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caffeine decreases heart rate?

I don't think so. agonists at the adenosine receptors reduce heart rate and are used in supraventricular tachyarrythmias by slowing conduction through the atrioventricular node. it seems at least counterintuitive and more likely flat out wrong that it "reduces" heart rate, it increases it. can this be changed or am i mistaken? — Preceding unsigned comment added by 198.49.6.225 (talk) 08:36, 22 April 2015 (UTC)

The source says it promotes bradycardia and also says there are heart rate increasing effects as well. It seems reasonable that there are competing effects. I have added a sentence regarding the increase in heart rate. Sizeofint (talk) 18:04, 22 April 2015 (UTC)

Overdose caused by powered caffeine supplements

I have added some information about the overdose potential of powdered caffeine supplements, sourced to a New York Times article. (The cited source shows up as a blog, but a shorter version of this appeared in the print edition.) This seems like information that our article ought to have, given that a number of fatalities have occurred. Looie496 (talk) 13:14, 19 May 2015 (UTC)

Addiction

With respect to caffeine addiction our current text appears to take one side in the debate.

  • This 2015 pyschiatry textbook descibes "continued caffeine use despite knowledge of a persistent or recurrent pyschological or physical problem caused or exacerbated by caffeine" [1]
  • This paper from 2014 discusses the controversy ""Academics and clinicians, however, have not yet reached consensus about the potential clinical importance of caffeine addiction (or ‘use disorder’1) [1]. The DSM-5 designated caffeine withdrawal as a formal disorder, an important step towards recognizing the potential to develop clinically significant problems related to caffeine use [2]. Moreover, caffeine use disorder was included in Section III (conditions for further study), acknowledging the merit of the condition while conveying the need for further research before an official designation. Of note, the World Health Organization (WHO) has long included caffeine on its list of psychostimulants that produce withdrawal or dependence disorders in the ICD-10."[2]
  • This review speaks about an effect on dopamine systems "Through these interactions, caffeine is able to directly potentiate dopamine neurotransmission, thereby modulating the rewarding and addicting properties of nervous system stimuli." [3]
  • This 2013 review states "an increasing number of clinical studies are showing that some caffeine users become dependent on the drug and are unable to reduce consumption despite knowledge of recurrent health problems associated with continued use" [4]

Now of course others do say it is not addictive. We should likely present both. Doc James (talk · contribs · email) 01:12, 11 July 2015 (UTC)

The biggest problem here is that non-research models do not define an addiction consistently or use an evidence-based definition to define that pathology. The second biggest problem is that, thanks to the file drawer effect, no one has bothered to publish a negative finding of caffeine-induced ΔFosB induction in D1-type neurons in nucleus accumbens compared to control drugs (or maybe no molecular biologist cares enough to conduct a single study to confirm a caffeine addiction model, since that finding is really all it would take). The first problem goes back to the whole diagnostic models of addiction don't have an actual pathophysiological basis or evidence to support their "labels". While I think it's perfectly fine to indicate that some literature asserts that caffeine is associated with an "addiction", it should be clear that this statement does not imply a contradiction with the research model unless the evidence for that statement is based upon the research model (e.g., any of the following would be sufficient evidence to assert that caffeine is addictive: clear reward system activation + activation of the mesolimbic pathway in particular in human neuroimaging studies, the presence of a drug/nautral reward cross-sensitization effects in animals, evidence that it is self-administrated in a manner similar to other addictive drugs in animal models, evidence of dopamine/calcium signaling in D1-type MSNs in animals, or evidence of ΔFosB induction in D1-type MSNs in animals). I just spent the past 5 hours looking for evidence of any of this and the strongest evidence I could find is that D1 receptors are activated in a part of the nucleus accumbens in animals from high-dose caffeine; however, this effect only occurs during acute use, but not chronic use, due to an adenosine A1 receptor desensitization effect which attenuates the agonist-like action on dopamine D1 receptors caused by caffeine-induced adenosine A1 receptor antagonism (in plain English: a form of drug tolerance occurs with repeated caffeine use).
I did read the paper on children that you linked above a few hours ago, but that doesn't say that it activates the reward system; the language it uses is that it modulates the rewarding properties of addictive stimuli, which need not involve the D1-type MSN pathway (it also doesn't preclude inhibitory effects by caffeine, as some other papers suggest with chronic use - mentioned in 1 of the linked PMIDs below). That modulatory effect could occur in any dopaminergic signaling pathway that interacts with the D1-type MSN pathway as a downstream effect. Some of the cell signaling literature that I read over the past few hours mentioned the a modulatory effect between caffeine and other drugs (cocaine), and suggested that it involved D2-type receptors (which it effects through adenosine A2 antagonism) and the desensitization effect between adenosine/dopamine A1 and D1 that I mentioned above (covered in PMID 18088379 PMID 17532111). It does indicate a that it isn't compulsively and increasingly self-administered like other addictive stimulants though: "Caffeine and drugs of abuse are both considered reinforcing and are both self administered in naturalistic settings and in the laboratory. In animal models of self-administration, caffeine is administered irregularly, is typically observed after prolonged caffeine exposure followed by abstinence, and is not seen under the same conditions which reliably produce cocaine or amphetamine self-administration"
The strongest clinical evidence I've found against an addiction model is this evidence of SPECT neuroimaging of the nucleus accumbens in humans and associated cell signaling evidence in animals at high doses:
  • textbook[1] cites this paper on humans[2]
The strongest nonclinical evidence that I've come across against an addiction model is that it isn't consistently self-administered like other addictive drugs in animals, it doesn't continue to produce an agonist-like effect on D1-type receptor with chronic use due to tolerance (meaning that if it is addictive, then unlike other psychostimulants, dopamine receptors don't play a significant role in producing an addiction), and there's a fairly large amount of evidence that it is markedly less rewarding in animals compared to other stimulants. The following covers the relative lack of drug reward compared to other stimulants:
This review[3] cites the following primary source[4] - these papers indicate that its (weakly) rewarding properties are not due to activation of dopamine receptors in D1-type NAcc MSNs, or in any other dopamine pathway for that matter.
TL;DR: I'm fine with indicating that some sources say that caffeine is addictive, so long as we make a clear distinction between the models/definitions which identify "addiction" using an arbitrary cluster of symptoms and the model which actually involves the use of a biomarker and signal transduction pathways to study a real disease. Seppi333 (Insert 2¢) 04:35, 11 July 2015 (UTC)
"Real disease" is not appropriate terminology. Most of psychiatry is studied based on symptoms and signs not neurimaging and biochemistry. And we do not typically state they are not diseases. Caffeine either has no addiction or low addiction and that information is useful. The literature does not agree that ΔFosB must be present first. Doc James (talk · contribs · email) 04:45, 11 July 2015 (UTC)
When you say "the literature does not agree that ΔFosB must be present first", are you referring to the hand-wavy bullshit pushed out by diagnostic classification systems? In any event, can you show me the literature you're referring to which supports that claim? I have never read any papers asserting that. Seppi333 (Insert 2¢) 05:03, 11 July 2015 (UTC)
Yes I am referring to the "hand-wavy bullshit" diagnostic systems that form the basis of psychiatric diagnosis. The DSM5 is an example. Mental illnesses are not diagnosed based on lab tests or medical imaging. Doc James (talk · contribs · email) 16:20, 11 July 2015 (UTC)
By the way we at Wikipedia should simply state the major positions on a topic. We are not here to advocate a single position or world view. You comments above seem to imply that the biological model of mental illness is the only one worth mentioning. It however is not. Doc James (talk · contribs · email) 16:28, 11 July 2015 (UTC)

