Q: Does a small cup of coffee result in a 45% reduced blood flow to the brain?
tl;dr NO!
this means, yes, sure, while there is a significant decrease in measured cerebral blood flow, this is not nearly in the range claimed and surely not for the dosage claimed.
this is not something to be concerned about. For several reasons. One is that this effect is largely compensated by reactive mechanisms and habituation.
The other biggest restriction to the claim is that this not entire brain blood flow, but region specific.
It does not follow what the claim alludes to: caffeine does not decrease brain function and health across the board to be of overly acute concern.
A vast oversimplification and exaggeration for caffeine doses commonly consumed. As shown at the end of this answer✶, the claimant also misreports its own 'source' which already is itself an alarmist and non-scientific piece of campaigning journalism. For adults low and moderate caffeine consumption seems to be more beneficial than detrimental.
Q: MRI images taken before and after 1 cup of coffee showed a decrease in blood flow to the brain by 45%. When the blood flow reduction was measured exactly, it was actually 52% less blood flow to the brain, after just one small cup of coffee.
a) This implies that 1 small cup of regular coffee, which should be between 80–175 mg caffeine, reduces on average cerebral blood flow (CBF) by 45–52% –– This is not the case. For 250mg the average lies usually ~20–30%.
b) If meant to imply that even in one person it could go to these numbers: that's virtually unheard of for that dose. And a single measurement does only prove so much anyway. Even under well controlled experimental settings.
c) If meant to show that one journalist had her CBF measured after an uncontrolled experiment and CBF did decrease by that amount:
- The claim presents a source that did not include these numbers either.
- even if it did, go to b.
The most widely consumed psychoactive compound is caffeine, which is found in various drinks and foods, such as coffee, tea, soft drinks and chocolate. Caffeine is a well-known cerebral vasoconstrictor, which significantly reduces resting cerebral perfusion by antagonizing adenosine receptors in the human brain, especially A1 and A2A subtypes that mediate vasodilation. By using PET methodology, Cameron et al. quantified the magnitude of the decrease in CBF in 1990. A single dose of 250 mg caffeine reduced resting CBF, with decreases ranging from 22% to 30%; this is in line with later studies using ASL and PET. Recently, Turnbull and colleagues evaluated the literature with respect to the effects of acute caffeine intake (45 to 400 mg) on CBF in adult subjects.
Trials investigating intakes of ≥175 mg observed significant decreases in CBF in all study populations. Studies that administered lower doses only reported significant decreases in caffeine-naïve or low-caffeine consumers, but not in habitual consumers. Altogether, the authors of the recent review concluded that there is some evidence for a dose-response relationship between caffeine intake and CBF, with greater sensitivity in caffeine-naïve study subjects as compared to habitual caffeine consumers. Interestingly, a global reduction by approximately 20% in gray matter CBF (measured with ASL perfusion MRI) was not only observed two hours after the intake of a single dose of 184 mg caffeine (equivalent to one strong espresso coffee), but also following the consumption of 2820 mg black tea solids containing 184 mg caffeine that is equivalent to about six cups of tea. This suggests that flavonoids (~902 mg) in black tea did not affect the acute decrease in CBF following the intake of caffeine in healthy male subjects with a mean age of 24 years.
Even though a robust blood flow decrease in response to acute caffeine consumption was observed, neural activity was enhanced, as adenosine’s effects are antagonized. Cognitive performance, however, was not changed. This might partly be explained by results from calibrated blood oxygenation level-dependent (BOLD) functional MRI experiments. It was shown that after caffeine intake, the cerebral metabolic rate of oxygen consumption remained stable in some, but not all studies, because the decrease in CBF was compensated for by an increase in oxygen extraction. More importantly, long-term effects are unclear. Vascular adenosine receptors may be upregulated during long-term caffeine use to preserve the CBF at a level that would have existed in a caffeine-naïve state. Another main issue are the effects of caffeine withdrawal. CBF may be abnormally high due to overnight withdrawal from caffeine or abnormally low due to recent caffeine ingestion. Due to its widespread use, caffeine is therefore a potential confounder in many cerebral perfusion studies, complicating the interpretation of the study results.
