Caffeine is a central nervous system stimulant [of the methylxanthine classification] and is the single most consumed psychoactive substance worldwide. According to the University of Villanova, over 90% of adults in the United States consume on a daily basis. What’s more, over 50% of American adults ingest over 300 mg of caffeine daily – usually via beverages like coffee, tea, soda, and energy drinks.
When ingested, caffeine acts primarily as an adenosine receptor antagonist whereby it binds to adenosine receptors (A1, A2A, A2B, A3) and inhibits their activation. More specifically, caffeine prevents the neurotransmitter adenosine from agonizing adenosine receptors, and by doing so, reduces drowsiness and fatigue.
Caffeine also modulates activation of other neurochemical targets, including: the inositol trisphosphate receptor 1, ryanodine receptors (RYR1, RYR2, RYR3), ionotropic glycine receptors, and cyclic-AMP. Most individuals use caffeine with the intention of increasing mental alertness, enhancing cognitive function, and/or improving athletic performance.
In medical settings, caffeine is sometimes recommended for the management of conditions such as: bronchopulmonary dysplasia, orthostatic hypotension, apnea of prematurity, and major depressive disorder. Regardless of the reason for which you use caffeine, if you’re a regular caffeine consumer, you may be curious as to how long it takes for the caffeine that you ingest to “kick in” or elicit a neurophysiologic effect – after consumption.
How long does it take for Caffeine to “kick in”?
The amount of time it takes for caffeine to “kick in” varies among caffeine consumers due to: mode of caffeine administration, genetically-mediated differences in caffeine metabolism, and concurrent substance use. Nevertheless, research suggests that, when consumed in the format of a caffeinated beverage (e.g. coffee, tea, cola), caffeine usually takes effect or “kicks in” within 10 to 20 minutes of ingestion.
According to the U.S. Institute of Medicine (2001), ~99% of caffeine consumed via beverages is absorbed via the GI tract within 45 minutes of ingestion – and distributed throughout body water. After being distributed throughout body water, caffeine efficiently crosses the blood-brain-barrier (BBB) and modifies neurotransmission via antagonism of adenosine receptors.
Antagonism of adenosine receptors substantially upregulates excitatory neurotransmission throughout the brain and causes users to feel as though they’re under the influence of caffeine. Moreover, caffeine reduces cerebral blood flow via vasoconstriction; alters neuroelectrical activity (i.e. brain waves); and activates the sympathetic nervous system – each of which may contribute to its rapid onset of action.
Non-beverage caffeine formats (Gum & Capsules)
Consumption of caffeine in non-beverage formats such as: chewing gum and/or capsules will yield a different rate of absorption and onset of action (than beverage formats). Research suggests that caffeine within caffeinated gum is absorbed quickly and exerts a faster onset of action than beverage formats. If you chew caffeinated gum, the effect of caffeine may become noticeable in less than 10 minutes of gum administration.
On the other hand, administration of caffeine in the format of caffeine capsules is associated with slower absorption, longer times to reach peak plasma concentrations, and a slower onset of action – compared to beverage formats. It is estimated that caffeine capsules may require between 20 and 40 minutes to elicit a noticeable effect (or “kick in”).
Research by Liguori, Hughes, and Grass (1997) noted that caffeine peaked in plasma: ~42 minutes after coffee intake; ~39 minutes after cola intake; and ~67 minutes after caffeine capsule ingestion. Though differences in the average time to reach peak plasma concentrations weren’t significantly different following consumption of caffeinated beverages (coffee and cola), there was a significant delay in the attainment of peak plasma concentrations following capsule administration (compared to the beverages).
Genes (CYP1A2 and ADORA2A) influence caffeine’s onset of action
In addition to the mode of caffeine administration as an influencer of how long it’ll take for caffeine to “kick in,” differences in gene expression among caffeine consumers might impact how quickly caffeine takes effect. Because caffeine is most extensively metabolized by the enzyme CYP1A2, genetically-mediated differences in CYP1A2 expression are most likely to influence its rate of metabolism – and how rapidly it takes effect.