it's not the only one worth mentioning IMO. All 3 models are notable, hence they should be covered. The evidence-based model is just the only correct model of an addiction, by any definition, because it's the only evidence-based model. I vocalize my opinion on talk pages, but I seldom act on my biases when I edit articles; e.g., yesterday I added coverage of the DSM-5 and ICD-10 in that section. Seppi333 (Insert 2¢) 17:47, 11 July 2015 (UTC)

You are welcome to your opinion that the biological model is the "only correct model of an addiction". There are many forms of evidence out their. And some of the other models are based on non laboratory based evidence. Doc James (talk · contribs · email) 18:47, 11 July 2015 (UTC)
That "opinion" is me paraphrasing the National Institute of Mental Health director's statement (about all current diagnostic models of any/all mental health disorders, not just addictions), which is apparently why he supports the Research Domain Criteria system.[5]

While DSM has been described as a “Bible” for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been “reliability” – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever.

In any event, I wouldn't make an assertion like that simply based upon my perception of one model being more correct than another. That line of thinking is fairly retarded IMO. Seppi333 (Insert 2¢) 19:12, 11 July 2015 (UTC)
I am not saying that psychiatry is not different than the rest of medicine. The majority of the clinical research done is based on the DSM and ICD diagnostic criteria. Doc James (talk · contribs · email) 19:16, 11 July 2015 (UTC)
Add: I didn't notice your first reply; my argument wasn't relevant to diagnosing addiction, rather it was about whether or not "caffeine addiction" was supported by some form of evidence w.r.t. the neuroscience (NAcc neuroimaging), psychology (self administration), molecular biology (ΔFosB), or pharmacological (dopamine/glutamate/other receptor/ion channel activation in D1-type NAcc MSNs) component of the addiction model.
FWIW, while a brain biopsy could actually be used to diagnose an addiction using the evidence-based model, I doubt anyone would opt to have a hole drilled into their skull for the sake of that particular diagnosis. That's really not even necessary to identify an addiction using this model though - anyone with a drug addiction and a working knowledge of operant conditioning (this is extensively covered in all high school/college level introductory psychology courses) should be able to recognize that their compulsion is being driven by positive reinforcement. Recognizing the difference between drug addiction and drug dependence is as simple as asking oneself whether one's drug use behavior has been associated with removing something "bad", which is negative reinforcement (i.e., drug use occurred in response to withdrawal symptoms or any other undesirable stimulus), or the addition of something "rewarding" or "approachable", which is positive reinforcement (i.e., drug use begets more drug use). There are no other possible drug-induced compulsive disorders because any compulsion is just a pathologically (positively and/or negatively) reinforced behavior; so, I really have no clue why current diagnostic models don't just follow that framework which predates both the first edition of the DSM and ICD. Seppi333 (Insert 2¢) 19:12, 11 July 2015 (UTC)
Refs

References

  1. ^ Miller PM (2013). "Chapter III: Types of Addiction". Principles of addiction comprehensive addictive behaviors and disorders (1st ed.). Elsevier Academic Press. p. 784. ISBN 9780123983619. Retrieved 11 July 2015. Astrid Nehlig and colleagues present evidence that in animals caffeine does not trigger metabolic increases or dopamine release in brain areas involved in reinforcement and reward. A single photon emission computed tomography (SPECT) assessment of brain activation in humans showed that caffeine activates regions involved in the control of vigilance, anxiety, and cardiovascular regulation but did not affect areas involved in reinforcement and reward.
  2. ^ Nehlig A, Armspach JP, Namer IJ (2010). "SPECT assessment of brain activation induced by caffeine: no effect on areas involved in dependence". Dialogues Clin Neurosci. 12 (2): 255–263. PMC 3181952. PMID 20623930. Caffeine is not considered addictive, and in animals it does not trigger metabolic increases or dopamine release in brain areas involved in reinforcement and reward. ... these earlier data plus the present data reflect that caffeine at doses representing about two cups of coffee in one sitting does not activate the circuit of dependence and reward and especially not the main target area, the nucleus accumbens. ​[10],​[11],​[12] ... Therefore, caffeine appears to be different from drugs of dependence like cocaine, amphetamine, morphine, and nicotine, and does not fulfil the common criteria or the scientific definitions to be considered an addictive substance.42 {{cite journal}}: zero width space character in |quote= at position 420 (help)
  3. ^ Puglisi-Allegra S, Ventura R (2012). "Prefrontal/accumbal catecholamine system processes high motivational salience". Front Behav Neurosci. 6: 31. doi:10.3389/fnbeh.2012.00031. PMC 3384081. PMID 22754514. A DA-independent reward mechanism for caffeine has been shown (Sturgess et al., 2010).{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Sturgess JE, Ting-A-Kee RA, Podbielski D, Sellings LH, Chen JF, van der Kooy D (2010). "Adenosine A1 and A2A receptors are not upstream of caffeine's dopamine D2 receptor-dependent aversive effects and dopamine-independent rewarding effects". Eur. J. Neurosci. 32 (1): 143–54. doi:10.1111/j.1460-9568.2010.07247.x. PMC 2994015. PMID 20576036. the D1 receptor is not involved in the rewarding effects of caffeine. ... The current data indicates that caffeine has aversive effects at high doses and neither rewarding nor unpleasant effects at low doses. Previous work in rats has indicated that caffeine induces mild preferences at low doses (Brockwell et al., 1991; Bedingfield et al., 1998; Patkina & Zvartau, 1998) and aversions at high doses ... Indeed the rewarding effects of caffeine seen by Brockwell et al.(1991) were at one dose and small. This is similar to our current data; the lower doses of caffeine on our dose-response curve are weakly, but non-significantly rewarding. Also consistent, the rewarding effects of caffeine in humans are mild or absent in individuals with limited caffeine experience
  5. ^ Thomas Insel. "Transforming Diagnosis". National Institute of Mental Health. Retrieved 17 June 2015.