Interestingly, the observed effects of caffeine on CBF may explain its efficacy as a contrast booster in functional MRI studies. In fact, by acting as a cerebral vasoconstrictor, caffeine causes an increase in the concentration of deoxyhemoglobin, and thus decreases the BOLD baseline resting signal. During activation, the human vasculature responds from below-normal baseline levels with a normal increase in blood flow, resulting in an overall increase in the BOLD contrast. The benefit of an increased BOLD signal contrast can be used to improve, for example, image resolution, the acquisition scheme, or the task design of functional MRI experiments.
–– Peter J. Joris et al: "Cerebral Blood Flow Measurements in Adults: A Review on the Effects of Dietary Factors and Exercise", Nutrients; 10(5): 530, 2018. doi
Note of the dosage, 250mg caffeine in the first and 175 in the second reference above. Drip coffee of 7oz, 207ml results in ~115–175 mg caffeine. Thus in caffeine naïve users the CBF reduction was up to 30% with what is not a cup, but either a strong cup regarding mg caffeine or just a bucket.
Resting CBF was reduced by an average of 24%. The reproducibility of the results was verified in one subject who was scanned on 3 different days. The dynamic changes are similar to those previously reported for baseline CBF reductions induced by hypocapnia and hyperoxia.
–– Liu TT: "Caffeine alters the temporal dynamics of the visual BOLD response", Neuroimage, 23(4):1402-13, 2004.
and
The available literature suggests that cardiovascular effects experienced by caffeine consumers at levels up to 600 mg/day are in most cases mild, transient, and reversible, with no lasting adverse effect.
Stroke occurs when blood flow to an individual's brain is interrupted, causing cell death within the brain due to a lack of proper oxygenation. A stroke may manifest in two primary ways: via blockage of a blood vessel supplying the brain (ischemic stroke), or via bleeding into and around the brain (hemorrhagic stroke). Stroke symptoms include sudden numbness or weakness, sudden confusion, trouble speaking or understanding speech, sudden issues related to balance, and/or sudden severe headache with no known cause.
Overall, 31 total studies evaluated the relationship between caffeine consumption and stroke incidence and/or mortality. All of these observational studies assessed correlations between stroke and self-reported coffee and/ or tea consumption. Ten of the 31 stroke-related studies evaluated stroke risk by subtype.
There was no statistically significant relationship between coffee and/or tea consumption at any level of consumption investigated and risk of stroke in 19 of 31 the studies. The majority of studies in this group were longitudinal in design except for one large cross-sectional study (n 1⁄4 12,959 subjects). All observational studies included approximately 3500 to 200,000 participants, reported a mean follow-up period ranging from approximately 2 to 30 years and considered coffee and tea consumption levels varying from 95 to !760 mg/caffeine a day.
Nine out of 31 studies reported statistically significant decreased risks of stroke in some coffee and tea consumers, though these decreases in risk were not always consistent across consumption groups, study sub-populations or stroke subtype within individual studies. Again, these studies were large cohort studies including several thousand participants (ranging from approximately 6400 to 402,000 in number), with mean follow-up periods ranging from approximately 5 to 19 years and with a wide variation of coffee and tea consumption levels (<45 to !475 mg/caffeine a day). Within these nine studies, the levels of consumption at which investigators reported decreased risks varied, ranging from 190 to !475 mg/day of caffeine from coffee and 180–225 mg/day of caffeine from tea.
Four of these nine studies considering stroke subtypes reported decreased relative risks in the combined stroke categories (i.e., all stroke sub-types combined), but these decreases disappeared when further parsing the population by stroke sub-type.