Caffeine may “kick in” at a rapid rate in persons who are fast CYP1A2 metabolizers, but its effect may be of lesser magnitude and/or shorter-lived due to more efficient hepatic metabolism and systemic elimination. On the other hand, caffeine may “kick in” at a slower rate in persons who are slow CYP1A2 metabolizers, but its effect may be of greater magnitude and/or longer-lasting due to less efficient hepatic metabolism and systemic elimination. (Read more: “How Long Does Caffeine Stay In Your System?”).
If you’re unsure about why caffeine isn’t taking effect quickly (or taking effect at all) – genes that encode for CYP1A2 expression may be to blame. It’s also possible that expression of the ADORA2A gene will impact how quickly you notice the effect of caffeine. Research by Domschke, Gajewska, Winter, et al. (2012) reported that differences in ADORA2A gene expression may influence specifically how a person reacts to caffeine, as well as the magnitude of those reactions.
Carrying certain ADORA2A variants might cause increased anxiety and/or arousal following caffeine intake – compared to other variants, which could lead some individuals to report a faster and/or more pronounced onset of caffeine action – than others. If you consistently notice caffeine “kicking in” quickly and facilitating a potent anxiogenic effect, your ADORA2A gene expression might be culpable.
- Source: https://www.ncbi.nlm.nih.gov/pubmed/22293536
- Source: https://www.ncbi.nlm.nih.gov/pubmed/22012471
Substances administered with caffeine
If you’re using substances along with caffeine such as: medications (prescription or over-the-counter), supplements, and/or illicit drugs – these substances may alter caffeine’s onset of action, magnitude of effect, and/or duration of effect. Concurrently-administered drugs can interact with caffeine pharmacokinetically (absorption, metabolism, elimination) and/or pharmacodynamically (neurochemical effects).
Certain concurrently-administered agents may cause pharmacokinetically-mediated interactions via CYP1A2 (CYP450 1A2) isoenzymes. Co-administration of substances that induce CYP1A2 enzyme activity will expedite the rate of caffeine metabolism and clearance, whereas co-administration of substances that inhibit CYP1A2 enzyme activity will slow the rate of caffeine metabolism and clearance.
Examples of CYP1A2 inducers include: tobacco, omeprazole, insulin, modafinil, Nafcillin, beta-Naphthoflavone. If you’re using a CYP1A2 inducer with caffeine, you might notice a faster onset of caffeine action, but a lower magnitude of effect.
Examples of CYP1A2 inhibitors include: Ciprofloxacin (and various fluoroquinolones), Fluvoxamine (i.e. Luvox), St. John’s wort, and Verapamil. If you’re using a CYP1A2 inhibitor with caffeine, you might notice a delayed onset of caffeine action, but a greater magnitude of effect.
In addition to pharmacokinetically-mediated interactions, many co-administered substances may interact with caffeine’s pharmacodynamics. Specifically, some co-administered agents may augment (or enhance) the neurochemical actions of caffeine, whereas other co-administered agents may counteract (or attenuate) its neurochemical actions.
Because caffeine acts as an adenosine receptor antagonist, co-administration of a substance that competitively agonizes adenosine receptors may substantially reduce (or completely block) the effect of caffeine due to opposing neurochemical action – resulting in caffeine never “kicking in.” Additionally, co-administration of a substance that acts as a CNS depressant (e.g. a benzodiazepine) may reduce the magnitude of caffeine’s effect and make it increasingly difficult for a user to notice caffeine “kicking in.”
Oppositely, co-administration of a substance that augments caffeine’s neurochemical actions (e.g. amphetamine) should bolster the magnitude of its effect – and make it easier for users to notice caffeine “kicking in.” In brief, if you notice caffeine “kicking in” at a slower or faster rate than the general population, it could be due to other substances you’re using.
