Lec 10 & 11- Caffeine Flashcards
(37 cards)
what is pure caffeine known as?
1,3,7-trimethylxanthine
how much caffeine is consumed a day?
Around 6 billion caffeine-containing drinks are consumed worldwide every day
About 30,000 kg of caffeine per day
how much caffeine is in coke, tea, chocolate and coffee?
coke = 33
tea = 50
choc =12
coffee = 80-120
what are the sources of caffeine?
Tea, coffee, mate, cocoa, cola nut and guarana
how many cups of tea are drunk daily in the UK?
165 million
in terms of monetary value traded worldwide, where does coffee rank?
second after oil
physiology of caffeine
It is an adenosine A1 and A2A receptor antagonist
=The effects of caffeine on human physiology and behaviour occur primarily because caffeine antagonises (blocks) the action of endogenous adenosine (i.e., adenosine produced, as a result of metabolic activity, in the body) at adenosine A1 and A2a receptors
Difference between caffeine and adenosine
how does adenosine work
Caffeine has opposing effects, for example, adenosine causes vasodilation (the dilatation of blood vessels, which decreases blood pressure) and caffeine cause vasoconstriction (the constriction of blood vessels, which increases blood pressure).
Adenosine modulates neural activity=
Activation of adenosine postsynaptic receptors by endogenous adenosine slows neural activity
Caffeine prevents activation of adenosine receptors by adenosine, thus removing this brake on neural activity
define tolerance to caffeine..
how do we become tolerant?
Prolonged exposure to caffeine leads to changes in adenosine signalling that oppose the effects of caffeine (tolerance)
With prolonged exposure to caffeine, the body attempts to restore normal performance through alterations in the endogenous system – eg through changes in concentrations. The adenosine system then becomes more sensitive and we become partially tolerant to effects of caffeine.
metabolism of caffeine
After consuming a caffeine-containing drink or food, caffeine is rapidly absorbed from the gastrointestinal tract into the bloodstream, and peak concentration in blood is reached after about 30 to 60 minutes. It is then distributed throughout the entire body including the brain. It takes about 15 minutes to reach the brain and is detectable in saliva soon after consumption.
Caffeine does not accumulate in the body, however, because it and its metabolites are efficiently excreted. For adults, the elimination half-life of caffeine is around 3 to 7 hours
Who was the first person to investigate caffeine? and what did he find?
Hollingworth 1912
compared pp who swallowed caffeine in a capsule in doses between 1 and 6 grains versus placebo capsule which contained ‘sugar of milk’
= Caffeine appears to speed up performance on simple motor tasks like tapping. This is not the pp motivation but a physiological response of caffeine.
=large doses of caffeine (390 which is about 3 or 4 cups of coffee) disrupts performance on hand steadiness task and causes shakiness.
He concludes that caffeine can have some positive effects by increasing motor performance
Smit and Rogers 2000 study
demonstrate that we are sensitive to caffeine at levels that not only occur in coffee and tea, but also in chocolate and cola beverages (levels 0, 12.5, 25, 50 and 100)
=Caffeine has effect on RT and people are faster with caffeine than placebo
=Relative to placebo, performance is also better with caffeine on rapid number search task.
=One strange finding was that low doses of caffeine produce similar effects to higher dose
the effects on performance were more marked in individuals with a higher level of habitual caffeine intake,
BUT vast majority of literature look at caffeine consumers and will stop them consuming caffeine before the test, this may effect the interpretation of data. .. therefore perhaps is effect of caffeine withdrawal, not that caffeine speeds up reaction time but that placebo slows down reaction time
what is the withdrawal reversal hypothesis?
- Acute (e.g., overnight) caffeine withdrawal lowers alertness and degrades mental performance
- Caffeine restores alertness and mental performance to, but not above, baseline (normal) levels
Goldstein 1969 study
3 main findings:
1- caffeine consumers rated themselves as feeling less alert before administration of the treatments (caffeine or placebo) than did the non-consumers.
