The Impact of Alcohol : The heart and the circulatory system

Lichtenstein (2003) states that 15 million deaths in the late 1990s could be attributed to cardiovascular disease. The American Heart Association has pointed out that coronary heart disease and the related cardiovascular disease is the number-one killer in the US, accounting for almost one in two deaths among Americans and more deaths than are caused by all the forms of cancer combined. The impact on disability and the attendant economic loss are enormous.
Atherosclerosis (‘hardening of the arteries’) is the term used to describe a number of pathological events occurring in arteries and which are responsible for coronary heart disease, stroke and diseases of the peripheral circulatory system (Fisher 1991). Atheroma (from the Greek ather = porridge) comprises deposits of fatty material on the walls of arteries – a material comprising cholesterol, triglycerides, brous tissue and red blood cells. As it builds it restricts blood ow and if this is in the coronary artery then heart attack and death may follow, as the heart muscle does not receive suf cient oxygen. Atheroma has also been associated with the development of cataracts, macular degeneration in the retina and the development of cancers (Emerit et al. 1991; Tunick et al. 1994). If the atheroma accumulation (plaque) is ruptured a blood clot may form which not only can accelerate the blockage of the artery concerned but also may break loose and plug another artery, increasing the risk of heart attack or, if the newly blocked artery is in the brain, a stroke.
Plainly, the intake of saturated fats and cholesterol increases the risk, although it must be realised that four- fths of the cholesterol is made in our bodies and does not come through the diet. The quantity of cholesterol produced is increased in proportion to the level of saturated fatty acids in the diet (polyunsaturated fatty acids reduce blood cholesterol), and also the trans saturated fatty acids, i.e. those that are produced industrially by catalytic hydrogenation (Krisetherton 1995). High sugar intake can lead to high formation of saturated fats in the body. Indeed, any imbalance in metabolism such that there is an excess of calories over those needed to sustain the body will lead to an accumulation of fat. Obesity, hypertension, diabetes, sedentary living and the use of cigarettes all increase the risk of atherosclerosis.
As cholesterol and other lipids such as the triglycerides are insoluble in aqueous systems, they are transported through the body by combination with proteins, as lipoproteins. The principal carrier of cholesterol is low-density lipoprotein (LDL) and there is a strong positive correlation between its level and the risk of atherosclerosis. Hence LDL is frequently referred to as ‘bad cholesterol’. A lower percentage (20–30%) of the blood cholesterol is in the form of high-density
lipoprotein (HDL), which is responsible for transporting cholesterol away from the arteries to the liver where it is metabolised. This role has caused HDL to be named ‘good cholesterol’, such that high levels of HDL appear to afford protection against heart attack. Thus there is an inverse correlation between levels of HDL and atherosclerosis.

Alcohol : Direct and indirect impacts on body health

There are at least two ways in which an alcoholic beverage such as beer might impact bene cially on the body: rst, through a direct physiological impact on bodily tissues and functions (which will be focused upon here); second, through indirect impact, but founded equally on a physiological interaction. The mellowing in uence that moderate consumption of alcohol has, with its calming and relaxing impact, will of itself have a sparing effect on stress-related illnesses (Morrell 2000). Cleophas (1999) concludes that there is a signi cant psychological component in the bene cial relationship between moderate alcohol consumption and mortality.
In either instance it will be recognised that excessive alcohol consumption will shift the status quo in a negative direction. We will address the incontrovertible direct damage to body organs that can be caused by overconsumption, and there is no denying the antisocial impact of excessive alcohol consumption in terms of behavioural changes and drink driving. One problem emphasised by many writers is the impact of underreporting alcohol consumption.
Dr Thomas Stuttaford (who for years has written a most engaging column in The Times) presents a fascinating experiential account of the likely reasons why his patients in rural Norfolk enjoyed a lesser incidence of cardiovascular problems and tended to live longer than did their counterparts in London (Stuttaford 1997). First, they had enjoyed less sedentary lives, with less dependence on the automobile. Second, they took aspirin daily to counter the osteoarthritis brought on by working in soggy agricultural conditions. Third, they weren’t teetotallers. And their chosen drink was beer, with the occasional celebratory whisky. It is of course not possible to con rm with any certainty that there was a causal link between any of those three factors and Stuttaford’s observations on mortality. Indeed, the reader will recognise the dif culty of pursuing robust research in this entire area, for the simple reason that studies relating health to any type of food intake must inherently try to remove as many interfering factors as possible and this is not easy:

