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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.
To Drink or Not to Drink
Most people drink for reasons other than alcohol’s health benefits, and many of them are already using alcohol in amounts that appear to promote cardiovascular health. But the accumulated research on alcohol’s positive effects presents a challenge to physicians. On the one hand, mild to moderate drinking seems better for heart health than abstinence for select people. On the other hand, heavy drinking is clearly dangerous. It can contribute to noncardiovascular conditions such as liver cirrhosis, pancreatitis, certain cancers and degenerative neurological disorders, and it plays a part in great numbers of accidents, homicides and suicides, as well as in fetal alcohol syndrome. (No conclusive evidence links light to moderate drinking to any of these problems.)
Heavy drinking also contributes to cardiovascular disorders. Too much alcohol raises the risk of alcoholic cardiomyopathy, in which the heart muscle becomes too weak to pump efficiently; high blood pressure (itself a risk factor for CHD, stroke, heart failure and kidney failure); and hemorrhagic stroke, in which blood vessels rupture in or on the surface of the brain. Alcohol overindulgence is also related to “holiday heart syndrome,” an electrical signal disturbance that disrupts the heart rhythm. The name refers to its increased frequency around particular holidays during which people engage in binge drinking.
Given the potential dangers of alcohol, how can individuals and their physicians make the decision as to whether to include alcoholic beverages in their lives and, if so, in what amounts? The ability to predict accurately an individual’s risk of a drinking problem would be a great boon; the least disputed possible consequence of moderate drinking is problem drinking. Individual risk can be approximated using family and personal histories of alcohol-related problems or conditions, such as liver disease or, of course, alcoholism. Even when known factors are taken into account, however, unpredictable events late in life may result in deleterious drinking changes.
Exactly because of these dangers, public health concerns about alcohol until recently have been appropriately focused solely on the reduction of the terrible social and medical consequences of heavy drinking. And the correlation between total alcohol consumption in society and alcohol-related problems has been used to justify pushes for abstinence. Ultimately, however, a more complex message is necessary. Merely recommending abstinence is inappropriate health advice to people such as established light drinkers at high risk of CHD and at low risk of alcohol-related problems—which describes a large proportion of the population. Of course, the most important steps for this group are proper diet and exercise; effective treatment of obesity, diabetes, high blood pressure and high cholesterol; and avoidance of tobacco. But there is a place on that list of beneficial activities for light drinking. Most light to moderate drinkers are already imbibing the optimal amount of alcohol for cardiovascular benefit, and they should continue doing what they are doing.
Abstainers should never be indiscriminately advised to drink for health; most have excellent reasons for not drinking. Yet there are exceptions. One case is the person with CHD who “goes clean”—quits smoking, switches to a spartan diet, starts exercising and, with good intentions, gives up the habit of a nightly bottle of beer or glass of wine. This self-imposed prohibition should be repealed. In addition, a number of infrequent drinkers might think about increasing their alcohol intake to one standard drink daily, especially men older than 40 and women older than 50 at high risk of CHD and low risk of alcohol-related problems.
But women also have to consider one possible drawback of alcohol: several studies link heavy drinking—and a few even link light drinking—to an increased risk of breast cancer, a less common condition than heart disease in postmenopausal women but certainly quite a serious one. For young women, who are generally at low short-term risk of CHD and therefore may not benefit greatly from alcohol’s positive cardiovascular effects, this possible breast cancer link looms larger in estimating the overall risks and benefits of alcohol. And for all women, the upper limit on moderate drinking should be considered one drink a day.
The only clear-cut message regarding alcohol and health, then, is that all heavy drinkers should reduce or abstain, as should anyone with a special risk related to alcohol, such as a family or personal history of alcoholism or preexisting liver disease. Beyond that, however, the potential risks and benefits of alcohol are best evaluated on a case-by-case basis. I believe that it is possible to define a clear, safe limit for alcohol consumption that would offer a probable benefit to a select segment of the population. The ancient Greeks urged “moderation in all things.” Three decades of research shows that this adage is particularly appropriate when it comes to alcohol. (Feature article, abridged. From Scientific American, February, 2003)
Exercise 6. Would you recommend moderate amounts of alcohol to the following groups of patients? Why? Why not?
