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Exercise 2. Read the information about alcohol provided by NewScientist.com to check some of your answers in Exercise 1.

What is it?Ethanol produced by the action of yeast on sugars.

What does it do?Ethanol is a biphasic drug: low doses have a different effect to high doses. Small amounts of alcohol (one or two drinks) act as a stimulant, reducing inhibition and producing feelings of mild euphoria. Higher doses depress the central nervous system, initially producing relaxation but then leading to drunkenness - characterised by poor coordination, memory loss, cognitive impairment and blurred vision. Very high doses cause vomiting, coma and death through respiratory failure. The fatal dose varies but is somewhere around 500 milligrams of ethanol per 100 millilitres of blood.

How does it work?At low doses (5 milligrams per 100 millilitres of blood), alcohol sensitises NMDA receptors in the brain, making them more responsive to the excitatory neurotransmitter glutamate, so boosting brain activity. These effects are most pronounced in areas associated with thinking, memory and pleasure. At higher doses it desensitises the same receptors and also activates the inhibitory GABA system.

How long is its history?

4000BC - Wine and beer making in Egypt and Sumeria

3500BC - Bronze-age vessels show evidence of wine consumption in eastern Mediterranean

800BC - Distillation of spirits in India

AD625 - Mohammed orders his followers to abstain from alcohol

1850s - New York bartenders invent the cocktail

1920-33 - Prohibition in the US. Alcohol was also illegal in Finland from 1919 to 1932 and in various Canadian provinces at various times between 1900 and 1948.

 

Exercise 3. Now read more detailed information about the effects of alcohol on the brain provided by Anthony Dekker D.O., Director of Ambulatory Care and Community Health at Phoenix Indian Medical Center.

What are the effects of alcohol on the brain?

The product of the oldest chemical reaction studied by man, alcohol, continues to challenge researchers. Since the original work on alcohol's neurological effects in the early 20th century, new theories have regularly emerged. What we have learned is that alcohol is a sedative-hypnotic in the acute intoxication phase for most patients. But it diminishes the quality of sleep. Individuals with sleep apnea often experience longer and more severe apneic episodes and hypoxia, or oxygen deprivation, after drinking alcohol.

In other individuals, though, alcohol may act as a stimulant. Indeed, its association with violent and self-abusive behavior is well documented*. At intoxicating levels, alcohol is a vasodilator (it causes blood vessels to relax and widen), but at even higher levels, it becomes a vasoconstrictor, shrinking the vessels and increasing blood pressure, exacerbating such conditions as migraine headaches and frostbite. Researchers have also thoroughly documented the effects of alcohol on the developing fetus. Approximately one third of all babies born to alcoholic mothers will develop Fetal Alcohol Syndrome or Effects (FAS or FAE), causing central nervous system dysfunctions including Attention Deficit Disorder (ADD) and impaired IQ. There are also growth and facial abnormalities associated with these infants.



In the early 1900s, H. Meyer and Charles Ernest Overton originally theorized that the effect of alcohol was achieved by altering the lipid environment of cell membranes. This theory, however, requires much higher concentrations of alcohol than are clinically observed. A recent theory, supported by several researchers, pins alcohol's effect on voltage and ligand-gated ion channels that control neuronal activity. Two distinct ligand-gated channels have been identified, inhibitory ones (GABA receptors and strychnine-sensitive glycine receptors) and excitatory ones (N-methyl-D-aspartate (NMDA) and non-NMDA glutamate-activated channels and the 5HT3 subtype of serotonin receptors).

The inhibitory aspect occurs due to a hyperpolarization of neurons, secondary to an influx of chloride ions. The neuron becomes less likely to achieve the threshold membrane potential. The excitatory receptor is dependent on the NMDA and non-NMDA glutamate receptors that control the influx of sodium and calcium, which bind to endogenous neurotransmitters (glutamate or aspartate) and depolarize the neuronal membrane. The NMDA receptor seems to have a high permiability to calcium, which acts as a catalyst to several intracellular events.

Chronic exposure to alcohol seems to alter the NMDA receptors and this may play a role in the clinical symptoms of alcohol withdrawal. In vitro studies have demonstrated an increase in the binding sites for MK801 (dizocilpine) in neurons chronically exposed to alcohol. This rise may account for the acclimation process, in which greater concentrations of alcohol are needed to cause experimental and clinical symptoms of intoxication. NMDA can cause seizure activity. Mice that have been exposed to chronically elevated levels of alcohol reveal increased numbers of NMDA receptors and NMDA related seizure activity. The NMDA antagonist MK801 has been shown to decrease the severity of seizures in these mice during withdrawal. Through a complex process of cell membrane ion pumps and neurotransmitter stimulation, the multi-faceted effects of alcohol and alcohol withdrawal are becoming better understood.

