CAFÉ & CAFEÍNA

Os efeitos do café no ser humano não podem ser comparados ao da cafeína isolada.

A substância mais pesquisada e conhecida do café é a cafeína, descoberta na Alemanha em 1820 pelo químico Ferdinand Runge. Deste então a ciência médica dedicou uma atenção quase que obsessiva e exclusiva à cafeína e muito pouca aos demais compostos bioativos do café, como a niacina, sais minerais e os ácidos clorogênicos/quinídeos, dentre centenas de outros, a maioria voláteis. A grande maioria dos artigos médico-científicos avaliam os efeitos da cafeína sobre o organismo humano ou sobre tecidos isolados, algo que não pode ser extrapolado para o café. Caso a ciência fosse realmente rigorosa, poderíamos dizer que ainda são necessários mais estudos com o café (café torrado e moído, café solúvel, café descafeinado, etc), particularmente conhecendo o teor final de seus componentes, pois a maioria deles, ao contrário da cafeína, que é termoestável, são termolábeis. Por isto nem todos os cafés possuem a mesma composição e assim os mesmos efeitos sobre o organismo humano.

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A SUMMARY OF THE PHYSIOLOGICAL EFFECTS OF CAFFEINE

Soon after drinking a cup of coffee, or tea or cola, caffeine is distributed throughout the body. As it is similar to substances normally present in the tissues, caffeine could affect all the systems of the body: nervous, cardiovascular, respiratory and so on. However, caffeine does not accumulate in the body, so its effects are short-lived and transitory.

Whether or not caffeine's effects are physiologically important (or even noticeable) depends on a number of factors. Every individual reacts differently to caffeine. For example, caffeine may stay in the body of pregnant women for up to 3 times as long as is usual in adults, whereas smokers eliminate caffeine twice as quickly as non-smokers. This may help to explain why women often feel more sensitive to coffee in the latter stages of pregnancy, or why heavy smokers are usually heavy coffee drinkers as well. Some of the effects of caffeine, such as those on the heart and blood vessels, are contradictory and have no net effect - others may only be noticeable when regular consumers suddenly cut out caffeine. The body can become habituated to caffeine so that regular users are less sensitive to the stimulant effects than others. In fact, people tend to regulate their coffee consumption according to their experience - as many cups of coffee in the morning as they find give a pleasant, stimulating effect - perhaps none a few hours before going to bed.

Of all the physiological effects of coffee, the best known is that it is a stimulant to the nervous system. One or two cups of coffee can make one feel more awake, alert and able to concentrate. Caffeine has been shown to counteract fatigue and restore flagging performance. However, in sensitive individuals, caffeine may delay the onset of sleep, decrease sleep time and even lower the subjective quality of the sleep. Caffeine has various effects on mood, ranging from pleasant stimulation and mood elevation to anxiety, nervousness and irritability, but these are transient and dose-related.

Other physiological effects of caffeine, in the short term, include increases in blood pressure, plasma catecholamines, plasma renin and serum free fatty acids; the production of urine and of gastric acid are also increased. Regular consumption in normal individuals rapidly leads to tolerance and has no adverse effects.

The vast bulk of scientific and epidemiological evidence points to the conclusion that normal, regular consumption of coffee and caffeine containing beverages is not associated with heart or cardiovascular diseases, damage to the foetus, benign breast disease or cancer of any kind. Some people with irregular heartbeat syndromes may choose to drink decaffeinated coffee since caffeine has been known to precipitate arrythmias or ventricular premature beats, as do alcohol, exercise, stress and many drugs.

Standard reference

Evaluation of Caffeine Safety, a scientific status summary by the Institute of Food Technologists' Expert Panel on Food Safety and Nutrition, 1987. Food Technology, Institute of Food Technologists, Chicago, 41(6):105-113.June 1987

CAFFEINE CONTENTS

COFFEE

The amount of caffeine in a cup of coffee can vary greatly, depending on its origin or the composition of the blend, the method of brewing and the strength of the brew. Instant, or soluble, coffee generally contains less caffeine than roast and ground coffee, but may be consumed in greater volume. Robusta coffees have about twice as much caffeine as arabicas. A 'cup' is usually understood to contain 150 ml (5 oz in the United States) but an espresso may be as small as 40 ml.

The U.S. Food and Drug Administration gives the following ranges for caffeine contents:

(mg per 5 oz cup)

	range	average
Roast and ground -drip method -percolator	60-180 40-170	115 80
Instant coffee	30-120	65

Consumer surveys

An interesting survey of caffeine contents in cups of coffee was conducted in Canada (Stavric et al, reference below). Whether the coffee was prepared by housewives at home, for sale in commercial outlets, or by individuals at work, the mean caffeine content was about 80 mg per cup (about 350 mcg per ml). The means for roast and ground coffee, both drip and percolator brewed, were below 85 mg; for instant coffee 71 mg. However, the range of measurements was so wide that, for most individuals, it would be inaccurate to use these figures as a basis for calculating the exact amount of caffeine consumed in a day. The size of the cup/serving varied from 25 ml (Greek coffee) to 330 ml at home and from 130 ml to 280 ml in the out-of-home situation.