● heavy drinkers
● pregnant women
● diabetics
● patients with CHD
● people with family history of alcoholism
● young people
● obese people
● women older than 50
Exercise 7. You are going to interview your fellow-students. Make up 10 questions about the key facts discussed in the article.
Exercise 8. Summarize all the information discussed in this unit and speak on the effects of alcohol on human organism.
Unit 13. Sex and Gender
A woman is only a woman, but a good cigar is a smoke.
Rudyard Kipling
Exercise 1. What do you know about the sexes?
1. What are the physiological differences between individuals of male and female gender? What organs and organ systems differ between males and females?
2. What mechanisms and when determine the sex of the future individual?
3. What are the functions of reproductive hormones (sex hormones)?
4. What are the secondary sexual characteristics?
5. Why do women generally live longer than men?
6. Do men and women really have different patterns of mental activity and emotions? Are they genetically or socially programmed?
Exercise 2. Read the text to check some of your answers in Exercise 1.
Why is life expectancy [2] longer for women than it is for men?
Bertrand Desjardins, a researcher in the demography department of the University of Montreal, explains.
Men dying sooner than women makes sense biologically: because 105 males are born for every 100 females, it would assure that there are about the same number of men and women at reproductive ages. But even though women showed a longer life expectancy in almost every human society in the last decade of the 20th century, the size of the advantage varied greatly. For example, in the U.S. life expectancy was 73.4 years for males and 80.1 years for females, a difference of 6.7 years, whereas in France it was 7.8 years and in the U.K., 5.3 years. The discrepancy was much greater in some countries, with the difference in Russia reaching more than 12 years, but in others, such as India (0.6 year) or Bangladesh (0.1 year), it was much less.
The diversity in worldwide longevity alone indicates that the difference in mortality between the sexes is not purely biological and that there are intervening social factors. The current range of situations actually reflects different stages of a three-part historical evolution. Women most probably have a biological advantage that allows them to live longer, but in the past--and in several places, still today--the status and life conditions of women nullified this benefit. Today, given the general progress in female life conditions, women have not only regained their biological advantage, but have gone much beyond it, both because they tend to engage in fewer behaviors that are bad for health than men do and because they better profit from current advances in health care and living conditions.
The biological advantage that women have is taken as a certainty, because the mortality of males is higher than that of females from the very outset of life: during the first year of life, in the absence of any outside influence which could differentiate mortality between the sexes, male mortality is 25 to 30 percent greater than is female mortality. The genetic advantage of females is evident. When a mutation of one of the genes of the X chromosome occurs, females have a second X to compensate, whereas all genes of the unique X chromosome of males express themselves, even if they are deleterious. More generally, the genetic difference between the sexes is associated with a better resistance to biological aging. Furthermore, female hormones and the role of women in reproduction have been linked to greater longevity. Estrogen, for example, facilitates the elimination of bad cholesterol and thus may offer some protection against heart disease; testosterone, on the other hand, has been linked to violence and risk taking. Finally, the female body has to make reserves to accommodate the needs of pregnancy and breast feeding; this ability has been associated with a greater ability to cope with overeating and eliminating excess food.
Even though many biological and genetic factors have been identified, their overall effect is impossible to measure, especially given the influence of social factors on mortality. The extraordinary economic and social progress, that has occurred since the 18th century, has been accompanied by a dramatic reduction of the social differences between men and women and of the burden of motherhood, which had previously negated women's biological advantage. But the recent mortality trends have gone much farther than the mere recovery of an original advantage, creating instead a new advantage of greater magnitude for women. Observations indicate that the growing excess male mortality in industrial countries could be explained by the rise of so-called "man-made diseases," which are more typically male. These include exposure to the hazards of the workplace in an industrial context, alcoholism, smoking and road accidents, which have indeed increased considerably throughout the 20th century.
But if these diseases are the only explanation for longer female life expectancy, why has the gap continued to grow even though male and female behavior and life conditions have been converging in recent years? Part of the paradox can certainly be explained by the fact that this convergence is not absolute: male smokers tend to smoke more cigarettes than female smokers do, and men drive more recklessly than female drivers do, for instance.