Placebo-like effect from caffeine (?)
If you consistently notice caffeine “kicking in” within seconds or 1 to 2 minutes of administration, this rapid response could be attributable to a placebo-like effect. A placebo-like effect is defined as a favorable effect and/or substantial change in neurophysiology as a result of preexisting expectation or belief.
In other words, if you strongly believe that caffeine will “kick in” and enhance your focus immediately after ingestion – this preexisting expectation may rapidly alter your neurophysiology in ways that are consistent with the expectation. As a result, you may notice better focus, heightened energy, and/or altered consciousness within seconds or 1-2 minutes following your caffeine intake.
Because the effect of caffeine is unlikely to be noticeable within just 1 minute of oral ingestion, if you experience a rapid effect, a placebo-like effect might be responsible. That said, because caffeine takes effect at different rates among users, it’s impossible to know the extent to which a placebo-like effect might account for its rapid onset of action in any given person.
Perhaps in certain users a placebo-like effect is fully responsible for rapid responses to caffeine ingestion, whereas in others a placebo-like effect may be partially responsible for immediate responses. Specifically, expectation-mediated neurophysiologic changes may synergize with the pharmacodynamic action of caffeine to yield a more potent effect.
It’s also possible that placebo-like responses play zero role in facilitation of rapid responses to caffeine – for a subset of the populace. In any regard, if you respond to caffeine rapidly, a placebo-like effect should be considered as a potential explanation – or partial explanation.
Variables that influence how quickly caffeine “kicks in” or takes effect
There are many different variables that might dictate how long it takes for caffeine to take effect following administration – or the amount of time it takes you to notice its effect. Variables that probably influence the rate at which caffeine “kicks in” include: administration specifics (modality, timing, empty vs. full stomach); user genetics (e.g. CYP1A2); caffeine dosage; and preexisting caffeine tolerance. Other variables like: age, body composition, and organ function (liver and kidney) – could also impact the amount of time it takes for caffeine to exert an effect.
Mode of administration: The modality of caffeine administration may determine how quickly it takes effect – and the significance of its effect. While most people consume caffeine orally via beverages and/or pills – caffeine is sometimes administered sublingually or intravenously. Sublingual and intravenous administration are known to “kick in” faster than orally-administered formats.
Timing: It is also thought that the time of day at which caffeine is administered could influence its onset of action. Administration of caffeine in the morning may yield a faster onset of action and more noticeable effect than at night for some users – due to circadian interaction (i.e. chronopharmacodynamics).
Morning coffee consumption is generally synergistic with the body’s endogenous production of stimulatory hormones and neurotransmitters (e.g. cortisol) and activity of adenosine. Because stimulatory neurotransmitter and hormone (e.g. cortisol) production usually peaks in the morning, and adenosine activity is lowest after sleeping – you might have an easier time noticing caffeine “kicking in” throughout the morning (compared to the afternoon or evening).
Some people derive benefit from consuming coffee prior to mid-day 15-minute power naps (i.e. “coffee naps“) such that when they awaken from their nap, the coffee they consumed prior to sleeping “kicks in” with a more potent effect (due to reduced adenosine receptor activation). That said, consuming coffee in the evening generally is antagonistic to one’s circadian biology – and may not exert as strong of an effect (due to circadian-caffeine mismatch).
Food vs. empty stomach: Additionally, whether you take caffeine with food or on an empty stomach could influence the speed at which it takes effect. Some research suggests that consuming caffeine on a full stomach slows its absorption (especially if the foods consumed were high-fiber), whereas ingesting caffeine on an empty stomach should speed up its absorption.
That said, foods like broccoli, brussels sprouts, and cauliflower activate CYP1A2 enzymes which should expedite caffeine metabolism and its corresponding onset of action. In summary, persons who consume caffeine on an empty stomach or with foods that activate CYP1A2 activity – should experience faster onsets of action than those who consume caffeine after a meal.