DECAFFEINATED COFFEE

Whatever method of decaffeination is used, the decaffeinated green coffee must contain less than 0.1 % caffeine (dry weight basis) to comply with EC regulations. This corresponds to about 3mg caffeine in a cup of decaffeinated coffee.

OTHER BEVERAGES

Tea contains more caffeine than coffee weight for weight, but less weight is used, in general, to brew a cup of tea. In the Canadian study referred to above, both the type of tea used and the steeping time affected the caffeine concentration of samples prepared in the laboratory as follows:

(mean, mcg per ml)

	2 minutes	5 minutes
Tea-bag	238	402
Loose tea	189	295

The average caffeine concentration of samples of tea prepared at home was lower, at 159 mcg per ml, but with a wide variation.

The caffeine content of a cup of tea is usually less than 60 mg, but a strong cup of tea may contain more caffeine than a weak cup of regular coffee.

Cocoa and chocolate drinks contribute 4-Smg caffeine per cup to the diet, dark chocolate and cooking chocolate 20-26mg per ounce (0.7-0.9mg per gram). Many soft drinks, including colas and "peppers", contain caffeine, which as well as being present in cola nuts is often added as a flavour ingredient. A 12-ounce serving may contain 30-60mg caffeine. The major brands of cola on sale in the UK contain about 120mg caffeine per litre.

DRUGS

Caffeine is present in many prescription and non-prescription (over-the-counter) drugs, including some taken for headache, pain relief, appetite control, staying awake, colds, asthma and fluid retention. The caffeine contents of drugs varies from 7mg to 200mg per tablet.

LEVELS OF CAFFEINE CONSUMPTION

Caffeine is generally consumed in amounts less than 300mg per day, roughly equivalent to:

3-4 cups of roast and ground coffee

5 cups of instant coffee

5 cups of tea

6 servings of some colas or

10 tablets of some painkillers

It has been suggested that the British consume more caffeine on average than Americans, but there are no large scale studies to support the observation. The nine, normal subjects recruited by Dr M.S. Bruce and his colleagues, as habitual caffeine users, for a study in London (reference below) were found to consume on average 428mg caffeine a day, with a range from 230mg to 670mg.

Customary caffeine consumption has been classified as follows:

Low caffeine users: less than 200mg per day

Moderate caffeine users: 200-400mg per day

High caffeine users: more than 400mg per day

References

Bruce M.S. et al. British Journal of Clinical Pharmacology,22: 81-87. 1986.

Lecos C. The latest caffeine scorecard. FDA Consumer, March 1984.

Stavric B. et al. Variability in caffeine consumption from coffee and tea: possible significance for epidemiological studies. Fd Chem Toxic 26(2):111-118. 1988.

NEUROIMAGEM & ALCOOLISMO

Apesar de a Organização Mundial da Saúde reconhecer o alcoolismo como doença desde 1967, muita gente ainda acredita que parar de beber é, sobretudo, questão de força de vontade. Avanços recentes nas técnicas de imagem cerebral, entretanto, comprovaram que a dificuldade de se livrar do vício é muito mais resultado de falhas do cérebro do que de falta de determinação.
Tomografias e ressonâncias magnéticas mostram que o excesso de bebida “reesculpe” conexões cerebrais, destruindo a capacidade de a pessoa sentir prazer sem beber e de agir conscientemente. Não é à toa que, a cada ano, 500 mil pessoas se internam em clínicas de desintoxicação nos EUA e outro 1 milhão procura o Alcoólicos Anônimos (AA). No Brasil, levantamento do Hospital das Clínicas (SP) aponta que 15% da população abusa de álcool.
As alterações que a bebida provoca no cérebro ajudam a entender por que mesmo os métodos mais eficientes de combate ao vício, como o do quase septuagenário AA, apresentam taxas de sucesso que não ultrapassam 50%.
“As pesquisas feitas a partir de imagens do cérebro de alcoólatras corroboraram o que a gente já sabia pela observação. Os pacientes bebem compulsivamente porque o excesso de álcool provoca alterações cerebrais, e não por serem sem-vergonhas”.
Após cair na corrente sangüínea, o álcool segue para uma região do cérebro conhecida como núcleo accumbens, onde ocorre um aumento de concentração de dopamina -neurotransmissor ligado à sensação de prazer.
O consumo abundante e repetido da bebida faz com que a ligação entre álcool e prazer fique registrada no córtex frontal. É essa memória que cria a obsessão pelo álcool, transformando o beber social em compulsão. Estudos recentes com animais em laboratório indicam que a bebida também modifica a estrutura dos gânglios basais, causando danos semelhantes aos observados em portadores de transtorno obsessivo-compulsivo.
O cérebro reprogramado pelo álcool passa a demandar martinis, uísques e vodcas com freqüência e em quantidades cada vez maiores. Uma imagem do drinque é suficiente para detonar o desejo incontrolável de beber, como demonstram imagens do cérebro de alcoólatras em recuperação.