Underlying mechanism

In the text we have some research that does not conclude their is a mechanism and other research that does. We need to balance both. Doc James (talk · contribs · email) 21:25, 22 July 2015 (UTC)

You have research saying that it modulates reward. Electrolytes modulate reward. Are sodium chloride and magnesium addictive? No. Do they affect drug reward? Yes. It is not indicative That the addiction mechanism exists. Seppi333 (Insert 2¢) 08:58, 23 July 2015 (UTC)
It's disappointing to see an editor I respect so much ignoring WP:BRD. Looie496 (talk) 16:01, 23 July 2015 (UTC)

This review speaks about an effect on dopamine systems "Through these interactions, caffeine is able to directly potentiate dopamine neurotransmission, thereby modulating the rewarding and addicting properties of nervous system stimuli." [5]. I have not seen the same said about taking sodium chloride. We should not ignore part of the literature. Doc James (talk · contribs · email) 19:57, 23 July 2015 (UTC)

Aside from its well-known effects on sleep and arousal, which are primarily mediated by antagonism of the adenosine A1 receptor, caffeine is also known to interact with the dopamine system to exert some of its behavioral effects (Cauli and Morelli, 2005; Fredholm and Svenningsson, 2003). These actions are likely mediated through inhibition of the adenosine A2A receptor, which is primarily localized to dopamine rich areas of the brain (Fredholm, 1999). Adenosine A2A receptors are co-localized with dopamine D1 and D2 receptors (Kudlacek et al., 2003) and have been shown to form heterodimers (Fuxe et al., 2003). In addition, activation of adenosine A2A receptors decreases dopamine binding at the D2 receptor (Salim et al., 2000). Through these interactions, caffeine is able to directly potentiate dopamine neurotransmission, thereby modulating the rewarding and addicting properties of nervous system stimuli... In rats, caffeine administration leads to increased locomotor activity (Nehlig et al., 1992), which can be blocked by administration of dopamine receptor antagonists (Garrett and Holtzman, 1994); (Kuribara and Uchihashi, 1994). Caffeine can also induce rotational behavior in rats with unilateral lesions of the nigrostriatal dopamine cells in a manner that mimics dopamine (Garrett and Holtzman, 1995; Herrera-Marschitz et al., 1988). Finally, caffeine can potentiate the effects of dopamine on rotational behavior in animals with this same lesion (Jiang et al., 1993). When taken together, these studies suggest that caffeine interacts with the dopaminergic system to produce some of its behavioral effects.

Greater text Doc James (talk · contribs · email) 20:00, 23 July 2015 (UTC)

We cannot put in Wikipedia's voice stuff that is directly refuted by other high quality sources [6] Doc James (talk · contribs · email) 20:07, 23 July 2015 (UTC)
Wherein the above do you think you read a "biomolecular mechanism of addiction"? It says it affects the dopamine system, i.e., the VTA and nigrostriatal dopamine nuclei through A2A-D2 and A1A-D1 heterodimers. Not once does it suggest that it exerts chronic DA stimulation in the nacc through this effect. What you're writing in the article is WP:OR. Seppi333 (Insert 2¢) 20:46, 23 July 2015 (UTC)
It clearly states that there are potential mechanisms by which it affect the DA system. Thus "directly potentiate dopamine neurotransmission" Doc James (talk · contribs · email)
This is a bit too complex to explain in simple terms, so I'll just elaborate on it in the pharmacodynamics section at some point. I pointed out before that chronic stimulation of A1A-D1 heterodimers produces tolerance to the effect in neurons. That's a key point, as D1-type MSNs in the NAcc shell are what mediate drug reward, and these A1A-D1 receptors (and not the A2A-D2 heterodimers) would be prevalent heterodimer in D1-type neurons. Zinc is a perfect example of something that potentiates dopamine neurotransmission without being addictive. I wrote about it a while back in dopamine transporter. In any event, I don't really care about this anymore - it's wrong and it's misleading, but it's just one article. Seppi333 (Insert 2¢) 16:17, 26 July 2015 (UTC)
Just for the record, your use of the following quotation to conclude that something is addictive, or even just rewarding, is still WP:OR.

Through these interactions, caffeine is able to directly potentiate dopamine neurotransmission, thereby modulating the rewarding and addicting properties of nervous system stimuli.

If the positive modulation of dopamine neurotransmission were necessary and sufficient for something to be addictive, every electrolyte which positively modulates dopamine neurotransmission (e.g., zinc and calcium) would be addictive and every rewarding stimulus would be addictive regardless of whether or not it is reinforcing since all rewarding stimuli trigger DA release in the portion of the reward pathway which synapses onto D1-type neurons in the nucleus accumbens shell; rewarding stimuli, however, are not necessarily reinforcing; this is why an addictive stimulus is defined as one which is both rewarding and reinforcing - reward does not imply reinforcement or vice versa. The most you can state based upon any ref currently cited in this article is that caffeine is reinforcing; that quote does not state or even imply that caffeine use is a rewarding stimulus or addictive. Seppi333 (Insert 2¢) 19:52, 8 August 2015 (UTC)
There are a number of sources that state that caffeine has a low addiction potential not just this one. This references gives caffeine an abuse potential liability index of 5 [7] along with LSD and PCP.
We can have a RfC Seppi if you want wider input. If so can you clarify what you are wanting? Do you want the statement that caffeine has a low risk of addiction removed? Or are you arguing that the sources do not mention a mechanism for addition? Doc James (talk · contribs · email) 05:24, 9 August 2015 (UTC)
You can start an RFC if you want, but community consensus doesn't trump WP:V - that ref does not support the assertion that a biomolecular mechanism exists, hence the underlined contention clause ("Some state that research does not provide support for an underlying biochemical mechanism for caffeine addiction") that you wrote in is not supported by a reference. The implication that "Others state otherwise" is your OR. Seppi333 (Insert 2¢) 06:41, 9 August 2015 (UTC)
You say it doesn't. I say it does. So we disagree. We have already established that. I am happy to ask for further opinions. Doc James (talk · contribs · email) 07:15, 9 August 2015 (UTC)