*Under the influence of alcohol, the brain experiences impairments in the following regions:

•Frontal Lobe - Loss of reason, caution, inhibitions, sociability, talkativeness and intelligence.

•Parietal Lobe - Loss of fine motor skills, slower reaction time, shaking.

•Temporal Lobe - Slurred speech, impaired hearing.

•Occipital Lobe - Blurred vision, poor distance judgement.

•Cerebellum - Lack of muscle coordination and balance.

•Brain Stem - Loss of vital functions.

 

Exercise 4. Do you agree with the statements below? Give reasons for your choice.

  1. Alcohol may have sedative-hypnotic and stimulatory effect on people.
  2. Alcohol affects circulatory system.
  3. So far scientists have not completely uncovered the mechanism of its activity.
  4. The effect of alcohol is most pronounced in the brain.
  5. Chronic exposure to alcohol produces no changes of brain structures.

 

Exercise 5. Some scientists argue that alcohol can produce significant positive effect on one’s health. The article below provides evidence for this point of view. Read the article and find answers to the questions:

  1. What disorders can alcohol protect from?
  2. What are the mechanisms involved?

 

Drink to Your Health?

By Arthur L. Klatsky

Three decades of research shows that drinking small to moderate amounts of alcohol has cardiovascular benefits. A thorny issue for physicians is whether to recommend drinking to some patients.

 

America has always had trouble deciding whether alcohol is a bad thing or a good thing. Millions who remember Prohibition, when all alcoholic beverages were illegal, now witness a constant stream of advertisements from producers of alcoholic beverages encouraging people to drink. Despite alcohol’s popularity today, however, many still consider abstinence a virtue. Certainly, heavy drinking and alcoholism deserve deep concern for the terrible toll they take on alcohol abusers and society in general. But worry about the dangers of abuse often leads to emotional denials that alcohol could have any medical benefits. Such denials ignore a growing body of evidence indicating that moderate alcohol intake wards off certain cardiovascular conditions, most notably heart attacks and ischemic strokes (those caused by blocked blood vessels). A few studies even show protection against dementia, which can be related to cardiovascular problems.

 

The Alcohol Effect

A discussion of moderate drinking requires a working definition of “moderate.” Simple definitions of light, moderate or heavy are somewhat arbitrary, but a consensus in the medical literature puts the upper limit for moderate drinking at two standard-size drinks a day. Studies show that drinking above that level can be harmful to overall health, although sex, age and other factors lower and raise the boundary for individuals.

The main medical benefit of reasonable alcohol use seems to be a lowering of the risk for coronary heart disease (CHD), which results from the buildup of atherosclerosis (fatty plaque) in the arteries. Atherosclerosis restricts blood flow to the heart and can promote the formation of vessel-blocking clots. It can thereby cause angina (chest discomfort resulting from low oxygen levels in the heart muscles), heart attack (the death of heart tissue that occurs when a blood clot or narrowing of the arteries prevents blood from reaching the heart) and death, often without warning. The condition usually starts at a young age but takes decades to blossom into overt CHD. The most common form of heart disease in developed countries, CHD causes about 60 percent of deaths from cardiovascular ills and about 25 percent of all deaths in those nations.

Pathologists uncovered the first clues to the value of alcohol in the early 1900s, noting that the large arteries of people who died of alcoholic liver cirrhosis seemed remarkably “clean”—that is, free of atherosclerosis. One explanatory hypothesis assumed that alcohol was a nebulous solvent, essentially dissolving the buildup in the arteries; another explanation held that heavier drinkers died before their atherosclerosis had a chance to develop. Neither idea truly explained drinkers’ unblocked arteries, however.

A more telling hint emerged in the late 1960s, when Gary D. Friedman of the Kaiser Permanente Medical Center in Oakland, Calif., came up with a novel idea: use computers to unearth unknown predictors of heart attacks. The power of computing could first identify healthy people who had risk factors similar to heart attack victims. Such factors include cigarette smoking, high blood pressure, diabetes, elevated levels of low-density lipoprotein (LDL, or “bad”) cholesterol, low levels of high-density-lipoprotein (HDL, or “good”) cholesterol, male gender, and a family history of CHD. Friedman then searched for predictors of heart attacks by comparing the patients and the newly found controls in hundreds of ways—for example, their exercise and dietary habits and their respective levels of various blood compounds. The computers spit out a surprising discovery: abstinence from alcohol was associated with a higher risk of heart attack.