Medicamentos

Além de derrubar de vez o mito de que o alcoólatra não abandona o vício porque não quer ou porque é fraco, os avanços nas técnicas de neuroimagem estão ajudando também no desenvolvimento de medicamentos que aumentam as chances de cura.
É o caso do acamprosato, disponível no mercado brasileiro há menos de seis meses e que alivia os sintomas da síndrome de abstinência e, assim, ajuda a evitar recaídas. A prescrição para indivíduos com insuficiência hepática ou renal é sua única contra-indicação.
Há cerca de dois anos no mercado, o naltrexone também diminui a compulsão e ajuda o alcoólatra a permanecer abstinente. Antes desse medicamento, a única droga aprovada nos EUA para tratar a dependência do álcool era o dissulfiram.
O remédio impede que o álcool ingerido seja metabolizado e causa náuseas, aumento da pressão arterial, rubor facial e grande desconforto em quem bebe. “Ele funciona como um breque psicológico e ajuda o paciente a mudar de hábito, mas não diminui o desejo”.Os novos remédios aumentam as chances de sucesso, mas não são panacéia e só surtem efeito quando combinados a tratamentos tradicionais, como terapia cognitiva (em que o paciente discute o que o leva a beber e aprende estratégias para se afastar do vício) e aconselhamento grupal.

Neuroimaging Identifies Brain Regions
Possibly Involved in Alcohol Craving
News Release from NIAAA

Viewing pictures of alcoholic beverages activates the prefrontal cortex and the anterior thalamus in alcoholics but not in moderate drinkers, report Medical University of South Carolina (MUSC) researchers in the April Archives of General Psychiatry.

The research team is the first to use fMRI (functional magnetic resonance imaging) to examine whether alcohol cues stimulate specific brain regions.

"The activated brain regions are known to be associated with attention and regulating emotion and are prominent components of working models of alcohol craving," said National Institute on Alcohol Abuse and Alcoholism Director Enoch Gordis, M.D. "Whether the activity in these areas accompanies craving or is in part responsible for it remains to be determined."

"The regions activated in this study should not yet be interpreted as correlates of craving per se," said lead author Mark S. George, M.D., of the Departments of Psychiatry, Radiology, and Neurology at MUSC. "Our next project uses fMRI scans to measure subjective craving in real time so that we can relate subjective craving temporally to the presentation of visual cues."

Unique Brain Activity

For the current study, the researchers recruited eight male and two female alcoholics and an equal number of moderate-drinking (no more than 14 drinks per week) controls matched according to age and gender. The alcoholics met DSM-IV criteria for alcohol dependence, drank an average of seven drinks per drinking day, and drank on about 70 percent of days in the month before testing. They were not severe alcoholics or in treatment at the time of study.

All 20 subjects viewed pictures on a screen while lying on their backs in a 1.5-Tesla MRI scanner. For nine minutes, they were shown a series of photographs of alcoholic beverages followed by a series of nonalcoholic beverages (e.g., coffee, juice, soda) in random order.

To heighten their responses to alcohol cues, the subjects were given a sip of an alcoholic beverage before viewing the images. The researchers compared mean group images of brain activity during the alcohol and nonalcohol pictures, exposing in the alcoholic group several brain areas with unique activity during the alcohol pictures.

"Our goals were to learn whether certain brain areas would be activated for the alcohol cues but not the neutral cues and whether brain areas in alcoholics would be activated differently than those of moderate drinkers," said Raymond F. Anton, M.D., a lead study author and Scientific Director of the NIAAA-funded MUSC Alcohol Research Center. "In fact, we saw clearly that certain brain regions in alcoholics activated in response to viewing pictures with alcohol-specific content. It appears that the alcoholics paid greater attention to the alcohol images."

"This work confirms a significant biological and brain component to alcoholism and provides information toward understanding the differences between alcoholics and nonalcoholics," said Dr. George.

Neuroadaptation

Future studies may examine regional brain activity following the administration of naltrexone, a medication believed to reduce alcohol craving, say the authors. Imaging studies are expected eventually to predict risk for both uncontrolled drinking and relapse and to evaluate potential anticraving medications.

Although many alcoholics report craving, an intense desire or "drug hunger" for alcohol, researchers have not arrived at a common understanding of the phenomenon. Most agree that craving involves neuroadaptation -- changes in brain cell function resulting from long-term alcohol consumption. Neuroadaptation produces an imbalance in brain activity and enhanced memories of alcohol reward that may increase drinking or, during periods of abstinence or reduced drinking, lead to relapse. Alcohol-related stimuli known as cues may trigger the neuroadapted brain to crave alcohol.

While animal experiments suggest that craving is associated with certain brain regions (neuroanatomy) and neurotransmitters (neurochemistry), such models are limited by the animals' inability to report how they feel.

In humans, craving is experienced differently at different stages of alcohol addiction and differently among drinkers at any single stage, complicating attempts to measure it accurately. To improve both measurement and understanding of the craving phenomenon, researchers are looking to new technologies such as the fMRI technique used in this study.