I do not say it doesn't. I say it's your WP:OR. This isn't a debate about a fact, it's about a policy violation. If you still disagree, let's go to Wikipedia:No original research/Noticeboard. Seppi333 (Insert 2¢)

Done Doc James (talk · contribs · email) 13:50, 9 August 2015 (UTC)
Much better now, thanks. Seppi333 (Insert 2¢) 22:24, 9 August 2015 (UTC)
Okay happy we figured something out. Doc James (talk · contribs · email) 05:05, 10 August 2015 (UTC)
I came across a 2015 primary source which appears to explain its mechanism in the nucleus accumbens - it's statements are consistent with all the existing sources, so I included it and expanded upon the corroborating statements from the other sources; however, it'll need to be replaced with a review when one is published. I imagine there's a secondary reference to the source on the NIDA site somewhere right now though. Seppi333 (Insert 2¢) 22:47, 12 August 2015 (UTC)
Seppi both of us know that consensus is that we do not use primary sources. We can have this discussion based on secondary sources. When a secondary source reviews this primary source we can discussion further.
Also it would be greatly appreciated if you could write in more simple language. Doc James (talk · contribs · email) 12:00, 13 August 2015 (UTC)
I actually didn't bother looking for a secondary source for it, simply because it didn't actually say anything the other citations didn't assert in their quotations; it wasn't hard to find a review citing it though: PMID 26051403[1] from June was written by a few of the same authors[2] and includes the conclusion of the primary source as a statement in the abstract.
Like I said before though, caffeine's pharmacodynamics in the dopamine system are rather complicated because they're off-target effects; in other words, dopaminergic effects are not mediated as a direct action of caffeine binding at a target, they're (at least) one step removed from its adenosine receptor targets. In any event, it's a bit difficult to simplify the language in that section because D1-type receptors (DRD1/DRD5) and D2-type receptors (DRD2, DRD3, DRD4) in the nucleus accumbens are heavily expressed on distinct groups of nucleus accumbens neurons (MSNs). I don't mind simplifying the language, but we'll probably have to omit an explanation of how caffeine potentiates dopamine neurotransmission due to its complexity. The sentence about punishment/reinforcement in D2-type/D1-type neurons respectively could just be restated as the associated activity in those neurons "decreases reward"/"increases reward" respectively. The technical explanation has the benefit of describing the cognitive function (reinforcement/punishment involving perceived reward) governed by each group of neurons though.
I'll read through the review later today and look for any new statements to quote – in the meantime, what parts of the text did you have in mind for rephrasing? Seppi333 (Insert 2¢) 14:04, 13 August 2015 (UTC)
What is wrong with "Some state that research does not provide support for an underlying biochemical mechanism for caffeine addiction. Other research states it can affect the reward system."? Doc James (talk · contribs · email) 15:16, 13 August 2015 (UTC)
That's awkwardly worded, but I agree it is the right information for this article to give. Looie496 (talk) 15:43, 13 August 2015 (UTC)
Nothing. If you like that statement, we can put it first, then follow it with a more technical explanation. Agree it's awkwardly worded though. Seppi333 (Insert 2¢) 23:19, 14 August 2015 (UTC)
I think what Doc James is saying (and I agree) is that the more technical material is not appropriate for this article. It might be appropriate for an article on the physiology of addiction, but not here. Looie496 (talk) 12:52, 15 August 2015 (UTC)
Yes this is a general encyclopdia and we should be writing for a general audience. Doc James (talk · contribs · email) 16:28, 15 August 2015 (UTC)
Hmm, ok. I'm fine with retaining the current version in that section, as what it says is in line with the sources, although I'm going to revise what I wrote originally and tailor it to the pharmacodynamics section. Its dorsal striatal DAergic+glutamatergic activity would likely play a role in its locomotor-activating effects and we don't even mention DA or glutamate in the article ATM. Using what I wrote originally, I'll cut the last sentence (explicitly covering MSN function or these pathways isn't necessary), revise the preceding ones accordingly, and add coverage of its subregional effect on adenosine/glutamate/DA release and receptors at normal/high/chronic dosing using the 2008 and 2015 review on the topic. I really don't feel like describing the dynamics of a GPCR heterotetramer in any article, so I'm going to keep the part on A1-DRD1, A2A-DRD2, A1-A2A heteromers limited to stating the role they play in caffeine's effect on neurotransmitter signaling. Will get around to this sometime later today or tomorrow. Seppi333 (Insert 2¢) 18:17, 15 August 2015 (UTC)
Maybe we need a subarticle on Pharmacology of caffeine and we leave just a single simple paragraph overview in this article? Doc James (talk · contribs · email) 19:39, 15 August 2015 (UTC)
Eh, it's not really that long IMO. The content I'd add is going to be about a paragraph, though I'll probably end up copyediting/pruning existing content or merging related subsections, so it may end up about the same size. Seppi333 (Insert 2¢) 22:21, 15 August 2015 (UTC)

Reflist

References

  1. ^ "Allosteric mechanisms within the adenosine A2A-dopamine D2 receptor heterotetramer". Neuropharmacology. June 2015. doi:10.1016/j.neuropharm.2015.05.028. PMID 26051403. caffeine-induced increases in D2R availability in the ventral striatum were associated with caffeine-induced increases in alertness (Volkow et al., 2015). ... Fig. 2. Brain maps showing significant differences in D2R/D3R availability (nondisplaceable binding potential or BPND), between placebo and caffeine ... Furthermore, caffeine has also been shown to release dopamine in a subregion of the ventral striatum by blocking presynaptic A1R localized in dopaminergic terminals (Ferre, 2008) {{cite journal}}: Unknown parameter |authors= ignored (help)
  2. ^ "Caffeine increases striatal dopamine D2/D3 receptor availability in the human brain". Transl Psychiatry. 5: e549. April 2015. doi:10.1038/tp.2015.46. PMC 4462609. PMID 25871974. We show a significant increase in D2/D3R availability in striatum with caffeine administration, which indicates that caffeine at doses consumed by humans does not increase DA in striatum. Instead we interpret our findings to indicate that caffeine's DA-enhancing effects in the human brain are indirect and mediated by an increase in D2/D3R levels and/or changes in D2/D3R affinity. {{cite journal}}: Unknown parameter |authors= ignored (help)
  3. ^ "An update on the mechanisms of the psychostimulant effects of caffeine". J. Neurochem. 105 (4): 1067–1079. 2008. doi:10.1111/j.1471-4159.2007.05196.x. PMID 18088379. On the other hand, our 'ventral shell of the nucleus accumbens' very much overlaps with the striatal compartment simply described by De Luca et al. (2007) as 'nucleus accumbens shell,' where both studies show that caffeine does not modify the extracellular levels of dopamine. Therefore, the results of both experimental groups are basically the same and point to differential effects of caffeine in different striatal subcompartments. In fact, analyzing the effects of the intrastriatal perfusion of an A1 receptor antagonist in several other striatal compartments showed striking differences compared with the shell of the nucleus accumbens. Thus, A1 receptor blockade significantly increased the extracellular concentration of dopamine, but not glutamate, in the core of the nucleus accumbens and in the caudate–putamen and the effect was more pronounced in the most medial compartments (Boryczet al. 2007). In summary, a subregional difference in the A1 receptor-mediated control of glutamate and dopamine release exists in the striatum ... A2A receptors play a crucial role in the sleep-promoting effects of adenosine and the arousal-enhancing effects of caffeine (Huang et al. 2007; Ferre´ et al. 2007a). Those A2A receptors are localized in the ventrolateral pre-optic area of the hypothalamus and their stimulation promotes sleep by inducing GABA release in the histaminergic tuberomammillary nucleus, thereby inhibiting the histaminergic arousal system ... chronic caffeine exposure counteracts both motor activation and dopamine release in the nucleus accumbens induced by caffeine or an A1 receptor antagonist ... An additional factor that might play a significant role in caffeine tolerance is the significant increase in plasma and extracellular concentrations of adenosine with chronic caffeine exposure ... Caffeine produces its motor and reinforcing effects by releasing the pre- and post-synaptic brakes that adenosine imposes on dopaminergic neurotransmission in the SSM {{cite journal}}: Unknown parameter |authors= ignored (help)

