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Caffeine Coursework

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Caffeine Coursework

Postby red.ninja13 » Sun Mar 15, 2009 11:34 pm

Hi i am doing my A2 Coursework on the effect of caffeine on reaction speed and short term memory. I am going to give my "test subjects" ProPlus tablets, the tablet packet states that you shouldnt take more then 2 tablets in 3 hours (100mg) however, having researched caffeine, i believe that it is safe to take upto 300mg (6 tablets). Do you think it is safe for me to give someone upto 5 tablets in one go?

Also, is it ok to have two dependant variables in this experiment? As i am testing the effect of caffeine on reaction speed and short term memory.

Thanks in advance for any help :D
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Postby futurezoologist » Tue Mar 17, 2009 12:33 pm

One serving of coffee has approximately 80mg of caffeine so i cant see that a person who had 4 coffees in one go would have too bad of an effect but it wouldn't be good for you i suspect, all depends on the willingness of your test subjects. I wouldn't give them six in one hit though, concentration of caffeine may be too high, but if you have done your research then you probably know as good as anyone.

About the dependent variables; looks like two separate investigations there as i cannot see any link between them, but it depends on how formal you want it.

Hope that helps a bit.
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Re: Caffeine Coursework

Postby mcar » Fri Mar 20, 2009 10:57 am

red.ninja13 wrote:I am going to give my "test subjects" ProPlus tablets, the tablet packet states that you shouldnt take more then 2 tablets in 3 hours (100mg) however, having researched caffeine, i believe that it is safe to take upto 300mg (6 tablets). Do you think it is safe for me to give someone upto 5 tablets in one go?


Consider carefully the pharmacokinetics and drug to drug interactions when you would like to let someone take those tablets. You check for any untoward interactions and compatibilities of their chemical constituents. Of course you have researched the safe levels, however some values I believe are subject to change since medicine is also a changing field. Obtain also consent from your test subjects; with that you and your subjects will be at least legally protected .
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Re: Caffeine Coursework

Postby red.ninja13 » Sun Mar 22, 2009 7:39 pm

Thanks for your help. i am trying to do section on biological info, and i just dont understand this passage from wikipedia, can anyone explain it to me?

"Caffeine's principal mode of action is as an antagonist of adenosine receptors in the brain.
Like alcohol and nicotine, caffeine readily crosses the blood–brain barrier that separates the bloodstream from the interior of the brain. Once in the brain, the principal mode of action is as an antagonist of adenosine receptors.[45] The caffeine molecule is structurally similar to adenosine, and binds to adenosine receptors on the surface of cells without activating them (an "antagonist" mechanism of action). Therefore, caffeine acts as a competitive inhibitor.
Adenosine is found in every part of the body, because it plays a role in the fundamental ATP-related energy-metabolizing system, but it has special functions in the brain. There is a great deal of evidence that brain adenosine concentrations are increased by various types of metabolic stress (including anoxia and ischemia), and act to protect the brain by suppressing neural activity, and by increasing blood flow.[46] Thus caffeine, by counteracting adenosine, has a generally disinhibitory effect on brain activity. Exactly how these effects translate into increases in arousal and alertness is a difficult question, though.
Adenosine release mechanisms in the brain are complex.[46] There is evidence that adenosine functions as a synaptically released neurotransmitter in some cases, but stress-related adenosine increases appear to be produced mainly by extracellular metabolism of ATP. It is not likely that adenosine is the primary neurotransmitter for any group of neurons, but rather that it is released together with other transmitters by a number of neuron types. Unlike most neurotransmitters, adenosine does not seem to be packaged into vesicles that are released in a voltage-controlled manner, but the possibility of such a mechanism has not been completely ruled out.
Several classes of adenosine receptors have been described, with different anatomical distributions. A1 receptors are widely distributed, and act to inhibit calcium uptake. A2A receptors are heavily concentrated in the basal ganglia, an area that plays a critical role in behavior control, but can be found in other parts of the brain as well, in lower densities. There is evidence that A 2A receptors interact with the dopamine system, which is involved in reward and arousal. (A2A receptors can also be found on arterial walls and blood cell membranes.)
Beyond its general neuroprotective effects, there are reasons to believe that adenosine may be more specifically involved in control of the sleep-wake cycle. McCarley and his colleagues have argued that accumulation of adenosine may be a primary cause of the sensation of sleepiness that follows prolonged mental activity, and that the effects may be mediated both by inhibition of wake-promoting neurons via A1 receptors, and activation of sleep-promoting neurons via indirect effects on A2A receptors.[47] More recent studies have provided additional evidence for the importance of A2A, but not A1, receptors.[48]"
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