Additional methodological problems are presented by a number of ‘confounding
factors’ such as age, sex, body mass index, diet, physical activity, smoking, coffee
consumption, educational attainment, type A/B behaviour, socio-economic status,
and medical history, that may be factors in particular health problems in persons who have been the subjects of the reported studies. For example, a generally
poor nutritional condition could possibly play a signi cant role in various health
problems associated with heavy drinkers.
Butterworth (1993)

Studies based on individuals’ reporting of their dietary intake are not as controlled as those in which feeding trials are performed with laboratory rats with de ned diets. Yet, of course, what is observed with a rat does not necessarily extrapolate to the human. We must critically evaluate the breadth of evidence that is presented. Most assume that if suf cient evidence of diverse origin is offered then ‘there must be something in it’. Much of the attention that has been paid to the impact of alcohol on the body has been for its negative effect on those who abuse it. These effects are amply described in the Oxford Textbook of Medicine (Weatherall et al. 1996) and, in more prosaic form, by Stuttaford (1997). In the discussions that follow I refer to these impacts and the reader is referred to those texts for more information.

The Impact of Alcohol on Health

The effect alcohol, including in the form of beer, might have on the overall state of healthfulness of the body. What harm might it do and might it actually do some good? And let us start from a baseline statement that alcohol is relatively non-toxic, with an oral LD50 for the rat of 13.7 g/kg (i.e. the amount of ethanol which will kill half of the animals in an experimental population) (Bakalinsky and Penner 2003) Increasingly the evidence is that there appear to be bene ts in drinking beer (and other types of alcoholic beverage). Guallar-Castillon et al. (2001) concluded that the consumption of total alcohol (wine and beer) was associated with a lower prevalence of sub- optimal health. Hospitalisation is less acute for daily moderate drinkers (Longnecker & McMahon 1988), especially for women who had consumed between 29 and 42 alcoholic beverages in the fortnight prior to lling in the questionnaire. Artalejo et al.
(2000) found that moderate drinkers in Spain were less likely than abstainers to use healthcare services. Meanwhile Wiley and Camacho (1980) showed that moderate alcohol consumption (17–45 drinks per month) was associated with the most favourable adjusted health scores.
Beer drinkers were shown by Richman and Warren (1985) to have signi cantly lower rates of morbidity (sickness) than expected – one drink per day giving 15% less disability than was the case for the general population. There will be those reading this who will not be able to countenance such ndings.
If these people nd it hard to swallow that drinkers, imbibing in moderation, could be less ill, then they might note that they have certainly not been shown to be more sick. However, we must stress always that many of these studies are dealing with correlation, not necessarily causality. Some will argue that there may be other confounding factors not explored in the studies, and that those who tend to drink in moderation may have other lifestyle attributes that are the true reason for their enhanced healthiness. However, the sheer frequency of studies that have demonstrated the bene ts of restricted alcohol intake, weigh heavily in support of the merits of sensible drinking.
In the mid-1990s, the Department of Health within the British government addressed the matter of recommended safe limits for drinking. After (we presume) careful consideration of the scienti c and medical evidence available up to that stage, they increased the recommended limit for men from 21 units to 28 units per week, with the advice to
women being to drink no more than 21 units per week (previously it had been 14). They stressed that the daily maximum should be 4 units and that binge drinking (the equivalent of taking all of the weekly allocation at one sitting) is absolutely undesirable.
Individuals differ substantially in their bodily response to alcohol. Various factors will play a role, including body weight, general state of health, amount of activity, and whether the alcohol is being consumed on its own or alongside food. The UK guidelines are precisely that: blueprints to give some guidance to people to judge sensibly what is and what is not an advisable amount of alcohol to consume. They are not recommendations to drink: they are certainly not instructions. Rather they are a common-sense judgement on what is likely to be healthful for a sensible and healthy adult. And the fact that the levels were increased is testimony to the burgeoning evidence that there is real merit in moderate consumption of alcohol.
The author of a newspaper article in California once highlighted the number of times I had invoked the word ‘moderation’ when she interviewed me. I make no apology for using the word again here (particularly as a glance at the thesaurus in my computer offers the word temperance as a suggested alternative!). As the reader should surmise from what follows, there is more than ample evidence for the harmful effects of sustained, heavy intake of alcohol in all its forms. However, it will be noted that the serious ailments are primarily associated with extreme alcoholism, and a consequence of vastly more alcohol ingestion than is the norm for the great majority of adults.