Since then, dozens of investigations in men and women of several racial groups in various countries have correlated previous alcohol use with current health. These studies have firmly established that nondrinkers develop both fatal and nonfatal CHD more often than do light to moderate drinkers. In addition, in 2000 Giovanni Corrao of the University of Milan-Bicocca in Italy, Kari Poikolainen of the Järvenpää Addiction Hospital in Finland and their colleagues combined the results of 28 previously published investigations on the relation between alcohol intake and CHD. In this meta-analysis, they found that the risk of developing CHD went down as the amount of alcohol consumed daily went up from zero to 25 grams. At 25 grams—the amount of alcohol in about two standard drinks—an individual’s risk of a major CHD event, either heart attack or death—was 20 percent lower than it was for someone who did not drink at all. New data about alcohol protecting against death from CHD are even more impressive. At a meeting of the American Heart Association last November, it was announced that those who had one or two alcoholic drinks a day had a 32 percent lower risk of dying from CHD than abstainers did.

The possible mechanisms by which alcohol has such an apparently profound effect on cardiovascular health primarily involve cholesterol levels and blood clotting. Blood lipids play a central role in CHD. Numerous studies show that moderate drinkers have 10 to 20 percent higher levels of heart-protecting HDL cholesterol. And people with higher HDL levels, also known to be increased by exercise and some medications, have a lower risk of CHD.

That lower risk stems from HDL’s ability to usher LDL cholesterol back to the liver for recycling or elimination, among other effects. Alcohol seems to have a greater influence on a different HDL subspecies (HDL3) than on the type increased by exercise (HDL2), although both types are protective. (The biochemical pathways in the liver that could account for alcohol’s ability to raise HDL levels remain incompletely known; it is thought that alcohol probably affects liver enzymes involved in the production of HDL.) Three separate analyses aimed at determining specific contributions of alcohol all suggest that the higher HDL levels of drinkers are responsible for about half of the lowered CHD risk.

Alcohol may also disrupt the complex biochemical cascade behind blood clotting, which can cause heart attacks when it occurs inappropriately, such as over atherosclerotic regions in coronary arteries. Blood platelets, cellular components of clots, may become less “sticky” in the presence of alcohol and therefore less prone to clumping, although data on this question remain ambiguous. Overall, alcohol’s anticlotting capacity is not as well established as its HDL effect, and some effects, such as platelet clumping, may be reversed by heavy or binge drinking. In addition, studies have shown a beneficial effect on CHD risk in people who have far fewer than two drinks a day—say, three or four drinks a week. Anticlotting could be a major factor in the protection accorded by alcohol in these small amounts, which seem insufficient to affect HDL levels greatly.

Before accepting alcohol’s benefits, an epidemiologist attempts to locate hidden factors possibly at work. For instance, could lifelong abstainers differ from drinkers in psychological traits, dietary habits, physical exercise habits or other ways that might account for their higher CHD risk without the need to invoke the absence of alcohol? Were such traits to explain away alcohol’s apparent protection, they would need to be present in both sexes, various countries and several racial groups. Considering that no such traits have been identified, the simpler and more plausible explanation is that light to moderate alcohol drinking does indeed enhance cardiovascular health.

In fact, the available evidence satisfies most standard epidemiological criteria for establishing a causal relation. The numerous studies examining light and moderate alcohol intake and health reach consistent conclusions. The positives associated with alcohol can be attributed to biologically plausible mechanisms. Alcohol offers specific enhancement of cardiovascular health, not general protection against all illness. And alcohol’s effect can be identified independent of known “confounders,” other alcohol related factors that could be responsible for a subject’s cardiovascular condition.

Because heavy drinking is not more protective than lighter drinking, this absence of a clear dose-response relation is also a weakness. Nevertheless, the collected data make a strong case for the cardiac benefits of controlled drinking.

 


Date: 2016-03-03; view: 917


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Exercise 8. In the following text the paragraphs are mixed. Put them in the correct logical order. The first and the last paragraphs are in their right places. | To Drink or Not to Drink
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