2- Second, over the next 2 h, caffeine versus placebo increased alertness in consumers; however, even after the highest caffeine dose, their alertness increased only to the level of alertness rated by non-consumers when they received placebo. Therefore caffeine only increased alertness to the (baseline) level
3- Third, caffeine barely affected alertness in non-consumers despite there being a considerable room for an increase in scores
=also found that high caffeine had little effect on regular drinkers but large effect in non-drinkers, these people reacted negatively to caffeine; principal complaints were jitteriness, nervousness, and “upset stomach.”
how can we avoid the self-selection bias
Randomise caffeine consumers to short-term versus long-term caffeine abstinence. Take people who are caffeine consumers and ask them to become abstain for a period of time and ask other consumers to carry on as normal and then compare. For the people who abstain, their withdrawal symptoms begin to decrease and eventually disappear. Their systems have therefore adjusted to life without caffeine and tolerance is lost. Can compare them to people who are withdrawn just overnight
what is Phenylketonuria (PKU)
PKU is an inherited metabolic disorder in which people are born with inability to metabolise PKU, therefore it builds up and results in elevated levels and cog impairments.
- High neonatal blood level of phenylalanine (1 in 10,000 in UK) and metabolites in urine, including phenylpyruvate (phenylketone)
- Deficiency of phenylalanine hydroxylase (PAH) activity due to mutation in gene coding for PAH (300 PAH mutations identified)
=tyrosine deficiency leads to dopamine deficiency =
=elevated phenylalanine leads to impaired myelin production and maintenance
Rogers et al 1995 study
They investigated caffeine reinforcement by assessing changes in preference for a novel flavoured fruit juice drink consumed with or without caffeine (70 mg). The drinks were consumed at breakfast on 10 consecutive weekdays. Changes in preference for the target drink during conditioning were examined by subtracting subjects’ ranked preference for the target drink on day 0 from their ranked preference for this same drink on day 10. Mood was assessed on each of the conditioning trials 1 h after the drink was consumed.
Based on their caffeine intake, subjects were divided into low and moderate users
= low users showed, overall, an increase in preference for the target drink relative to the other drinks. This change in preference was not significantly affected by the caffeine content of the target drink.
=In contrast, subjects who were habitually consuming caffeine at the higher level developed a relative dislike for the target drink if it lacked caffeine, and showed an increase in preference for the drink if it was caffeinated.
=Mood in the low caffeine consumers was largely unaffected by the ingestion of caffeine, but tended to be lowered in regular users who received the noncaffeinated drink. They felt less clearheaded, less energetic and less lively, and more tired than the moderate users who received caffeine.
Yeomans et al 1998 -
This study examined whether 100 mg caffeine could reinforce preference for the flavour of a novel herbal tea drink in moderate caffeine users, both after overnight caffeine abstinence and 2 h after receiving 100 mg
= Liking for the tea increased significantly over four days for subjects receiving caffeine, and decreased significantly in those without caffeine.
Rogers et al 2013 study
-caffeine withdrawal at 10:30am associated with some detrimental effects including slower RT times
-caffeine withdrawal also associated with greater sleepiness, lower self reported mental altertness and poorer cog performance - all of which are reveresed by caffeine
In contrast to medium-high caffeine consumers, (non-tolerant) non-low consumers experience an increase in anxiety/jitteriness after caffeine which offsets any benefit for mental alertness and mental performance arising from reduced sleepiness.
Tolerance in consumers develops to anxiety (Rogers 2010) but not to the effects on sleepiness as the beneifits in mental alertness and mental performance only return levels to a normal state of affairs.
anxiety and jitteriness have neg effects on performance- Eysenck 2007 - anxiety reduces attentional control and increases threat stimuli processing.
an important dissociaiton in this study was between sleepiness/wakefulness and mental alertness, which previously were measured as lying on continuum Rogers 2010).
what is the difference between addiction and dependence
- ‘Addiction is restricted to the extreme or psychopathological state where control over drug use is lost.’ – loss of control is key.
- ‘Dependence refers to the state of needing a drug to function within normal limits; it is often associated with tolerance and withdrawal (symptoms), and with addiction as defined above.’
what is the underlying mechanism for cognitve decline and diet?
vasuclar disease which leads to cerebral ischaemia.
what is Atherosclerosis?
a disease in which fatty plaques develop on the inner wall of arteries, resulting in obstruction of blood flow
what are the fatty acids that have beneficial effects in relation to atherosclerosis and associated effects
n-3 fatty acids (alpha-linolenic acid, DHA and EPA)
what is ischemia and how is it effected by caffeine?
ischemia is a condition in which there is insufficient blood flow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus to the death of brain tissue or cerebral infarction / ischemic stroke
When someone suffers from ischemia, adenosine is released, this feeds back to reduce the adverse effects of ischemia. Through chronic exposure to caffeine, and caffeine’s effect of adenosine, it sensitises this and creates adenosines protective response to ischaemia