Beer: a vice or a staple part of the diet?

Were we able to transport ourselves back to the Middle Ages and enquire in England, Flanders, Bavaria or Bohemia about the key features of the popular diet, ale or beer would unquestioningly and unhesitatingly be listed alongside meat, bread, milk and vegetables. The questioner would be regarded as being mightily peculiar if he or she were to question ale’s legitimate place on the table. It was neither a comfort food nor an extravagance. It was an integral part of the food intake in all walks of society. In eighth-century England a monk might consume eight pints of ale a day. Beer in Britain has long been considered to be a key part of the diet, as much so as wine in France. Henry Brougham MP (Brougham 1830) said that ‘To the poor the beer is next to a necessity of life.’
Over 50 years ago the nutritive value of beer was emphasised. An admittedly weakish beer [3% alcohol by volume (ABV) in the austere early post-war years] was claimed to provide 200 calories and a fth of a working man’s requirement for calcium, phosphorus,nicotinic acid and ribo avin (Bunker 1947). The satisfaction of having at least part of one’s dietary intake in a pleasurable form was not sneered at then.
Perhaps the rst person to conduct a serious study of the impact of abstinence, moderation and excessive drinking on health was statistician Raymond Pearl. On the basis of interviews with over 2000 workers in Baltimore, he concluded almost 80 years ago that on average moderate drinkers lived longer than abstainers and much longer than those who were heavy drinkers (Pearl 1926).
Yet now, at the dawn of the twenty- rst century, beer-drinking is regarded in many societies as a vice. It is surely astonishing that in the United States it is possible to buy cigarettes at the age of 18, but it is not legal to purchase alcohol until the age of 21. It would be a struggle to identify any merit associated with smoking, with the possible exception of its role as an anxiety relaxant. By contrast there is accumulating evidence that alcohol, including beer, in moderation can have a bene cial impact on health and wellbeing.
In passing, let us consider the legal age at which, in the US, it is possible to partake of other activities that surely might be considered a genuine risk to health and wellbeing, not only for the partaker but also for those around them. A child may legally drive a car, with relatively few restrictions, at the age of 16. More alarmingly, 35 states in the US have no licensing or registration requirements for guns (www.soros.org/crime/ higlights.htm). Seven states lack a legal minimum age for buying a ri e or shotgun from an unlicensed dealer, while six states have no legal minimum age for a child to possess a handgun. In ve states there is a minimum age – 16 in New York, Georgia, Vermont and Alaska, and just 14 in Montana. But the minimum legal age for drinking alcohol in all 50 states is 21!
Opinions about the relative merits and de-merits of smoking, driving, guns and alcohol will of course differ between individuals. Certainly if we consider the respective virtues of smoking, weapon use and alcohol (in restraint), then it seems to this author that there may be a warped set of priorities in one country at least. Nonetheless beer is the second most popular drink in the United States, with annual average per capita consumption at 357 8-ounce servings, after sodas and other soft drinks (861) (Beverage Digest 1998). Worldwide production of beer in 1999 ran at 0.13 billion litres.

Several drugs and hormones have an effect on body weight.