Of particular note is one study of 6358 Japanese adults without a history of stroke or heart disease; this study reported that green tea drinkers drinking more than several cups of tea every two to three days were at decreased relative risk of developing cerebral hemorrhage compared to individuals who drank several cups of green tea per week or less. These results were only statistically significant in green tea drinkers; no relationship between tea consumption and stroke was reported among roasted tea drinkers, suggesting that the results may be more related to green tea as a beverage than caffeine as an ingredient.
Three studies out of the 31 total stroke-related studies reported an increased relative risk of stroke associated with some level of coffee consumptio. The first study, a cohort study of 499 hypertensive older and middle-aged Hawaiian men followed for 25 years, reported a statistically significant association between consumption of at least 5 cups of coffee per day (!475 mg caffeine) and thromboembolic (i.e., ischemic) stroke (RR 1⁄4 2.3, 95% CI: 1.4, 4.0) (Hakim 1998). This particular analysis excluded men with diabetes, and adjusted for age, blood pressure, total cholesterol, triglycerides, alcohol use, and physical activity. This study also excluded past and current smokers from all analyses, and did not identify a statistically significant association for hemorrhagic stroke in any coffee consumption category. The second study, a case-control study of 237 patients at an Italian hospital who have experienced ischemic stroke, reported an increased risk among those reporting at least 5 cups of coffee per day (!475 mg caffeine, OR 1⁄4 15.3, 95% CI: 2.4, 97.5). However, this estimate is limited because of the small number of cases within this consumption category (n 1⁄4 16), and even smaller number of matched controls (n 1⁄4 2); the model used for this estimate adjusted for social class, education, alcohol consumption, smoking, diabetes mellitus, hypertension, cholesterol, BMI, physical activity and family history of AMI and stroke. Associations were not statistically significant in the other consumption categories. The third study, a case-control study of 390 individuals, mean age 68–70, interviewed shortly after experiencing acute ischemic stroke (median follow-up: 3 days), reported that the risk of experiencing a stroke within one hour of coffee consumption was higher compared to the risk of experiencing a stroke during periods of coffee non-consumption (RR 1⁄4 2.0, 95% CI: 0.4, 2.4) (Mostofsky 2010). When further considering daily intake of caffeinated coffee in the previous week, the investigators noted that the increased risk of stroke in the hour after consuming coffee was only elevated among those consuming 1 or fewer cups per day (95 mg caffeine/day). Those who consumed coffee more regularly were not at increased risk of stroke in the hour after consuming coffee. The statistical significance of these results were retained after sensitivity analyses accounted for coffee consumption at certain times of day and select stroke triggers (i.e., physical activity, anger, alcohol consumption, cigarette smoking).
Overall, the weight of evidence (28 out of 31 studies) suggests that there is no statistically significant association between caffeine consumption (in the form of coffee and/or tea) and the relative risk of stroke.
–– Duncan Turnbull, Joseph V. Rodricks, Gregory F. Mariano, Farah Chowdhury: "Caffeine and cardiovascular health", Regulatory Toxicology and Pharmacology 89 (2017). DOI: 10.1016/j.yrtph.2017.07.025
And this is not for "the brain, globally"
The CBF and cerebrovascular reactivity (CVR) to hypercapnia were measured with arterial spin labeled magnetic resonance imaging (MRI) before and 2 hours after administration. We found a significant global reduction with caffeine (20%) and tea (21%) in gray matter CBF, with no effect of decaffeinated tea, suggesting that only caffeine influences CBF acutely. Voxelwise analysis revealed the effect of caffeine to be regionally specific. None of the interventions had an effect on CVR. Additional research is required to conclude on the physiologic relevance of these findings and the chronic effects of caffeine and tea intake on CBF.
