The World of Caffeine (49 page)

The short-term effects of caffeine on blood pressure are just the opposite. People not used to caffeine experience an immediate increase in blood pressure, that is, a moderate pressor effect, and a related reduction in heart rate, or bradycardia, of brief duration, usually less than four hours. These effects apparently cease when caffeine is consumed regularly and a tolerance develops.
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These studies considered people with normal blood pressure. But what if your blood pressure is high to begin with? What will caffeine do to you then? In 1984 D. Robertson, a medical researcher, undertook a study of hypertensives and found that, as in the earlier study of people with normal pressure, acute responses of elevated blood pressure and slowed heart rate were observed to occur the first day and to disappear thereafter. Robertson concluded that the acute response to caffeine was actually less in hypertensives than in normal people, and that “tolerance developed rapidly and completely.” Other researchers have concluded that there was no association between caffeine consumption and all or any causes of mortality among this large group of hypertensives.

An interesting aside is that, in days gone by, caffeine was sometimes used by anesthetists during surgery to increase dangerously low blood pressure. Its effect was transitory, and it would not be considered reliable enough to be the drug of choice today. Dr. Adriani, who was the anesthetist in chief at Charity Hospital New Orleans for many years, describes this procedure in a 1940 textbook he wrote. One of his students gave the following account in 1996: “I’m a Vintage’ nurse anesthetist. In my salad days, I used caffeine sodium benzoate as a stimulant to raise a patient’s blood pressure, during surgery. It is no longer used, as there are better drugs available. The dose I used was .5 gram, given subcutaneously.”

Lipids comprise a group of organic compounds, including fatty acids, waxes, phospholipids, and steroids, that are stored in the body as fat and used as energy reserves. Lipids contain cholesterol, as do all animal fats, and elevated serum cholesterol levels are strongly correlated with heart attacks, strokes, and early death.

Since the phenomenon was first noticed in 1970, many studies have confirmed that the use of unfiltered (sometimes mislabeled “boiled”) coffee can contribute significantly to an increase in serum cholesterol levels in both men and women, especially in those whose levels were elevated to begin with. A 1990 thesis published in the Netherlands reviewing twenty-four studies differentiated the effects of different brewing methods. In conclusions supported by subsequent European studies,
the author found
filtered coffee produced little if any increase in cholesterol levels,
while in contrast unfiltered coffee was correlated with an increase amounting to as much as 15 percent. The fact that different brewing methods produce such a variation in effects on lipid levels may help explain why the cholesterol-raising effects of coffee have been shown to vary widely between different nationalities. A dramatic example of this effect is the substantial drop of cholesterol levels over the last fifteen years in Finland paralleling the change from infusion to filter-drip as the most popular method of brewing coffee.

Most researchers think that some strong, naturally occurring ingredient of coffee is responsible for these effects and that caffeine is in no way implicated. Roasting itself forms fatty acids such as cafestol, kahweol, and their derivatives. Most of these lipids remain in the spent grounds, but the amount that get into your coffee cup can vary from 1 to 40 mg, depending on the fineness of the grind and the method of preparation. Many researchers think that there is an as yet unknown substance, present in the oil of all coffees, that acts as a cholesterol-raising factor.
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In any event, caffeine consumption levels seem to have no correlation with cholesterol levels.

More significantly for lay readers, the Framingham Heart Study also found that levels of coffee consumption had
“no
influence on the rate of coronary heart disease,
”
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and the study found no evidence to support the hypothesis that the level of caffeine consumption is related to the death rates from strokes in hypertensive patients.

Hemostasis is any process which stops bleeding, notably including the body’s coagulation process, or clotting. Fibrinolysis is the process by which the body breaks down clots, averting thrombosis, a pathological condition in which a thrombus, or blood clot, forms within a blood vessel. In an artery supplying the brain, these clots can result in a stroke, and in an artery supplying the heart, they can result in a heart attack.

No effect by either coffee or caffeine on the coagulation process has been observed.

However, very curious and interesting effects of caffeine on fibrinolysis have been suggested by recent research. In order to understand the importance of these effects, consider that reduced fibrinolysis is strongly associated with an increase in heart attacks. That is to say, when the process of breaking down clots is rendered less efficient, the resulting undissolved blockages can become dangerous and even life threatening. Conversely, an increase in the efficiency of fibrinolysis can help protect against heart attacks; drugs are now used to boost the body’s ability in this respect, helping to dissolve blood clots that the body cannot handle. Because studies have found that clot-dissolving time is reduced by regular coffee drinking but remains unaffected by decaffeinated coffee drinking, many researchers think that caffeine is probably the agent responsible for this difference. If this is true, caffeine must operate in effectively the same way as certain pharmaceutical products designed to reduce the risks of heart attacks and strokes, thus counterbalancing the otherwise deleterious effects of coffee on clotting time.
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Asthma, a respiratory disorder marked by a reversible airway obstruction, with attending difficulty in breathing, wheezing, cough, and thick mucus production, is the most common breathing affliction. As many as 10 percent of children suffer from asthma to the extent that they require medical treatment.
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Caffeine, at first administered in the vehicle of strong coffee, has been used to relieve the symptoms of asthma for hundreds of years. Its primary respiratory effect is an increase in the respiratory rate, which corresponds closely with plasma caffeine levels. In patients with asthma, caffeine functions as a relaxant of bronchial tissue or a bronchodilator. Today, theophylline, another methylxanthine, is also widely used for the same purpose, because it has almost twice the potency in this respect and is thought to be less toxic to the central nervous system than caffeine. Widespread experience in treating newborns with caffeine for neonatal apnea, or arrested breathing, which often occurs in premature infants, has presented an unusual opportunity to study its possible toxic effects. Although some agitation does occur at the levels used in treatment, there is an absence of toxicity in newborns. However, as with other potential detrimental effects of the methylxanthines, a definitive answer about its possible effects on growth and development awaits further research, for which reason the treatment of infants with caffeine is discontinued as soon as possible, usually after only a few weeks.