Trying to clarify

I don't want to discuss this at the NOR noticeboard; this is a better place. It seems to me that the discussion is getting too far into the weeds. Let me try framing the issue around these statements:

  1. The literature is inconsistent about whether caffeine is addictive.
  2. Some recent reviews point out that caffeine modulates dopamine activity and suggest that this modulation may be relevant to the addictive potential of caffeine. (Note http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777290/.)
  3. Addiction does not necessarily depend crucially on dopamine. Opiates and tranquilizers are addictive by a mechanism that depends on suppression of the brain's punishment/suffering system rather than activation of the reward system.
  4. Chronic consumption of caffeine results in up-regulation of the adenosine system. This effect is probably the basis of caffeine withdrawal syndrome, and may be sufficient in itself to account for addition (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777290/).


Looie496 (talk) 14:31, 9 August 2015 (UTC)

I think the problem is resolved now. That said, diagnostic models unfortunately have used the terms "addiction" and "dependence" interchangeably in the past, in turn affecting the use of terminology in literature. A withdrawal syndrome is associated with dependence, which, according to experimental evidence, is a distinct pathology from an addiction; that's not really surprising though since they're mediated through opposite types of reinforcement (dependence/withdrawal involves negative reinforcement whereas addiction involves positive reinforcement), which wouldn't necessarily involve the same neural pathways/brain structures/intracellular signaling since they're different cognitive processes.
As an aside, opiates/tranqs do activate the reward system, but typically not directly within the pathway itself; e.g., opiates disinhibit the reward pathway primarily through opiate signaling in the RMTg→VTA projection that synapses onto the VTA neurons that in turn project to the NAcc shell. Some addictive tranqs like PCP and ketamine do act directly on the VTA→NAcc shell pathway through its NMDARs though. I actually have no clue how propofol's pharmacodynamics produce an addictive signaling cascade though - it's associated with compulsive use and has been shown to induce ΔFosB in D1-type NAcc MSNs. Seppi333 (Insert 2¢) 23:03, 9 August 2015 (UTC)

Subpage content fork

Speaking of subpages, we need to apply WP:MEDRS to health effects of caffeine to prune out some highly outdated primary sources, then merge it back into this article since there's duplicate section topics of approximately the same length in both, but with different content/sourcing. That page is basically a WP:CFORK due to the duplicate topical coverage and difference in content.

I ran into the same problem with the related Health effects of MDMA/Effects of MDMA on the human body article - it was an abhorrently shitty content fork rife with bad sourcing compared to the parent article (aside: the page I'm referring to is located at Talk:MDMA/Effects of MDMA on the human body, mainly to prevent random people from restoring it while preserving the history). Seppi333 (Insert 2¢) 16:50, 16 August 2015 (UTC)

Yes, the useful content should be merged back into the main article. Sizeofint (talk) 20:26, 16 August 2015 (UTC)

  checkY Merger complete. Seppi333 (Insert 2¢) 00:23, 16 December 2015 (UTC)

Hello fellow Wikipedians,

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analogs

Here is an interesting 2D substituted caffeine diagram: [8] Nagelfar (talk) 00:26, 9 November 2015 (UTC)

Regulation

FYI, I don't know the current rules but awhile back Canada regulated its use in beverages. A well-known "lemon-lime" flavored soda that is known for having high caffeine in the United States has little if any caffeine in Canada because the drink had little if any naturally-occurring caffeine and (at the time at least) adding caffeine to that drink would put the drink under increased regulations. If memory serves, non-naturally-occurring caffeine was regulated as a dietary supplement in Canada back then. Anyone know the current laws on caffeine in foods in Canada? davidwr/(talk)/(contribs) 16:53, 28 November 2015 (UTC)

Reference for some infobox content

to content referenced by [1] is just part of that article's introduction. It is there referenced with the following review [2] Also, the onset of action seems a little long. Yak90 (talk) 14:19, 24 January 2016 (UTC)

It looks to me it is supposed to be sourced from Ribeiro JA, Sebastiao AM. Caffeine and adenosine. J Alzheimers Dis 2010;20 462(Suppl. 1):S3–15. though I am have a hard time finding the content in either of the papers. I sourced the intro to that paper because it was the only non-primary source I could find on Google Scholar at the time. If you can find something better please add it. Sizeofint (talk) 17:43, 24 January 2016 (UTC)

Self-assembly of Caffeine

Caffeine is known to exist in different polymorphic form. It has been shown that an anhydrous form of caffeine can undergo supramolecular self-assembly leading to gelation in alcoholic solvents including ethanol at very low concentration (1). This might bring some new application of caffeine in materials science.

