Legend has it that coffee was "discovered" around 850 AD in upper Egypt by a goat herded named Khaldi. One night, Khaldi's goats did not return home. When he found his goats, Khaldi saw them dancing around a shrub with red berries (coffee beans). After Khaldi tried some of the berries, he started to dance too. Khaldi spoke with some monks who used the berries to make a drink and....coffee was born!
Caffeine is an alkaloid from methylxanthines called 3,7-dihydro-1,3,7-trimethyl-1H-purine-2,6,-dione or 1,3,7-trimethylxanthine.
Caffeine may be the most popular drug in the world.
We consume caffeine in coffee, tea, cocoa, chocolate, some soft drinks, and some drugs. The actual source of caffeine is the coffee bean, tea leaf, cola nut, guarana. maté and cacao pod. Pure caffeine is odorless and has a bitter taste .
Theophylline is a dimethylxanthines that have two rather than three methyl groups 3,7-dihydro-1,3-dimethyl-1H-purine-2,6-dione; 1,3-dimethylxanthine ,
Is considerably weaker than caffeine and having about one tenth the stimulating effect of either. It has a stronger effect on the heart and breathing than caffeine. For this reason it is often the drug of choice in home remedies for treating asthma bronchitis and emphysema. The theophylline found in medicine is made from extracts from coffee or tea.
Caffeine has long been suspect of causing mal-formations in fetus, and that it may reduce fertility rates.
These reports have proved controversial. What is known is that caffeine does causes malformations in rats, when ingested at rates comparable to 70 cups a day for humans. Many other species respond equally to such large amounts of caffeine.
Caffeine also increases dopamine levels in the same way that amphetamines do (heroine and cocaine also manipulate dopamine levels by slowing down the rate of dopamine re-uptake).
Dopamine is a neurotransmitter that, in certain parts of the brain, activates the pleasure center. Obviously, caffeine's effect is much lower than heroin's, but it is the same mechanism. It is suspected that the dopamine connection contributes to caffeine addiction.
The binding of adenosine in brain causes drowsiness by slowing down nerve cell activity. In the brain, adenosine binding also causes blood vessels to dilate (presumably to let more oxygen in during sleep).
Caffeine binds to the adenosine receptor. So instead of slowing down, the cells speed up
Caffeine blocks adenosine reception so you feel alert. It injects adrenaline into the system to give you a boost. And it manipulates dopamine production to make you feel good.
Association of coffee and caffeine intake with the risk of Parkinson disease. Ross GW, Abbott RD, Petrovitch H, Morens DM, Grandinetti A, Tung KH, Tanner CM, Masaki KH, Blanchette PL, Curb JD, Popper JS, White LR. JAMA. 2000 May 24-31; 283(20):2674-9.
Department of Veterans Affairs, Honolulu, HI.
CONCLUSIONS: Our findings indicate that higher coffee and caffeine intake is associated with a significantly lower incidence of PD. This effect appears to be independent of smoking. The data suggest that the mechanism is related to caffeine intake and not to other nutrients contained in coffee.
Parkinson and coffee
Does caffeine intake protect from Alzheimer's disease?.
Maia L, de Mendonca A. Eur J Neurol. 2002 Jul;9(4):377-82
Dementia Clinics, Hospital of Santa Maria and Laboratory of Neurosciences, Faculty of Medicine of Lisbon, Portugal.
Caffeine intake was associated with a significantly lower risk for AD, independently of other possible confounding variables. These results, if confirmed with future prospective studies, may have a major impact on the prevention of AD.
Caffeine was on the International Olympic Committee (IOC) list of prohibited substances for many years. Athletes who tested positive for more than 12 micrograms of caffeine per milliliter of urine could be banned from the Olympic Games. This level can be reached after drinking about 5 cups of coffee. However, The IOC is REMOVED caffeine from the banned list in 2004.
Caffeine was taken off of the list of banned substances so that athletes who drink cola or coffee are not penalized. (References: World Anti-Doping Agency .)
xanthine alkaloids (caffeine, theobromine, and theophylline), Guarana Yerba maté
Caffeine is the most widely consumed behaviourally active substance in the western world. Neuroprotective effects of caffeine in low doses, chronically administered, have been shown in different experimental models. If caffeine intake could protect against neurodegeneration in Alzheimer's disease (AD), then higher levels of caffeine consumption in normal subjects as compared with AD patients should be detectable in the presumably long period before diagnosis when insidious pathogenic changes are taking place. A case-control study was used: cases were 54 patients with probable AD fulfilling the National Institute of Neurologic and Communicative Disorders and Stroke and the AD and Related Disorders Association criteria, in a Dementia Clinics setting. Controls were 54 accompanying persons, cognitively normal, matched for age (+/-3 years) and sex. Patients with AD had an average daily caffeine intake of 73.9 +/- 97.9 mg during the 20 years that preceded diagnosis of AD, whereas the controls had an average daily caffeine intake of 198.7 +/- 135.7 mg during the corresponding 20 years of their lifetimes (P < 0.001, Wilcoxon signed ranks test). Using a logistic regression model, caffeine exposure during this period was found to be significantly inversely associated with AD (odds ratio=0.40, 95% confidence interval=0.25-0.67), whereas hypertension, diabetes, stroke, head trauma, smoking habits, alcohol consumption, non-steroid anti-inflammatory drugs, vitamin E, gastric disorders, heart disease, education and family history of dementia were not statistically significantly associated with AD.
CONTEXT: The projected expansion in the next several decades of the elderly population at highest risk for Parkinson disease (PD) makes identification of factors that promote or prevent the disease an important goal. OBJECTIVE: To explore the association of coffee and dietary caffeine intake with risk of PD. DESIGN, SETTING, AND PARTICIPANTS: Data were analyzed from 30 years of follow-up of 8004 Japanese-American men (aged 45-68 years) enrolled in the prospective longitudinal Honolulu Heart Program between 1965 and 1968. MAIN OUTCOME MEASURE: Incident PD, by amount of coffee intake (measured at study enrollment and 6-year follow-up) and by total dietary caffeine intake (measured at enrollment). RESULTS: During follow-up, 102 men were identified as having PD. Age-adjusted incidence of PD declined consistently with increased amounts of coffee intake, from 10.4 per 10,000 person-years in men who drank no coffee to 1.9 per 10,000 person-years in men who drank at least 28 oz/d (P<.001 for trend). Similar relationships were observed with total caffeine intake (P<.001 for trend) and caffeine from non-coffee sources (P=.03 for trend). Consumption of increasing amounts of coffee was also associated with lower risk of PD in men who were never, past, and current smokers at baseline (P=.049, P=.22, and P=.02, respectively, for trend). Other nutrients in coffee, including niacin, were unrelated to PD incidence. The relationship between caffeine and PD was unaltered by intake of milk and sugar