Everyone knows from common experience that cigarette smokers have a far higher likelihood of being caffeine fanciers as well. Perhaps, as in Walsh’s words, “Under such a fact there may be more significance than science has yet elicited”—more significance than has been understood until recently, that is. Medical researcher D.R.Lima, in 1989, investigated the theory that
caffeine might help protect smokers against the development of chronic bronchitis and pulmonary edema.
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Both smokers and non-smokers were tested after smoking a cigarette with or without an accompanying cup of coffee. Coffee was found to provide protection against the adverse pulmonary effects of smoking. In researcher Jack James’ words, “The investigators concluded that regular intake of coffee might be beneficial to smokers in delaying the development of chronic obstructive lung disease.”
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Obviously more research is needed to define these benefits more precisely. However, based on current results
of studies of caffeine’s effects on pulmonary function, we can responsibly assert that caffeine may have important therapeutic potential in this respect.

In the 1970s, the American Heart Association recommended that people who wanted to quit smoking should concurrently stop drinking coffee and eliminate all sources of caffeine. Subsequent studies have suggested that the American Heart Association’s strategy only complicates matters. After all, sudden withdrawal from caffeine can have unpleasant consequences that certainly won’t ameliorate the withdrawal effects of stopping cigarette smoking and may even make them more difficult to cope with.

However, one caveat for those attempting to quit smoking is in order. We now know that cigarettes increase the rate of caffeine metabolism and shorten or attenuate its effects in smokers. This means that smokers must consume more caffeine to achieve the same effects as non-smokers, which may be one reason smokers drink more coffee than non-smokers. Therefore, cigarette smokers who are cutting down or eliminating tobacco should
reduce
their caffeine intake, especially if it was high to begin with, because, in the absence of smoking, caffeine will have a much stronger and longer-lasting effect on them than they had been accustomed to experiencing. To put it simply, if a heavy smoker is used to drinking four cups of strong coffee to wake up, he might find that, after discontinuing his cigarette habit, two cups will accomplish the same purpose.
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No disease inspires more dread than cancer, perhaps in part because, in our aging population, cancer’s incidence is on the rise. Although more potent treatments are developed every year, we are still far from attaining a complete understanding of what cancer is and what its causes are, and people are reasonably afraid of anything that they think causes the disease. In recent decades caffeine has sometimes been called a carcinogen; for example, a 1981 study created a concern more than a link with pancreatic cancer. As it turned out, this fear was unfounded.

Since early studies indicated a positive correlation between caffeine in high concentrations and cancer in animals, this connection has been widely studied. Results, however, have been contradictory, even though doses so high that they are unlikely ever to be experienced by people have invariably been used: Depending on the dose, the timing of administration, and the experimental protocol, caffeine appears to raise or lower cancer incidence.
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Much of the information putatively pertaining to caffeine as a possible cause of cancer is compromised by the fact that most studies have been based on usage profiles of coffee, not of caffeine itself, and because coffee contains more than 100 active chemicals, it presents a particularly complex matrix, within which it is difficult to disentangle the singular role of caffeine. We must wonder, for example, if or to what extent the suggestions of a positive correlation between coffee and bladder cancer are related to its caffeine content. Certainly skepticism about the role of caffeine is aroused when we consider those studies of bladder cancer in which the results of the use of decaffeinated coffee were indistinguishable from the results of the use of regular coffee.
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Coffee contains several other suspected carcinogens, including creosote, pymdine, and miscellaneous tars, all created by the heat of roasting,
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and some claim that the polycyclic aromatic hydrocarbons that are responsible for coffee’s taste and smell also cause cancer, although the fact that coffee contributes less that. 1 percent of dietary intake of these substances makes that notion seem alarmist.
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In addition, there are sticklers who admonish that carcinogenic dioxins in bleached coffee filters leach into the drink. To confuse matters even more, cafestol and kahweol, present in your cup of coffee in amounts proportional to the oil content, are non-mutagenic and in animal experiments have shown cancer-protective activity with relatively large doses.
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However, despite this confusion, because the possible relationship between coffee and cancer has been so extensively considered in the past thirty years, while there has been very little investigation of caffeine and cancer and tumor activity apart from the matrix of coffee, it is worth reviewing summaries of these results for whatever light they may shed on the question of caffeine.

Fibrocystic breast disease, a condition characterized by benign fibrous lumps in the breast, is not dangerous, but it can be very painful, and the cysts that it produces drive many women to their doctors for tests to rule out breast cancer. Since the late 1970s, some researchers have suspected a causal link between caffeine and this condition, and an early study suggested that caffeine abstinence might reduce symptoms of the disease. A 1986 National Cancer Institute (NCI) study of over three thousand women found no evidence of any correlation between caffeine use and benign tumors, fibrocystic breast disease, or breast tenderness.
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However, a subsequent study by the institute of more than fifteen hundred women concluded that women consuming 250 mg of caffeine (about as much as in two cups of coffee) daily experienced a 50 percent increase in the condition, while those consuming 500 mg experienced nearly a 150 percent increase. Such results have led one researcher to claim that a caffeine-free regimen supplemented by 800 mg of vitamin E daily can provide substantial relief for two-thirds of women with fibrocystic breast disease.
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