(1) Nonappa; Kolehmainen, E. Caffeine as a Gelator. Gels 2016, 2, 9. — Preceding unsigned comment added by Nonappa (talk • contribs) 17:40, 3 March 2016 (UTC)

Are you proposing this be added to the "Research" section? Sizeofint (talk) 19:18, 3 March 2016 (UTC)

Review

... of risks and benefits for neurological disease doi:10.1136/practneurol-2015-001162 JFW | T@lk 22:44, 16 March 2016 (UTC)

Semi-protected edit request on 8 August 2016

In the Physical and chemical properties, the line "It is weakly basic (pKa = ~0.6) requiring strong acid to protonate it.[138]" is incorrect, I would suggest changing it to:

"It is weakly basic (pKb = ~0.6) requiring strong acid to protonate it.[138]" and not referencing the book but the paper directly (see below).

The pKa value for caffeine is around 14:

https://www.sigmaaldrich.com/content/dam/sigma-aldrich/docs/Sigma-Aldrich/Product_Information_Sheet/c0750pis.pdf

I followed the citation 138 and in the book "Harry G. Brittain; Richard J. Prankerd (2007). Profiles of Drug Substances, Excipients and Related Methodology, volume 33: Critical Compilation of pKa Values for Pharmaceutical Substances. Academic Press. p. 15. ISBN 0-12-260833-X. Retrieved 15 January 2014." on the page 106 values of pKa for caffeine are indeed -0.13 and 0.18 - this is also incorrect, thus it would suggest that caffeine is an acid comparable in strengt to e.g. TFA. The table on the page 106 points out to the paper by ROBERT L. BENOIT AND MONIQUE FRECHEIT "Protonation of hypoxanthine, guanine, xanthine, and caffeine". In the paper, it were the pKb values that were measured not pKa (as stated in the last line of the abstract).

212.87.10.2 (talk) 12:54, 8 August 2016 (UTC)

I did a CTRL-F in that paper [9] and I'm not seeing where it has the 0.6 figure. Sizeofint (talk) 17:27, 8 August 2016 (UTC)
Not done: Like Sizeofint I cannot find anything in the article to support that change. The sheet does say the pKa is 14, but there's nothing about 0.6 in the pdf and there's no "pKb" either. EvergreenFir (talk) 01:02, 9 August 2016 (UTC)

Contradiction

In the lead, it says caffeine may be used to treat pulmonary dysplasia of prematurity and prevent apnoea of prematurity, then in the next section that it is used to treat or prevent pulmonary dysplasia of prematurity and treat, but not prevent, apnoea of prematurity. Which is correct? At least I try (talk) 03:03, 21 August 2016 (UTC)

I think the article is correct, fixed the lead. Sizeofint (talk) 04:09, 21 August 2016 (UTC)

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Semi-protected edit request on 18 February 2017

The range for caffeine per cup of coffee is in error. Ethiopian Harrar (a dry-processed coffee) has only 58 mg of caffeine per 8 ox drip. The upper range for Arabíca Coffee is 132 mg per cup (Columbia and Guatamala – both washed coffees) Robusta coffee is often at 200 mg per 8 oz. Fr Steven Clark (talk) 23:31, 18 February 2017 (UTC)

What is the source of this information? — Anita5192 (talk) 00:44, 19 February 2017 (UTC)
Not done: please provide reliable sources that support the change you want to be made. DRAGON BOOSTER ★ 08:14, 19 February 2017 (UTC)

Dubious unsourced sentence.

" It (caffeine) is found in the seeds, nuts, or leaves of a number of plants native to South America and East Asia and confers on them several survival and reproductive benefits." How does caffeine confer "survival and reproductive benefits" on the plants that contain it? Aside from the fact every living thing has evolved with its given characteristics because of some survival advantage (which is true for every living thing and does not need to be stated for each case), I am aware of no special thing about caffeine that confers a peculiar "survival and reproductive advantage". The sentence should end with "...East Asia." The rest of the sentence adds nothing, is unsourced, and is a waste of space.77Mike77 (talk) 16:35, 5 March 2017 (UTC)

@77Mike77: you are talking about a sentence in the WP:LEAD, where we are supposed to be summarizing the key aspects of the rest of the article. That later content is (supposed to be) more specific and detailed, and well cited. But therefore we don't also include those cites in the lead. Think of it like a paragraph with a topic sentence and then supporting sentences. The § Natural occurrence section of the article has several specific and cited examples of the benefits to the plants. DMacks (talk) 17:46, 5 March 2017 (UTC)

Fair point about the citation not needed in the lede, but the sentence is still poor, because it is incomplete and goes nowhere. Maybe if it said, "... confers on them several unusual survival benefits." But still. Does the article about rattlesnakes say that their venom "confers on them several survival and reproductive benefits"? It would be best if the lede did not slightly open the door on a tangential topic, only to drop it like a hot potato. Very awkward. But if such a low bar is the SOP at wikipedia, that isn't my problem. I've found that most articles here are soon carved in stone at a mediocre level, and are immune to improvement. Thanks for being polite.77Mike77 (talk) 21:47, 5 March 2017 (UTC)

I think the idea of that sentence is to summarize the Caffeine#Natural occurrence section. If you have a better idea please suggest it. There aren't too many people who work on this article and we're amenable to positive changes. Sizeofint (talk) 22:53, 5 March 2017 (UTC)

I suggest what I mentioned earlier, i.e. simply inserting the word "unusual" into the sentence, i.e.: "It is found in the seeds, nuts, or leaves of a number of plants native to South America and East Asia and confers on them several unusual survival and reproductive benefits." The word "unusual" suggests there is more to follow that explains it. It's a very minor change that I think would improve the sentence. Overall, I think the article is very good, it was just that sentence that seemed in need of improvement.77Mike77 (talk) 03:42, 7 March 2017 (UTC)

Is it unusual though? I think there are many plants that have protective chemicals. Caffeine is only given special attention because it is also psychoactive. Perhaps it might be better to just summarize which survival and reproductive benefits it confers. Sizeofint (talk) 04:05, 7 March 2017 (UTC)

I think it is unusual compared to the average plant. Like a skunk is an unusual animal.77Mike77 (talk) 23:42, 10 March 2017 (UTC)

Caffeine does predominantly induce unpleasant psychoactive effects (a form of operant punishment) in some individuals, and probably in other animals as well; in such cases, it necessarily induces aversive motivational salience towards the ingested caffeine-containing substance (i.e., the person avoids ingesting it again), such as coffee. Other more obvious phytochemical deterrents to herbivores are capsaicin (the spicy compound in hot peppers) and allyl isothiocyanate (the "spicy" compound in wasabi); these induce aversive motivational salience by causing unpleasant sensory stimulation via activation of a nociceptor called TRPV1. That said, these compounds are not universally effective at staving off predators due to classical conditioning and reinforcement learning; these substances can and do act as conditioned reinforcers in some individuals. Conditioned reinforcers induce attractive motivational salience (a.k.a. incentive salience - i.e., the person desires to ingest it again) after being repeatedly paired with pleasurable stimuli (e.g., tasty food) or desirable outcomes (e.g., increased task performance). Seppi333 (Insert 2¢) 22:27, 7 March 2017 (UTC)

Caffeine#During_pregnancy

I am updating a Cochrane Review on this, and I feel that this paragraph should be changed around. The first sentence presently states "Caffeine consumption during pregnancy does not appear to increase the risk of congenital malformations, miscarriage or growth retardation even when consumed in moderate to high amounts.[63]"

This is followed by a "however"... a cochrane review (that states there is not sufficient evidence to "confirm or refute caffeine avoidance during pregnancy", and other references from WP:MEDRS sources suggesting that pregnant women limit their caffeine intake.