French demographer Jacques Vallin has long been monitoring longevity in general and sex differences in mortality in particular. He adds to the above an interesting explanation of women's current mortality advantage that could explain the more recent trends: the dramatic increase in excess male mortality emerged as an equally dramatic progress in the general health conditions of our societies was taking place. He thus argues that beyond the negative behavioral or environmental factors that affect men more than they do women, there could be very well be a more fundamental difference in lifestyles that allows women to better benefit from the general progress in health. For example, although women now participate massively in the work force, their roles remain different and their professional activities are, on average, less prejudicial to their health. In addition, women often relate to their bodies, their health and their lives in general in a much different way than men do. To caricature, women seek beauty, men seek strength and power; thus, a woman's body must remain young and healthy as long as possible, whereas a man's body must be submitted to risks and challenges from an early age. The result is that women, much more than men, are attentive to their bodies and their needs and often carry on deeper dialogs more easily with their doctors. Hence, women, being more inclined to take care of their bodies and to prolong their lives, may be better able to glean greater profit from modern medical and social advances by practicing activities that are healthier and better protect their bodies. In this context, women's biological advantage now appears relatively minor in the total mortality differences between the sexes.
Exercise 3. Are the following statements true or false, according to the text?
Exercise 4. Sex Differences in the Brain.
Men and women display patterns of behavioral and cognitive differences that reflect varying hormonal influences on brain development. Before reading the next text guess if the following statements generally refer more to men or to women:
Exercise 5. Read the following article to check some of your answers in Exercise 4.
Girl Brain, Boy Brain?
The two are not the same, but new work shows just how wrong it is to assume that all gender differences are “hardwired”
By Lise Eliot
As MRI scanning grows ever more sophisticated, neuroscientists keep refining their search for male-female brain differences that will answer the age-old question, “Why can’t a woman think like a man?” (and vice-versa). Social cognition is one realm in which the search for brain sex differences should be especially fruitful. Females of all ages outperform males on tests requiring the recognition of emotion or relationships among other people. Sex differences in empathy emerge in infancy and persist throughout development, though the gap between adult women and men is larger than between girls and boys. The early appearance of any sex difference suggests it is innately programmed—selected for through evolution and fixed into our behavioral development through either prenatal hormone exposure or early gene expression differences. On the other hand, sex differences that grow larger through childhood are likely shaped by social learning, a consequence of the very different lifestyle, culture and training that boys and girls experience in every human society.
At first glance, studies of the brain seem to offer a way out of this age-old nature/nurture dilemma. Any difference in the structure or activation of male and female brains is indisputably biological. However, the assumption that such differences are also innate or “hardwired” is invalid, given all we’ve learned about the plasticity, or malleability of the brain. Simply put, experiences change our brains.
Recent research by Peg Nopoulos, Jessica Wood and colleagues at the University of Iowa illustrates just how difficult it is to untangle nature and nurture, even at the level of brain structure. A first study, published in March 2008 found that one subdivision of the ventral prefrontal cortex - an area involved in social cognition and interpersonal judgment, known as the straight gyrus (SG), - is proportionally larger in women, compared to men. (Men’s brains are about 10 percent larger than women’s, overall, so any comparison of specific brain regions must be scaled in proportion to this difference.) Wood and colleagues found the SG to be about 10 percent larger in the thirty women they studied, compared to thirty men. What’s more, they found that the size of the SG correlated with a widely-used test of social cognition, so that individuals (both male and female) who scored higher in interpersonal awareness also tended to have larger SGs.
In their article, Wood and colleagues speculate about the evolutionary basis for this sex difference. Perhaps, since women are the primary child-rearers, their brains have become programmed to develop a larger SG, to prepare them to be sensitive nurturers. Prenatal sex hormones are known to alter behavior and certain brain structures in other mammals. Perhaps such hormones—or sex-specific genes—may enhance the development of females’ SG (or dampen the development of males’) leading to inborn differences in social cognition.
The best way to test this hypothesis is to look at children. If the sex difference in the SG is present early in life, this strengthens the idea that it is innately programmed. Wood and Nopoulos therefore conducted a second study with colleague Vesna Murko, in which they measured the same frontal lobe areas in children between 7 and 17 years of age. But here the results were most unexpected: they found that the SG is actually larger in boys! What’s more, the same test of interpersonal awareness showed that skill in this area correlated with smaller SG, not larger, as in adults. The authors acknowledge that their findings are “complex,” and argue that the reversal between childhood and adulthood reflects the later maturation of boys’ brains, compared to girls. (Adolescents’ brains undergo a substantial “pruning” or reduction in gray matter volume during adolescence, which happens about two years earlier in girls, compared to boys.)
