Eighty-four men and 84 women drank enough alcohol to produce peak BrACs of .110g/210L for heavy and moderate drinkers and BrACs of .090g/210L for light drinkers. An Intoxilyzer 5000 was used to generate the concentration-time profiles. Mean (M) elimination rates (g/210L/h) were found to be higher for women (N=84, M=.0182, SD=.0033) than for men (N=84, M=.0149, SD=.0029), F(1, 144)=57.292, p<.001; higher for heavy drinkers (N=56, M=.0176, SD=.0038) than for light and moderate drinkers combined (N=112, M=.0160, SD=.0032), F(1, 144)=12.434, p<.01; and higher for older subjects (51-69 years, N=42, M=.0180, SD=.0038) than younger subjects (19-50 years, N=126, M=.0161, SD=.0033), F(1, 144)=14.324, p<.001. None of the two-way interactions (age×gender, age×drinking practice, gender×drinking practice) or the three-way interaction (age×gender×drinking practice) was statistically significant. Limitations of the current study and suggestions for further research are discussed.
... Following the consumption of alcohol, an individual's breath alcohol concentration (BrAC) is influenced by a variety of factors, such as whether food was consumed. The presence of food can be so important that reductions in peak BrAC have been reported to be as much as 20-57% when food is present in the stomach as compared to when alcohol is consumed alone (Jones and Jonsson, 1994;Pikaar et al., 1988;Roberts and Robinson, 2007;Sedman et al., 1976). While food delays stomach emptying (thus reducing BrAC), only recently has the role of nonalcoholic drink mixers consumed with alcohol been explored as another potential factor influencing BrAC. ...
Background:
Limited research suggests that alcohol consumed with an artificially sweetened mixer (e.g., diet soft drink) results in higher breath alcohol concentrations (BrACs) compared with the same amount of alcohol consumed with a similar beverage containing sugar. The purpose of this study was to determine the reliability of this effect in both male and female social drinkers and to determine if there are measureable objective and subjective differences when alcohol is consumed with an artificially sweetened versus sugar-sweetened mixer.
Methods:
Participants (n = 16) of equal gender attended 3 sessions where they received 1 of 3 doses (1.97 ml/kg vodka mixed with 3.94 ml/kg Squirt, 1.97 ml/kg vodka mixed with 3.94 ml/kg diet Squirt, and a placebo beverage) in random order. BrACs were recorded, as were self-reported ratings of subjective intoxication, fatigue, impairment, and willingness to drive. Objective performance was assessed using a cued go/no-go reaction time task.
Results:
BrACs were significantly higher in the alcohol + diet beverage condition compared with the alcohol + regular beverage condition. The mean peak BrAC was 0.091 g/210 l in the alcohol + diet condition compared with 0.077 g/210 l in the alcohol + regular condition. Cued go/no-go task performance indicated the greatest impairment for the alcohol + diet beverage condition. Subjective measures indicated that participants appeared unaware of any differences in the 2 alcohol conditions, given that no significant differences in subjective ratings were observed for the 2 alcohol conditions. No gender differences were observed for BrACs, and objective and subjective measures.
Conclusions:
Mixing alcohol with a diet soft drink resulted in elevated BrACs, as compared with the same amount of alcohol mixed with a sugar-sweetened beverage. Individuals were unaware of these differences, a factor that may increase the safety risks associated with drinking alcohol.
Human laboratory methods are valuable approaches to studying the etiology of alcohol misuse and interventions to ameliorate misuse because they offer advantages such as enhanced experimental control and relative efficiency compared to other methods. Yet, published reports from laboratory alcohol administration experiments typically do not provide a sufficient degree of detail for readers to replicate these procedures themselves. The primary goal of this chapter is to provide fine-grained details on experimental laboratory methods to assess subjective response and craving for alcohol: two mechanisms underlying alcohol misuse that we have learned the most about using laboratory alcohol administration paradigms. The detailed steps described here relied heavily on one research group’s approach with several alternatives offered. We describe the materials needed to conduct laboratory alcohol administration research followed by a step-by-step description of the methods involved in chronological order, beginning with day before procedures to prepare for a laboratory session; day of procedures, including calculating fixed doses of alcohol to target particular breath alcohol levels, pre-session baseline, beverage administration procedures; and day-after procedures. We conclude this chapter by discussing several key decisions investigators must make when designing a laboratory alcohol administration study. While there are several validated and reliable methods for conducting experimental laboratory research, investigators interested in subjective response and alcohol craving must carefully consider how their research questions and approaches align, while also taking into account the many potential logistical limitations.Key wordsExperimental proceduresSimulated bar laboratoryAlcohol dosePlacebo beverageStimulationSedationUrge
There are a significant number of individuals passing through the criminal justice system with substance misuse problems and it is essential that healthcare professionals (HCPs) working in the field of clinical forensic medicine are aware of the current drug trends in their area and have been trained to a standard to practice competently in this field.