Some hormones cause weight gain and others cause weight loss. Hormones that cause weight gain are of particular interest, because if researchers can study and understand how they work, they may be able to develop drugs that can interact with these hormones in a way that makes it easier for people to lose weight. Insulin is a hormone that helps turn glucose (the sugar found in food) into energy the body can use. High levels of insulin lead to weight gain, although the reason why is not fully understood. Drugs used to treat diabetes, such as insulin and medications that make the body produce more insulin, cause weight gain. Obese people often have higher levels of naturally occurring insulin than their leaner counterparts.
Female hormones, like progesterone and estrogen, are associated with weight gain. Obese women most commonly begin to gain weight after puberty, when their bodies begin to produce these hormones. Birth control pills contain estrogen and progesterone, and are associated with weight gain. Today, birth control pills cause less weight gain than in previous years because they contain lower levels of estrogen. Some women may gain more weight than usual during pregnancy, up to 110 pounds (50 kg), which may be related to differences in their hormone levels during pregnancy, as compared to other pregnant women. Women who gain excessive weight during pregnancy may never fully lose this weight. Changes in hormone levels also occur during menopause. These hormone changes lead to a change in fat distribution, including increased central obesity (fat around the midsection or waist). This fat distribution is associated with increased health risks, especially heart disease.
Thyroid hormones increase metabolism and cause weight loss. People with the disease hypothyroidism (underactivity of the thyroid gland) have a smaller amount of thyroid hormone. People with hypothyroidism are predisposed to weight gain.When these individuals are treated with a drug that contains thyroid hormones, they lose weight. Thyroid hormones are dangerous in very high levels and must be monitored closely when taken. An excess of thyroid hormones in the blood can lead to several health problems, including high blood pressure, nervousness, insomnia (trouble sleeping), menstrual cycle changes, heart palpitations (the feeling that the heart is pounding), and fever. Several hormones that may play a role in weight gain have recently been discovered. One of these is leptin, a newly discovered hormone produced in fatty tissue. Increased leptin decreases food intake and increases metabolism in rats and, according to some early studies, in humans as well. Other hormones released by the stomach—including neuropeptide Y, cholecystokinin (CCK), enterostatin, and polypeptide Y 3-36— tell the body it has consumed enough food and should stop eating. Another hormone, ghrelin, is produced by the
stomach. Ghrelin signals hunger and increases appetite.
Ghrelin concentrations increase in response to weight loss. This may make ghrelin partly responsible for people gaining weight back after a successful diet. Table 2.2 lists some of the hormones that influence body weight. Clearly, many hormones affect body weight. Some of these hormones are known, and some have not yet been discovered. By studying these hormones researchers can better understand what causes people to gain and lose weight. Eventually, researchers may be able to develop drugs that can change levels of these hormones in the body, thus giving people who are overweight or obese another weapon in the weight loss battle. Intensive study is required to identify the possible negative effects of increasing or decreasing the level of hormones in the body.

HEALTH RISKS ASSOCIATED WITH OBESITY

Obesity is currently the second leading cause of preventable death in the United States.1 Being overweight and obese can contribute to death by causing or worsening many different diseases, including but not limited to:

• High blood pressure;
• High cholesterol (overweight individuals often have higher levels of “bad” cholesterol and lower levels of “good” cholesterol);
• Obstructive sleep apnea (a condition where a person may stop breathing for a period of time while sleeping);
• Rheumatoid arthritis and osteoarthritis;
• Certain types of cancer, including breast, esophageal, stomach, colorectal, endometrial, and kidney cancer;
• In women: menstrual disturbances, infertility problems, and an increased incidence of birth defects in children;
• Increased daytime sleepiness and heat intolerance;
• Obesity may also contribute to gallbladder disease, gout, breathing problems, increased incidence of infections, liver diseases, and increased pain, especially in the lower back and knees.
  

Two of the biggest health problems that overweight individuals face are a greatly elevated risk of heart disease and stroke. The American Heart Association (AHA) has found a direct link between these health conditions and being overweight. Heart disease is now the number-one killer of women in the United States, and the rise of overweight and obesity can be directly correlated to it.
A person’s risk of developing these health conditions increases as his or her BMI increases, so obese individuals are at higher risk than overweight individuals. Weight loss of even 10 to 15 pounds (4.5 to 6.8 kg) in adults and children can decrease the risk of developing health problems such as diabetes and hypertension. This weight loss can also help to control or lessen the severity of these conditions in patients already afflicted with these conditions. As previously noted, adults with central obesity are at higher risk of developing many of these conditions than are people with evenly distributed body fat.
Obese children also have an increased incidence of health problems.As the prevalence of obesity has increased in children, there has been a similar rise in diseases that were previously rare in children, including type II diabetes and hypertension (high blood pressure). There is a high incidence of obesity among children with asthma, which may indicate a link between the two conditions. There is also an increase in bone and joint complications in obese children. During childhood, bone and cartilage is still growing and developing, and is not strong enough to bear excess weight.