–– Rishma Vidyasagar et al.: "The effect of black tea and caffeine on regional cerebral blood flow measured with arterial spin labeling", J Cereb Blood Flow Metab., 33(6): 963–968, 2013 doi: 10.1038/jcbfm.2013.40
And
Behavioural data showed that caffeine also improved performance in the oddball task with a significantly reduced number of missed responses. Our results are consistent with earlier studies demonstrating altered flow-metabolism coupling after caffeine administration in the context of our observation of a generalised caffeine-induced reduction in cerebral blood flow demonstrated by arterial spin labelling (19% reduction over grey matter). We were able to identify vascular effects and hence altered neurovascular coupling through the alteration of low-level task FMRI responses in the face of a preserved visual evoked potential. However, our data also suggest a cognitive effect of caffeine through its positive effect on the frontal BOLD signal consistent with the shortening of oddball EEG response latency.
–– Ana Diukova et al.: "Separating neural and vascular effects of caffeine using simultaneous EEG–FMRI: Differential effects of caffeine on cognitive and sensorimotor brain responses", Neuroimage, 62(1): 239–249, 2012. doi: 10.1016/j.neuroimage.2012.04.041
Region specific alterations:
- –– Xu F: "Does acute caffeine ingestion alter brain metabolism in young adults?", Neuroimage; 110:39-47, 2015. doi:10.1016/j.neuroimage.2015.01.046.
Entropy is an important trait of brain function and high entropy indicates high information processing capacity. We recently demonstrated that brain entropy (BEN) is stable across time and differs between controls and patients with various brain disorders. The purpose of this study was to examine whether BEN is sensitive to pharmaceutical modulations with caffeine. Both cerebral blood flow (CBF) and resting fMRI were collected from sixty caffeine-naïve healthy subjects before and after taking a 200 mg caffeine pill. Our data showed that caffeine reduced CBF in the whole brain but increased BEN across the cerebral cortex with the highest increase in lateral prefrontal cortex, the default mode network (DMN), visual cortex, and motor network, consistent with the beneficial effects of caffeine (such as vigilance and attention) on these areas. BEN increase was correlated to CBF reduction only in several regions (-0.5 < r < -0.4), indicating a neuronal nature for most of the observed BEN alterations. In summary, we showed the first evidence of BEN alterations due to caffeine ingestion, suggesting BEN as a biomarker sensitive to pharmaceutical brain function modulations.
–– Chang D: "Caffeine Caused a Widespread Increase of Resting Brain Entropy", Sci Rep., 8(1):2700, 2018. doi: 10.1038/s41598-018-21008-6.
As this was also raised in comments below the question: a 50% reduction of cerebral bloodflow usually produces prodromal syncopic symptoms, but the brain needs blood not like a vampire but mainly & acutely for oxygen. And caffeine doesn't much interfere with oxygenation of the brain.
In the nonsyncopal head-up tilted subjects as in the controls, blood pressure, heart rate, MCA vmean and brain oxygenation indices remained stable. The results suggest that during orthostasis, presyncopal symptoms relate not only to cerebral hypoperfusion but also to reduced brain oxygenation.
–– Madsen P et al.: "Near-infrared spectrophotometry determined brain oxygenation during fainting", Acta Physiol Scand., 162(4):501-7, 1998.
Cf also: Njemanze: "Critical limits of pressure-flow relation in the human brain", Stroke 23:1743–17478, 1992. // Antonio Franco Folino: "Cerebral Autoregulation and Syncope", Progress in Cardiovascular Diseases, Vol. 50, No. 1, 2007: pp 49-80. ("In 80% of symptomatic patients, the critical lower limit of mean flow velocity was at -50% of resting baseline while patients were lying supine.")
* From scientific paper, over sensationalistic misleading news, to propaganda of pure ideology
A note on the alleged source of the claim: this was one abc-reporter, Lisa Stark in a video entitled: "Dr Richard Besser caffeine warning-parents – Many common drinks available to your teenagers contain too much caffeine. 3:00 | 02/14/11", in a totally uncontrolled setting. We do not know anything about the health status of the reporter, proper procedure or a load of other confounders (her cup looked indeed quite large, but that's all we know for the really ingested dosage). This one measurement said that "blood flow was reduced by ~40%." How the extra 5% got into the claim is another mystery, but one I cannot explain here with what is available. The number of 52% reduction is not found in any way in the source given by claimant. It only strengthens the claim originating site likes exaggeration more than scientific study results.