Background:
Excessive alcohol consumption is a major public health problem in East Asian countries. Alcohol use leads to a cascade of problems including increased chances of risky behavior and a wide range of negative health consequences, from alcoholic liver disease to upper gastric and liver cancer. These alcohol effects are known to be influenced by ethnic variability and genetics.
Methods:
In this study, subjects were administered a single dose of alcohol (0.6 g/kg for men or 0.4 g/kg for women), and blood alcohol and acetaldehyde concentrations were measured eight times over 5 hours. To investigate genetically susceptible factors to alcohol metabolism, we selected single-nucleotide polymorphisms (SNP) of genes identified by prior genetic association studies for alcohol metabolism, alcohol consumption, alcohol dependence, and related traits, and performed genotyping on all subjects (n = 104).
Results:
We identified variations in the ADH1A, SRPRB, and PGM1 genes, which are directly associated with blood alcohol or acetaldehyde concentrations. Namely, the T allele of SRPRB rs17376019 and the C allele of PGM1 rs4643 were associated with lower blood alcohol levels, while the ADH1 rs1229976 C allele group exhibited markedly higher blood acetaldehyde levels than those of the ADH1 rs1229976 T allele group.
Conclusion:
This study demonstrates that genetic variations in ADH1A, SRPRB, and PGM1 are associated with variations in blood alcohol and acetaldehyde concentration after alcohol intake.
Whatever the reason for alcohol ingestion (and there are many, such as a food, social lubricant, or religious, ritual, or psychotropic drug), alcohol remains a toxin that can affect virtually every cell in the human body. It is not surprising, then, that alcohol-related effects on the mind and body represent one of the most important worldwide health problems today. In this article, we consider in detail how alcohol modifies diet and nutrient absorption and, conversely, how foods in the diet affect alcohol absorption and metabolism. In addition, we discuss how alcohol exerts its toxic effects on the gastrointestinal tract, particularly disruption of the gastrointestinal barrier, and how this disturbance might contribute to several systemic disorders, including alcoholic liver disease.
Ethylene glycol and methanol toxicity has the potential to cause morbidity and mortality [1, 2]. Along with supportive care and hemodialysis, ethanol has been utilized as a treatment option for many years, first investigated and used in the 1940s and 1950s [3–5].
IntroductionHistoryDiagnosing the Effects of Prenatal Alcohol ExposureRisk factors influencing FAS and FASD ConditionsPrevalence and Impact of FAS and FASDPreventionInterventionsAcknowledgmentsReferences
Ethylene glycol and methanol toxicity has the potential to cause morbidity and mortality [1, 2]. Along with supportive care and hemodialysis, ethanol has been utilized as a treatment option for many years, first investigated and used in the 1940s and 1950s [3–5].
In 1726, the Royal College of Physicians of Great Britain wrote to the Parliament drawing attention to the medical and social consequences of over-indulgence in alcohol [1]. By the nineteenth century, problems with public drunkenness, alcoholism, and addiction were beginning to reach alarming proportions. This was increasingly evident in the rapidly growing towns and cities of the industrial revolution where accidents at work were often alcohol-related [2]. Scientists and physicians were baffled by the question of what happens to ethanol in the body; was it a food, a poison, or a medicinal compound? Before the dawn of biochemistry, the pathways of drug metabolism and the fate of foreign substances in the body were unknown. But compared with many toxic drugs and chemicals, ethanol is a relatively weak pharmacological agent and its metabolism gives a quick source of energy to fuel the body processes, theoretically 7.1 kcal/g; 29 kj/g [3].