I feel that a health guidance document or reference from a national or international expert body should be used for the first sentence, followed by the cochrane review, and the other reviews (including the above review reference stating that caffeine does not appear to increase the risk of birth defects or low birth weight etc).

Here is my proposed edit, it changes around the paragraph:

This is a great improvement IMO. I'm thinking that the first paragraph might fit better under the "Specific populations" section though. Sizeofint (talk) 04:09, 23 March 2017 (UTC)
very good improvement to the section(you might use [10] for the last sentence which has a citation needed)--Ozzie10aaaa (talk) 10:58, 23 March 2017 (UTC)
Thanks User:Ozzie10aaaa, I am looking at your link but I am not familiar with these text books. Do you have a particular one in mind that you feel is a strong WP:MEDRS?JenOttawa (talk) 00:19, 24 March 2017 (UTC)
Thanks User:Ozzie10aaaa. I will sit down and look through this book later this weekend or early next week. JenOttawa (talk) 02:56, 25 March 2017 (UTC)


This meta-analysis from 2016 implies that higher caffeine intake (over 150 mg per day) is associated with pregnancy loss. However there are limitations with the meta-analysis such as possible confounding. Axl ¤ [Talk] 14:29, 23 March 2017 (UTC)
The paper is written by the same group as "Maternal caffeine intake during pregnancy is associated with risk of low birth weight" below (reference 8). Axl ¤ [Talk] 14:33, 23 March 2017 (UTC)
This review states that high maternal preconception caffeine intake (over 300 mg per day) is associated with increased risk of pregnancy loss. However, again the studies included were observational. I wonder if preconception caffeine intake is really a marker of during-pregnancy caffeine intake though. Axl ¤ [Talk] 14:40, 23 March 2017 (UTC)
Thanks for all the help with this and for your support. I have updated the page with the new edit. I will go through these references and add them in tonight. This all looks great! JenOttawa (talk) 16:17, 23 March 2017 (UTC)
User:Axl Is this what you had in mind with your suggested references? I can add the following into the article (the first reference is already in, the other two are your suggestions)

There is some evidence that higher caffeine intake by pregnant women may be associated with a higher risk of giving birth to a low birth weight baby,[3] and may be associated with a higher risk of pregnancy loss.[4] A systematic review, analyzing the results of observational studies, suggests that women who consume large amounts of caffeine (greater than 300 mg/day) prior to becoming pregnant may have a higher risk of experiencing pregnancy loss.[5]

Thanks again, JenOttawa (talk) 00:13, 24 March 2017 (UTC)

This new paragraph looks fine. Axl ¤ [Talk] 11:57, 24 March 2017 (UTC)
JenOttawa, did you mean to cite a 1973 paper in reference 47? Looks good otherwise. Sizeofint (talk) 16:38, 24 March 2017 (UTC)
Definitely not! Good catch, there must have been a mistake when I was pasting it in. Thanks for noticing User:Sizeofint. JenOttawa (talk) 02:43, 25 March 2017 (UTC)

During pregnancy

The UK Food Standards Agency has recommended that pregnant women should limit their caffeine intake, out of prudence, to less than 200 mg of caffeine a day – the equivalent of two cups of instant coffee, or one and a half to two cups of fresh coffee.[6] The American Congress of Obstetricians and Gynecologists (ACOG) concluded in 2010 that caffeine consumption is safe up to 200 mg per day in pregnant women.[7] For women of childbearing age, Health Canada recommends a maximum daily caffeine intake of no more than 300 mg, or a little over two 8 oz (237 mL) cups of coffee.[8]

The evidence for or against the importance of limiting caffeine intake during pregnancy is insufficient and of weak quality.[9] There are conflicting reports in the scientific literature about caffeine consumption during pregnancy.[10] A 2011 risk analysis review found that caffeine consumption during pregnancy does not appear to increase the risk of congenital malformations, miscarriage or growth retardation even when consumed in moderate to high amounts.[11] There is some evidence that the hormonal changes during pregnancy slow the metabolic clearance of caffeine from the system, causing a given dose to have longer-lasting effects (as long as 15 hours in the third trimester).[12] There is also some evidence that caffeine intake by pregnant women is associated with a higher risk of giving birth to a low birth weight baby.[13]

Caffeine's potential impact on female fertility, and its precise impact on pregnancy, is still being studied, but (as with many other substances in these circumstances) caution and moderation is warranted in any case until further information is known.[citation needed]