However, in both studies, Wood and colleagues added another test that reminds us to be cautious when interpreting any finding about sex differences in the brain. Instead of simply dividing their subjects by biological sex, they also gave each subject a test of psychological “gender:” a questionnaire that assesses each person’s degree of masculinity vs. femininity—regardless of their biological sex—based on their interests, abilities and personality type. And in both adults and children, this measure of “gender” also correlated with SG size, albeit in just as complicated a way as the correlation between “sex” and SG size. (Larger SG correlated with more feminine personality in adults but less feminine personality in children.)
In other words, there does seem to be a relationship between SG size and social perception, but it is not a simple male-female difference. Rather, the SG appears to reflect a person’s “femininity” better than one’s biological sex: women who are relatively less feminine show a correspondingly smaller SG compared to women who are more feminine, and ditto for men.
This finding—that brain structure correlates as well or better with psychological “gender” than with simple biological “sex”—is crucial to keep in mind when considering any comparisons of male and female brains. Yes, men and women are psychologically different and yes, neuroscientists are uncovering many differences in brain anatomy and physiology which seem to explain our behavioral differences. But just because a difference is biological doesn’t mean it is “hard-wired.” Individuals’ gender traits—their preference for masculine or feminine clothes, careers, hobbies and interpersonal styles—are inevitably shaped more by rearing and experience than is their biological sex. Likewise, their brains, which are ultimately producing all this masculine or feminine behavior, must be molded—at least to some degree—by the sum of their experiences as a boy or girl.
And so, any time scientists report a difference between male and female brains, especially in adults, it begs the question, “Nature or nurture?” Is women’s larger SG the cause of their social sensitivity, or the consequence of living some 30 years in a group that practices greater empathetic responding? Wood and colleagues are among the few neuroscientists to analyze male-female brain differences for their relationship to gender type, as opposed to strict biological sex. Their findings do not prove that social learning is the cause of male-female differences in the brain, but they do challenge the idea that such brain differences are a simple product of the Y chromosome. (From Scientific American Online, September 8, 2009)
Exercise 6. Answer the questions using the information from the text:
Exercise 7. Divide into two groups. Each group should read either Text A or Text B about differences between the sexes. Then tell other students what you have read about.
Text A. Enzyme Lack Lowers Women's Alcohol Tolerance
By Harald Franzen
An international team of researchers may have found one of the reasons why alcohol harms women more than men: women, it appears, are deficient in an enzyme that helps metabolize alcohol. The findings appear in the April issue of Alcoholism: Clinical and Experimental Research. "It has been known for a long time that, in general, both women and female animals are more susceptible to the negative or toxic effects of alcohol," team member Steven Schenker of the University of Texas at San Antonio says. "This is true for the liver, heart muscle and skeletal muscle, and it may be true for the pancreas and the brain. In other words, there is something about the female gender that makes them more susceptible to toxic amounts of alcohol."
In the past scientists attributed this susceptibility to women's smaller body size and their relatively higher percentage of fatty tissue. For this study, however, the researchers focused on what is known as first-pass metabolism. Before alcohol reaches the blood stream, it goes through the stomach, where so-called gastric alcohol dehydrogenase (ADH) isozymes break some of it down. "In an earlier study we found that women have less of this ADH activity than men do," notes lead author Charles Lieber of the Mount Sinai School of Medicine. "Accordingly, women have a lesser first-pass metabolism and, therefore, for a given dose of alcohol, their blood level is higher than it is for men."
Following up on that research, the team recently turned their attention to the makeup of ADH. They found that one of the enzyme's three components, glutathione-dependent fomaldehyde dehydrogenase (x-ADH), is deficient in women, thus explaining their lower ADH activity levels. To Schenker, the take-home message is clear: "Women simply need to be more cautious than males in terms of the amount of drinking they do." (From Scientific American Online, April 16, 2001)
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