Alcohol clamping is a technique that maintains a constant breath alcohol concentration (BrAC) for prolonged intervals, thereby reducing experimental variance in the time course of organ exposure to alcohol, when compared with oral alcohol administration paradigms. The technique employs an intravenous (iv) infusion of an ethanol solution at a rate that is intermittently adjusted based on real-time BrAC measurements. In earlier studies, when the clamped state was induced with an oral ethanol loading dose, the vagaries of gastric emptying and absorption were associated with a 45 min delay (RST: reliable start time) before collection of dependent measurements could be planned with confidence. The objective of the present study was to develop an induction method that provides an earlier RST, and to compare the performance of the two methods. The “quick-clamping” method replaced the oral loading dose with a preprogrammed infusion rate profile. A three-compartment physiologically-based pharmacokinetic (PBPK) model for ethanol was constructed, then tailored to each subject using individualized estimates of model parameters. The model was used to compute the infusion-rate profile that would produce the desired time course of BrAC when infused in the corresponding subject. The two clamping methods were compared in a two-session crossover study in 20 healthy young subjects (10 males, 10 females). Compared with the oral/iv method, quick clamping produced a comparable precision in the control of BrACs during the clamped interval, and provided a much earlier RST (mean ± SE for quick-clamp: 17 ± 4 min; for oral/iv clamp: 45 ± 7 min). The quick-clamping method enables, for the first time, the examination of the early-phase neuroadaptive responses to alcohol in human subjects.
Ethanol (also referred to as alcohol in this chapter) is probably the most widely investigated drug in the world, not only because of its ubiquitous use and its widespread abuse but also because of its unique pharmacological properties. Following administration, systemic concentrations of alcohol are a consequence of the absorption, distribution, and metabolism of alcohol, which display very unique characteristics and demonstrate substantial interindividual variability [1]. As the pharmacological effects of alcohol depend on its systemic concentrations, variability in the pharmacokinetics of alcohol can have a significant impact on its pharmacodynamic effects.
The factors that govern blood and tissue concentrations of ethanol are the rate of absorption from the site of administration, the distribution space for ethanol in the body, and the rate of its elimination. Ethanol is neither accumulated to any extent by specific organs nor preferentially bound to cellular components. It is eliminated principally by oxidative metabolism in the liver. Consequently, after absorption and distribution in tissue and extracellular water, the primary determinant of the duration and extent of its pharmacologic action is the rate of its oxidation by the liver. For this reason, the enzymatic pathways of ethanol metabolism and their control by genetic and environmental factors have been important areas for detailed study. Furthermore, the oxidation of ethanol can produce profound abnormalities in the metabolic functions of the liver as well as nutrient imbalance. Knowledge of these interrelationships is fundamental to the understanding and treatment of many of the medical consequences of alcohol abuse and alcoholism, some of which may be life-threatening. These aspects of the biochemistry and pharmacology of ethanol are the principal focus of this chapter.
The analytical toxicologist may be required to detect, identify, and in many cases measure a wide variety of compounds in samples from almost any part of the body or in related materials such as residues in syringes or in soil. This book gives principles and practical information on the analysis of drugs and poisons in biological specimens, particularly clinical and forensic specimens. After providing some background information the book covers aspects of sample collection, transport, storage and disposal, and sample preparation. Analytical techniques - colour tests and spectrophotometry, chromatography and electrophoresis, mass spectrometry, and immunoassay - are covered in depth, and a chapter is devoted to the analysis of trace elements and toxic metals. General aspects of method implementation/validation and laboratory operation are detailed, as is the role of the toxicology laboratory in validating and monitoring the performance of point of care testing (POCT) devices. The book concludes with reviews of xenobiotic absorption, distribution and metabolism, pharmacokinetics, and general aspects of the interpretation of analytical toxicology results. A clearly written, practical, integrated approach to the basics of analytical toxicology. Focuses on analytical, statistical and pharmacokinetic principles rather than detailed applications. Assumes only a basic knowledge of analytical chemistry. An accompanying website provides additional material and links to related sites. Written by an experienced team of authors,Fundamentals of Analytical Toxicology is an invaluable resource for those starting out in a career in analytical toxicology across a wide range of disciplines including clinical and forensic science, food safety, and pharmaceutical development.
Subjects consumed 0.28 g/kg (females) or 0.33 g/kg (males) of 40% v/v diluted pure ethanol during a forty-minute period. Blood alcohol concentrations (BAC) were determined by breath samples introduced into Borkenstein Breathalyzers. When a constant BAC was maintained for at least fifteen minutes (approximately one hour after the end of drinking), the subjects consumed a further 0.86 g/kg (females) or 1.00 g/kg (males) of 40% v/v diluted pure ethanol within five minutes. The data were compared with data from subjects in the postabsorptive state who consumed only 40% v/v diluted pure ethanol within five minutes. The time to the maximum BAC and the length of the plateau were shorter when a period of “social” drinking preceded the bolus consumption of alcohol. It is proposed that the period of “social” drinking increased the permeability of the gastric mucosa to H+ ions to such an extent that the enterogastric inhibitory reflex was diminished. This would facilitate gastric emptying and result in increased rates of alcohol absorption.