References

  1. ^ Poleszak, Ewa; Szopa, Aleksandra; Wyska, Elżbieta; Kukuła-Koch, Wirginia; Serefko, Anna; Wośko, Sylwia; Bogatko, Karolina; Wróbel, Andrzej; Wlaź, Piotr (July 2015). "Caffeine augments the antidepressant-like activity of mianserin and agomelatine in forced swim and tail suspension tests in mice". Pharmacological Reports. 68: 56–61. doi:10.1016/j.pharep.2015.06.138. Retrieved 12 September 2015.
  2. ^ Fredholm, Bertil B., et al. "Actions of caffeine in the brain with special reference to factors that contribute to its widespread use." Pharmacological reviews 51.1 (1999): 83-133.
  3. ^ Chen, Ling-Wei; Wu, Yi; Neelakantan, Nithya; Chong, Mary Foong-Fong; Pan, An; van Dam, Rob M (19 September 2014). "Maternal caffeine intake during pregnancy is associated with risk of low birth weight: a systematic review and dose-response meta-analysis". BMC Medicine. 12 (1). doi:10.1186/s12916-014-0174-6.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ Chen, Ling-Wei; Wu, Yi; Neelakantan, Nithya; Chong, Mary Foong-Fong; Pan, An; van Dam, Rob M. (2016-05-01). "Maternal caffeine intake during pregnancy and risk of pregnancy loss: a categorical and dose-response meta-analysis of prospective studies". Public Health Nutrition. 19 (7): 1233–1244. doi:10.1017/S1368980015002463. ISSN 1475-2727. PMID 26329421.
  5. ^ Tan, T. L. (1973-01-01). "[Physiology of nitrate reduction in Pseudomonas aeruginosa]". Zeitschrift Fur Allgemeine Mikrobiologie. 13 (1): 83–94. ISSN 0044-2208. PMID 4196566.
  6. ^ "Food Standards Agency publishes new caffeine advice for pregnant women". Retrieved 3 August 2009.
  7. ^ American College of Obstetricians and Gynecologists (August 2010). "ACOG CommitteeOpinion No. 462: Moderate caffeine consumption during pregnancy". Obstet Gynecol. 116 (2 Pt 1): 467–8. doi:10.1097/AOG.0b013e3181eeb2a1. PMID 20664420.
  8. ^ "It's Your Health – Caffeine". Health Canada. March 2010. Retrieved 8 November 2010.
  9. ^ Jahanfar, S; Jaafar, SH (28 February 2013). "Effects of restricted caffeine intake by mother on fetal, neonatal and pregnancy outcome". The Cochrane database of systematic reviews (2): CD006965. PMID 23450573.
  10. ^ Kuczkowski KM (2009). "Caffeine in pregnancy". Arch. Gynecol. Obstet. 280 (5): 695–8. doi:10.1007/s00404-009-0991-6. PMID 19238414.
  11. ^ Brent RL, Christian MS, Diener RM (2011). "Evaluation of the reproductive and developmental risks of caffeine". Birth Defects Res. B Dev. Reprod. Toxicol. 92 (2): 152–87. doi:10.1002/bdrb.20288. PMC 3121964. PMID 21370398.
  12. ^ Fredholm BB, Bättig K, Holmén J, Nehlig A, Zvartau EE (1999). "Actions of caffeine in the brain with special reference to factors that contribute to its widespread use". Pharmacol. Rev. 51 (1): 83–133. PMID 10049999.
  13. ^ Chen, Ling-Wei; Wu, Yi; Neelakantan, Nithya; Chong, Mary Foong-Fong; Pan, An; van Dam, Rob M (19 September 2014). "Maternal caffeine intake during pregnancy is associated with risk of low birth weight: a systematic review and dose-response meta-analysis". BMC Medicine. 12 (1). doi:10.1186/s12916-014-0174-6.{{cite journal}}: CS1 maint: unflagged free DOI (link)

Good Faith edit on caffeine and children

https://en.wikipedia.org/w/index.php?title=Caffeine&type=revision&diff=772817905&oldid=772063041

Should we leave this new sentence about caffeine and children out until a more recent WP:MEDRS citation is found?

Thanks. JenOttawa (talk) 15:00, 29 March 2017 (UTC)

You mean "There is no evidence that coffee stunts a child's growth"?
It is commonly stated that caffeine does stunt a child's growth.
It however appears to be an urban legand[12].
I think it is fine to include this. Doc James (talk · contribs · email) 15:24, 29 March 2017 (UTC)
Found a suitable source[13] Doc James (talk · contribs · email) 15:33, 29 March 2017 (UTC)
Thanks @Doc James:. I am not up to speed with the literature on caffeine and kids. I just noticed this new edit and was not sure if it was a suitable reference.JenOttawa (talk) 16:02, 29 March 2017 (UTC)
Agree that it was not a very good ref. But the content is the generally accepted position it appears. The new ref is somewhat better. Doc James (talk · contribs · email) 16:06, 29 March 2017 (UTC)

Student assessement

Check a few citations. Do the links work? Is there any close paraphrasing or plagiarism in the article? I did not find any broken links or plagiarism or close paraphrasing in this article. It appears to be a well research, well cited article with more information than I thought possible. Is each fact referenced with an appropriate, reliable reference? It does appear there are some facts that do not have a direct source. Some of them are what I would consider "common knowledge" while others, like the last paragraph in the opening section, about lethal caffeine doses, does indeed lack proper citations. This information is properly cited later in the article under the overdose section, so I am not sure if that is adequate or not.Davidjpboyd (talk) 04:17, 5 April 2017 (UTC)

Welcome to Wikipedia. Yes, the lead is supposed to the body so it isn't necessary to reference statements in the lead because they should be already referenced in the body. However, for controversial statements or medical topics this is often done regardless of the general practice. Sizeofint (talk) 22:27, 5 April 2017 (UTC)

Cosmetics

I see no mention of its use in cosmetics to, for example, reduce eye bags. Does it go into the blood? Is the effect through the skin similar to the oral effect? --Error (talk) 21:44, 1 March 2017 (UTC)

It is now also being sold in shampoos - Alpecin. May have no medical effect, just promotional sales woo. 60.242.247.177 (talk) 08:39, 7 April 2017 (UTC)

Function in Pain Killers - APC

For a long time aspirin-phenacetin-caffeine compound analgesic, was used as a remedy for fever and pain before phenacetin was banned. (Mentioned in other articles)

Why was caffeine used? 60.242.247.177 (talk) 10:58, 6 April 2017 (UTC)

Googling reveals that caffeine was used to reduce fever as quinine came from a related plant. This may be the real reason rather than pain reduction. These demonstrate some possible not necessarily acceptable sources.

https://books.google.com.au/books?id=pkzx2TeYYT8C&pg=RA3-PA645&lpg=RA3-PA645&dq=fever+reduction+caffeine+quonine&source=bl&ots=LGCL29Ixqg&sig=Xt8vtImiYbQMpLPHc-Z1y0j3DDU&hl=en&sa=X&ved=0ahUKEwix8qOk85HTAhUBwLwKHboxB38Q6AEIKzAD#v=onepage&q=fever%20reduction%20caffeine%20quonine&f=false

https://books.google.com.au/books?id=sUEEAAAAMBAJ&pg=PA23&lpg=PA23&dq=fever+reduction+caffeine+quonine&source=bl&ots=anTEOQwq67&sig=GFoKNQ22tzNVGWBKhcITVH7eBvQ&hl=en&sa=X&ved=0ahUKEwix8qOk85HTAhUBwLwKHboxB38Q6AEIKTAC#v=onepage&q=fever%20reduction%20caffeine%20quonine&f=false

http://www.botanical-online.com/english/feverremedies.htm This one from 1972 is a claim that caffeine in tea taken with aspirin (known antipyretic) does not reduce fever, but may increase body heat. 60.242.247.177 (talk) 08:32, 7 April 2017 (UTC)

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