The claimant's source accompanying written abc-news report ("New Report Warns of Energy Drink Health Risks for Children – By Liz Neporent, ABC Feb. 14, 2011") also doesn't show these numbers anywhere. But it should be perhaps noted that it was inspired by this study:
Sara M. Seifert & […] & Steven E. Lipshultz: "Health Effects of Energy Drinks on Children, Adolescents, and Young Adults", Pediatrics. 2011 Mar; 127(3): 511–528. 2011 Feb 14. doi: 10.1542/peds.2009-3592
Not even that publication contains the numbers claimed!
So. To be clear:
Q: When the blood flow reduction was measured exactly, it was actually 52% less blood flow to the brain, after just one small cup of coffee.
This is all invented out of thin air. The numbers 45% & 52% are nowhere to be found, the measurement was a single one, not "repeated with more precision", and neither status of the reporter nor the dose she took was disclosed, but apparently: no "small cup."
And to balance this study in children and adolescents, read (notice one of the lead authors is the same as for the study that inspired the devolution into FUD in HAF or ABC-news piece)
–– Jennifer L. Temple, Steven E. Lipshultz et al.: "The Safety of Ingested Caffeine: A Comprehensive Review", Front Psychiatry. 2017; 8: 80, 2017 May 26. doi:10.3389/fpsyt.2017.00080
In general it seems also noteworthy that the claim implied reasoning: "caffeine 🠦 CNS vasoconstriction 🠦 reduced cerebral blood flow 🠦 bad" is far too simplistic on a multitude of levels. The quality and comparability of studies is also often limited.
Caffeine and theophylline affect cerebral circulation, most likely through their effect as adenosine antagonists.
The often severe headaches, common in caffeine withdrawal, appear to be caused by vasodilation of cerebral blood vessels. This action is probably mediated by the action of the methylxanthines on adenosine receptors.
One study, for example, showed that relatively low doses (250 mg) of caffeine have similar effects on cerebral blood flow in non-users and heavy users, evidence against substantial tolerance in heavy users. Moreover, habitual caffeine use does not eliminate its acute effects or its enhancement of the stress response in some studies.
There are, however, opposing findings suggesting that tolerance to caffeine does develop perhaps in as little as five days. One team of investigators examined adults who consumed caffeine on a regular daily schedule and found evidence for significant tolerance. Similarly, Evans and Griffiths demonstrated the development of tolerance with a high dose of caffeine. In addition, the reticular formation in male rats has been shown to develop complete tolerance to caffeine within 2 weeks.
A variety of factors differentiating tolerance studies could have contributed to the observed discrepancy. Lower doses are less likely to lead to tolerance than higher doses or will do so less rapidly. The habitual coffee drinkers in some studies may have had different levels or durations of consumption. In the cases of acute dosing, caffeine consumed by subjects outside the laboratory on the day of the experiment may have varied.
This is particularly true when some investigators request in advance that subjects abstain from caffeine prior to the experiment, while others do not. Differences in age, gender, and arousal-relevant personality dimensions, such as extraversion and impulsivity, may have affected results. Finally, in the population at large, underlying genetic factors may make some people more susceptible to the development of caffeine tolerance. Unfortunately, there is no clear pattern in the studies to date that would specifically target one or more of these explanations. As a result, the tolerance issue remains unresolved.
–– Gene Alan Spiller: "Caffeine", CRC Press: Boca Raton, London, 1998.