Blood alcohol concentrations (BAL) were determined in order to monitor the absorption and diffusion-equilibration phases of alcohol in humans. Four hours after the last intake of food, the subjects consumed in five minutes 1 g. alcohol/kg. body weight dose either as 20% v/v or 40% v/v. The blood alcohol concentrations were determined by means of breath samples introduced into Borkenstein Breathalyzers. The concentration of alcohol in the solution ingested had no significant effect upon the times to the maximum blood alcohol level, the time to the plateau blood alcohol level or its duration. The plateau blood alcohol level itself was not affected. The maximum blood alcohol level (BAL max) was not dependent upon the concentration of the alcohol consumed but was significantly higher in females than males. Ninety-six percent of the population tested reached the BAL max within 105 minutes of the start of drinking. Forty minutes after the start of drinking, 93% of the population were within 20 mg.% of the BAL max.
Sixteen healthy men drank 1.43 g ethanol per kg of body weight as Swedish aquavit, export beer, and cognac during 90 min together with a 3-course meal. Capillary (fingertip) blood was drawn on 8 occasions starting at 0–10 min after the end of drinking and blood alcohol concentration (BAC) was determined by an enzymatic method. The peak BAC ranged from 0.97–1.41 mg/ml (mean 1.20 mg/ml) and this occurred 78 min after the end of drinking (range 0–230 min). The mean rate of disappearance of alcohol from blood (β) was 0.16 mg/ml/h (range 0.13–0.21) and the apparent volume of distribution of ethanol was 0.795 l/kg (range 0.64–0.93). The mean rate of ethanol elimination from the body was 128 mg/kg/h (range 99–160). The BAC increased on the average by 0.17 mg/ml (range 0.0–0.45 mg/ml) before reaching the maximum level. During the absorption phase, the BAC had attained on the average 83%, 91%, 95% and 98% of the final peak BAC within 5 min, 45 min, 109 min and 175 min, respectively, after ingestion. These results suggest that part of the dose of alcohol is rapidly absorbed into the blood despite the presence of undigested food in the stomach. However, the absorption of the remaining dose of alcohol might proceed for several hours.
Alcohol nomograms and charts based on population averages may induce substantial inaccuracies in the estimates of individual blood alcohol concen- tration levels (BACs). Also, many such charts require a compensating equa- tion to account for the metabolic elimination of alcohol over a period of time. Together, these two factors can lead to dangerous underestimates of BAC. This article outlines a one-tailed confidence interval approach for esti- mating expected BAC varying as a function of time and amount of alcohol consumed. The use of these data in BAC charts tailored to specific weight ranges precludes the use of a compensating equation and provides estimated BAC values which are much less likely to unsafely underestimate actual BACs.
Postsynaptic potentials of 30 masseter and digastric motoneurons evoked by stimulation of the facial and hypoglossal nerves were studied in cats. The afferent impulses from the facial and hypoglossal nerves evoked IPSP in masseter motoneurons with a latency of 5.3±0.3 msec and 5.8±0.2 msec, respectively. In digastric motoneurons EPSP and action potentials appeared after stimulation of the facial and hypoglossal nerves with a latency of 6.1±0.5 msec and 5.3±0.4 msec, respectively. The data obtained confirm the existence of connections between afferents of the facial and hypoglossal nerves and trigeminal motoneurons.
The effect of food deprivation on alcohol self-administration was examined in five women with bulimia nervosa and five healthy controls in a semi-naturalistic experimental design. In this within-subjects study, each individual underwent two food-deprived and two non-deprived sessions. The deprivation condition consisted of no food or caloric beverages for 19 hours prior to the experimental procedure. On each of the 4 days, subjects watched a 2–hour segment of an epic movie and were permitted to drink ad libitum. No differences were observed in the number of grams of alcohol consumed under deprived and non-deprived conditions for either group. Breath alcohol levels were significantly higher under the non-deprived condition despite equivalent amounts of alcohol consumed and similar ratings of the subjective sense of tipsiness. Bulimic women, consumed equivalent calories due to alcohol as control women but significantly fewer calories due to non-alcoholic beverages. These results do not support the hypothesis that food deprivation leads to increased self-administration of alcohol in women.