The Link between Weight and Health

Weight and health are strongly related to each other. Disease risk goes up slowly as weight gain pushes you out of the healthy weight range and into the overweight range.Your risk of disease and death increase significantly if extra weight puts you in the obese range. One study reported that obesity in middle age reduces life expectancy by seven years.
The list of weight-related diseases continues to grow. Increased weight raises blood lipids (cholesterol and triglycerides) and blood pressure, which are heart disease risk factors.Weight gain impairs the body’s ability to handle glucose (blood sugar) and contributes to a prediabetic condition called insulin resistance. Other medical conditions that are associated with increased weight include certain cancers, osteoarthritis of the knees and other weight-bearing joints, gastrointestinal tract disturbances, interrupted sleep and sleep apnea, and reduced fertility.To date, obesity has been linked with more than thirty medical conditions.
As weight goes out of the healthy range, risk increases for
• Heart disease
• High blood pressure
• Stroke
• Diabetes
• Several forms of cancer
• Metabolic syndrome (Syndrome X)
• Gallbladder disease
• Gout

It is not just big gains that carry ill health effects—the consequences of gradual or modest weight gain add up quickly. Even 10 or 20 extra pounds increases the risk of death among adults, as shown in a large study published in the New England Journal of Medicine.A recently published study found that just a 5% increase in the BMI over time had a negative impact on simple body functions like walking. Research on women, weight gain, and cancer found that women who gained 21 to 30 pounds since age 18 and were not on hormone replacement therapy were 40% more likely to get breast cancer than women who had gained no more than 5 pounds. The risk increased as the women’s weight increased. Similarly, another study found an 8% increase in the
risk of postmenopausal breast cancer for every 11 pounds gained.

Environmental Factors,Causes of Obesity

Along with genetics, environmental factors have been found to contribute to obesity. In particular, increased food consumption and an inactive (sedentary) lifestyle are environmental factors that very closely correlate with an increased risk of obesity. Americans have an ever-increasing number of energydense foods, packaged in enormous portions, conveniently available at low cost. Energy-dense foods contain large numbers of calories in very small portions. These foods promote the overconsumption of calories. Americans also consume 40% of their calories from fats, which is well above the level recommended by the American Heart Association (AHA). Fats are an extremely energy-dense form of nutrition. The AHA recommends that adults obtain less than 30% of their daily calories from fat. In the United States and in other developed countries, modern technology allows people to be less active in their daily tasks, since many things today are automated and do not require manual labor. For example, years ago people walked to most places. Today, people have access to cars and public transportation to take them to these same places, thus limiting the need for physical activity.
Decreases in physical activity can lead to weight gain. Ultimately, all the calories you eat are not utilized, or burned off. Calories that are not utilized are stored as fat tissue, which can lead to weight gain. Sedentary behavior is on the rise now that technology and automation are so widely available. All of the modern conveniences we now have accessible to us have eliminated the need for individuals to perform much of the physical activity that was once required for daily tasks at work and home (Table 2.1). Computers, cable and satellite television, movies on demand, and high-tech toys like video game systems have led to a decrease in physical activity in people of all ages. Reduced physical education requirements in schools across the nation have also caused physical activity to decline among adolescents. The CDC estimates that 70% of adults in the United States fail to meet minimal recommendations for physical activity. It also estimates that
about one-third of people over the age of 18 get no leisuretime physical activity at all.
Other environmental factors that have been linked to obesity are lower economic class, lower education level, and cessation (quitting) of smoking. The link between economic level, educational background, and obesity is not clear. One theory is that a person who is illiterate may not be able to read labels on food and may not be aware he or she is consuming high-fat, high-calorie foods that can lead to obesity.High-fat, high-calorie foods, such as the food served at most fast-food restaurants, are formulated to be cheap and great tasting. This food is readily available and affordable for people with lower incomes and it is speculated that these people may consume more of this type of food, which can lead to obesity.
People who quit smoking are also likely to gain weight and potentially become obese. It is believed that the nicotine withdrawal a person experiences when he or she quits smoking causes an increase in appetite that leads to an increased intake of calories and, thus, weight gain. This trade-off is not an easy one to handle. The harmful effects of smoking are many and include lung cancer, bronchitis (an infection of the tube that brings air to the lungs), and emphysema (a condition that results in labored breathing and increased risk of infections). Many people who quit smoking trade one health risk (smoking) for another (obesity) because they gain weight.