While non-adults should probably indeed abstain completely from caffeine, this is really not a reason for everyone to abstain entirely:
In general, caffeine produces long-term cerebral hypoperfusion while at the same time producing its alerting effect via nonselective blockade of adenosine A1 and A2a receptors in the basal forebrain and midbrain reticular formation (Fredholm 1995). However, the pharmacological effects of caffeine reach beyond that of sleep-wake regulation. Specifically, caffeine, independent of its stimulant effects, modulates adenosine pharmacology to induce beneficial changes in molecular signaling cascades that mediate synaptic plasticity. In fact, studies have shown that caffeine has a neuroprotective action against cognitive decline in neurodegenerative disorders such as Alzheimer’s disease (Dall’Igna et al 2007).
Normally, adenosine disrupts the underlying processes of learning and memory at the synaptic level whereas caffeine seems to reverse many of adenosine effects on sleep propensity and even learning and memory by blocking adenosine receptor signaling (Alhaider et al 2010a; 2011). One of the multiple mechanisms by which caffeine affects synaptic plasticity is thought to stem from its different affinities for distinct types of receptors present on the synaptic membranes and cytoplasmic calcium stores.
For instance, on the synaptic membrane level, caffeine blocks mainly adenosine A1 and adenosine A2a in the midbrain reticular formation and basal forebrain (Fredholm et al 1999). On the other hand, caffeine at higher concentration also activates ryanodine receptors, which cause an increase in calcium release from cytoplasmic calcium stores (McPherson et al 1991), leading to an increase in calcium-dependent signaling pathways. Additionally, caffeine inhibits the phosphodiesterase IV enzyme (Smellie et al 1979), which increases the level of intracellular cAMP and enables caffeine to enhance the cAMP signaling cascades involved in LTP and memory. It further enhances striatal glutamate-dependent and glutamate-independent release of dopamine. This is achieved by targeting adenosine receptors, namely A1 and A2a receptors on the presynaptic striatal glutamatergic, and A1 receptors on the presynaptic striatal dopaminergic terminals (Ferre 2010). In particular, a growing body of evidence suggests that endogenous adenosine interferes with synaptic plasticity through activation of the highly expressed adenosine A1 receptors in the hippocampus. For example, adenosine produces an inhibitory effect on LTP in rat hippocampal slices and disrupts the process of learning and memory at the synaptic level (de Mendonca and Ribeiro 1994). Additionally, studies show that adenosine inhibits the release of glutamate from nerve terminals, and prevents NMDA receptor mediated activity at the post-synaptic membrane (Dunwiddie and Masino 2001).
Moreover, it is thought that the increase in the levels of adenosine during prolonged wakefulness adversely affects hippocampus-dependent learning and memory through its action on A1 receptors. In contrast, the diverse effects of caffeine have been shown to be neuroprotective against SD induced insults to synaptic plasticity and memory function. Although, the precise mechanism by which caffeine prevents the effects of SD on memory and LTP is not clearly understood, it is postulated that caffeine protects against SD-induced LTP impairment by preventing the decrease in the levels of key signaling molecules such as CaMKII and CREB (Alhaider et al 2010a; 2010b; 2011). In view of this, it is quite possible that caffeine can prevent learning and memory impairment associated with SD through several mechanisms including antagonism of adenosine receptors, phosphodiesterase enzyme inhibition (Smellie et al 1979), and increasing calcium induced-calcium release (McPherson et al 1991). However, studies indicate that the concentration of caffeine typically consumed by humans (i.e. 40–180mg per cup) may act to improve learning and memory primarily by inhibiting adenosine receptors (Fredholm 1995). Thus, by antagonizing the abundant A1 receptors, caffeine disrupts the deleterious signaling cascades mediated by adenosine on both the pre-synaptic neurons and post-synaptic neurons leading to overall enhancement in synaptic plasticity.
–– Victor R Preedy (Ed): "Caffeine. Chemistry, Analysis, Function and Effects", Food and Nutritional Components in Focus, Vol 2, The Royal Society of Chemistry, 2012.