A gender difference in alcohol pharmacokinetics has been suggested to explain why women are more vulnerable to ethanol’s toxic
effects. The results of animal experiments suggest that females exhibit higher alcohol metabolic rates than males as a result
of hormonal differences. Experimental results examining gender differences in human alcohol metabolism have been inconsistent;
the diversity of experimental protocols and variety of pharmacokinetic parameters reported have made comparisons of these
studies very difficult. Variability in alcohol metabolic rate between individuals of the same sex is often significant, preventing
an assessment of gender differences in some studies. This chapter attempts to summarize the findings of studies from the last
decade that examined the role of gender and sex hormone differences on ethanol metabolism in men and women. The role of body
composition, genetic factors, gastric and hepatic alcohol dehydrogenase, and gastric absorption in creating gender differences
in alcohol metabolism is discussed. Suggestions are offered that may result in better cross-study comparisons and more consistent
experimental results.
Adverse drug–alcohol interactions represent a major problem in today’s society because of the increasing use of prescription
medication in the aging population and the recreational use and abuse of alcoholic beverages throughout adult life. Heavy
drinking and drunkenness are major public health problems and ethanol is the drug most frequently encountered in poisoning
deaths either alone or together with other substances. Drugs and alcohol can interact in a number of ways, such as by competition
for binding sites on hepatic enzymes, which opens the possibility for a metabolic interaction. This is often reflected in
a change in the blood or plasma concentration–time curve of alcohol and/or drug and a more rapid or slower rate of elimination
from the body (pharmacokinetic interaction). The combined influence of alcohol and other drugs might occur at certain receptor
sites or ion channels in the central nervous system and in this way modify behavioral response to drug treatment (pharmacodynamic
interaction). This review is concerned with the biological background and the mechanism underlying pharmacokinetic and pharmacodynamic
interaction between ethanol and other drugs. Examples are given of ethanol–drug interactions involving common medications
(e.g., acetaminophen, benzodiazepines, and other sedatives) as well as drugs of abuse, such as cocaine and GHB.
KeywordsDrug-Alcohol-Interactions
This chapter discusses sociocultural influences on the availability, access, diagnosis, and treatment of alcoholism for women,
particularly those in minority groups. Race/ethnicity and other sociocultural influences are presented in terms of the societal
context and the counselor-client relationship. The latest data on heavy drinking, alcohol-induced mortality, and alcoholism
treatment utilization are presented on African-American, Hispanic, and white women. Data also are presented on the ability
to pay for treatment through insurance or earnings. Information on Native Americans and Asian/Pacific Islanders is included
whenever possible.
The number of individuals passing through the criminal justice system with substance misuse problems is increasing, and doctors should be aware of current drug trends in their area. In the United States there is a well-established program of research on drug testing urine samples of people arrested by the police—the Arrestee Drug Abuse Monitoring Program (ADAM), which recently replaced the Drug Use Forecasting Program (DUF) (1). A smaller scale project in England, which involved testing the urine of detainees, showed high levels of recent drug consumption—61% had taken at least one drug (2). The figures, similar to those found in the United States (68%), may well be higher in reality, as detainees were excluded from testing who were unfit for interview due to alcohol, drugs, or medication, or who were considered mentally disordered or potentially violent.
A nonlinear relationship between the total area under the blood ethanol concentration-time curve and the orally administered dose (mg/kg) of ethanol was observed in fasting subjects. A preliminary model, based on physiological considerations, was elaborated and shown, for the first time, to describe the entire time course of blood alcohol concentrations after four different doses of alcohol. The model could be refined by further experimentation.
Introduction Substance misuse is a major and growing problem often resulting in drug-related criminal activity. Forensic physicians are seeing an increasing number of substance misusers in the setting of a police station [1]. These misusers may be intoxicated, withdrawing or dependent on alcohol or drugs. The police may request a medical assessment of substance misusing detainees in order to: assess their fitness for detention and fitness to be interviewed; conduct a mental state examination; undertake a comprehensive examination of their fitness to drive a motor vehicle; and perform an intimate search for drugs. Some substance misusers will, for a variety of reasons, attempt to hide their misuse from the authorities on arrest. Therefore, it is most important that examining forensic physicians make a conscious effort to look for any indication of substance misuse or dependence. A sympathetic approach from the doctor is more likely to result in disclosure and a reliable history from the detainee, who should be reassured that effective treatment will be given where necessary and that the overriding consideration of the doctor is their clinical safety and wellbeing. Criminality and drug use The relationship between crime and drug use is very complex and takes a number of forms, with much of the crime committed reflecting the lifestyle and circumstances of the drug users themselves. Drug-related crime encompasses any criminal activity which is committed either to fund the purchase of drugs or as a consequence of drug misuse.
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