Genetics,Causes of Obesity

Genetics clearly play a role in obesity. It has been noted that an
adopted child’s body weight is usually more similar to the body
weight of his or her biological parents than that of his or her
adopted parents. Identical twins usually have similar occurrences
of obesity. Studies have also shown that fraternal twins
do not show this same likelihood of obesity; when one twin is
overweight, the other is very often not. These examples help
demonstrate that genetics play a significant role in obesity.
Researchers participating in the Human Obesity Gene
Map project are in the early stages of determining which genes
contribute to obesity in people. Several alterations in normal
genes have been discovered in laboratory rodents and linked to
obesity in these animals. These genes include the ob or lep gene
and the Agouti gene. Researchers are working to find out if
these same genes contribute to obesity in humans.
Not all people who have obesity genes will be overweight.
Conversely, some people who are overweight will not have
these genes. This is because environmental factors also play
a major role in causing overweight and obesity.

WHEN ARE DIET PILLS, ERECTION, HAIR GROW DRUG RECOMMENDED?

DIET PILSS NEED?
Overall, in carefully selected patients, a doctor may prescribe appropriate drugs to be used in conjunction with diet and exercise to achieve weight loss. The only drugs recommended for use by the National Heart, Lung, and Blood Institute (NHLBI) are those that have been approved by the U.S. Food and Drug Administration (FDA). FDA-approved drugs have been studied and determined to be safe and effective for some, but not all, people.
According to the NHLBI, people who are appropriate candidates and should consider taking diet pills are adults with a BMI of greater than 30 kg/m2 or those with a BMI of higher than 27 kg/m2 who have health problems related to being overweight. Diet pills, like any other medication, have risks associated with their use. Therefore, diet pills should only be used by people who are at high risk of developing weight-related health problems. For people who are obese or overweight, the benefits of weight loss are generally greater than the risks associated with taking slimming pills. Several slimming pills have been studied for use in children; however, doctors only recommend using them in extreme situations.
The National Institutes of Health (NIH) has established guidelines on the use of diet pills. These guidelines are used by health-care practitioners both within and outside the United States. The information contained in these guidelines helps to determine who should and should not use weight loss medications. This is important because people who use diet pills inappropriately risk potentially devastating effects on their health.
ERECTION DRUGS NEED?When a man is aroused, nerve signals are sent from the brain and around the penis. These nerve signals cause chemicals to be released that relax the muscles in the penis. Normally, these muscles are constricted so that blood cannot flow into the penis. When these muscles relax, large amounts of blood are able to enter the penis, causing an erection. An erection is reversed when another chemical (known as phosphodiesterase type 5 [PDE5]) breaks down the chemicals that caused the muscles to relax in the first place. This causes the muscles in the penis to constrict again as blood leaves the penis. Cialis works by blocking PDE5. When PDE5 is blocked, more of the chemicals responsible for the erection remain, so the muscles in the penis do not constrict. This allows blood to stay in the penis longer, which allows the man to maintain an erection.
HAIR GROW DRUGS NEED?With at least forty treatments for baldness patented in 1996 and $200 million budgeted for clinical trials in 1997, you'd think someone might have figured out by now why men lose hair. But the lab guys know only one big thing: Hair follicles shrink and die. They've proved that this tragedy is triggered by the body's especially potent testosterone derivative, DHT. But researchers can still only theorize about why the perfectly normal presence of DHT leaves some otherwise healthy men mourning their hair as it swirls down the drain.
Propecia, the next treatment to grind its way through the FDA-approval machinery, probably within the year, will be Merck's promising finasteride tablet, Propecia. Finasteride inhibits the enzyme that turns testosterone into DHT--the first domino in the chain reaction that ends in follicle death. It first appeared in the guise of Proscar, a drug that combats prostate enlargement, another problem caused by DHT. Merck's trial results have raised high hopes for Propecia's effectiveness: More than half of those treated had "clinically significant increases in growth of new hair." Some baldsters, wanting to get the jump on the approval process, are already cadging prescriptions for Proscar from their physicians.