Genetics of caffeine user
As was already discussed, the genetics of a caffeine user may determine how quickly caffeine “kicks in” and the magnitude of its effect. Individuals who express the “A/A” variant of the rs762551 gene will metabolize caffeine at a fast rate, whereas persons who express the “A/C” or “C/C” variant of the rs762551 gene will metabolize caffeine at slow rate.
Faster metabolism of caffeine among individuals with the “A/A” genotype of rs762551 may yield quicker onset of caffeine action, but a less noticeable effect. If you have the “A/A” rs762551 genotype, you might struggle to detect caffeine’s effect – particularly if you only ingest a low dose.
Slower metabolism of caffeine among persons with the “A/C” or “C/C” genotype of rs762551 may yield slower onset of caffeine action, but a more noticeable effect. If you have either the “A/C” or “C/C” rs762551 genotype, it should be easy to detect caffeine “kicking in” – especially if you ingest a high dose.
Additionally, because the ADORA2A gene encodes for adenosine receptors in the brain, genetically-mediated differences in ADORA2A expression may impact the specific effects and magnitude of effects derived from caffeine consumption. Expressing one variant of ADORA2A may yield a quicker and/or more noticeable onset of caffeine action than expressing another.
Caffeine dosage (10 mg to 400 mg)
The exact dosage of caffeine that you administer might influence the time it takes for you to notice its effect. In most cases, the greater the dose of caffeine ingested – the more likely you’ll be able to consciously detect its effect within 10 to 20 minutes of administration.
On the other hand, the lower the dose of caffeine that you ingest – the less likely you’ll be able to notice its effect. Large doses of caffeine (such as between 300 mg and 400 mg) reach higher peak plasma concentrations and modulate neurophysiology to a greater extent than lower doses (such as between 10 mg and 50 mg).
If you administer a dose of 400 mg caffeine, this will exert nearly 4-fold the effect upon adenosine receptors and downstream neurochemical targets as a 100 mg dose. Greater antagonism of adenosine receptors with a higher dose of caffeine will yield more substantial increases in excitatory neurotransmission – and a more noticeable psychoactive effect.
In short, it should be easier to know exactly when caffeine “kicks in” following administration of a high dose – compared to a low dose (as a result of the more potent neurophysiologic effect). However, despite differences in one’s ability to notice the effect of caffeine at low and high doses, caffeine should take effect at approximately the same rate regardless of the dose.
Concurrent substance use
It is known that concurrent substance use could influence the rate at which caffeine takes effect. As was already mentioned, concurrent administration of agents that either induce or inhibit CYP1A2 can alter the rate of caffeine metabolism: inducers speed up its metabolism, whereas inhibitors slow its metabolism.
Concurrent use of a CYP1A2 inducer with caffeine is likely to expedite its metabolism, making it more difficult to notice caffeine “working.” Concurrent use of a CYP1A2 inhibitor with caffeine is likely to slow its metabolism, making it easier to notice caffeine “working.” The extent to which inducers and/or inhibitors of CYP1A2 will affect caffeine metabolism will be contingent upon their dosage.
Because caffeine exerts a stimulatory effect within the CNS, any co-administered agents that augment this effect might make it easier to detect the onset of caffeine’s action. Conversely, any co-administered agents that counteract its CNS stimulation – such as CNS depressants – might make it tougher to detect the onset of caffeine’s action. Oral contraceptives and cigarettes are two of the most common agents to alter caffeine’s effect and onset of action.
Level of caffeine tolerance
Persons with preexisting high tolerance to caffeine and/or psychostimulants with similar pharmacodynamics might struggle to detect when caffeine “kicks in” – particularly if low doses are administered. That said, individuals devoid of preexisting caffeine tolerance, or who have a very low caffeine tolerance, should have an easier time detecting when caffeine takes effect.
If you have a high tolerance to caffeine resulting from regular high-dose caffeine intake over a long-term, you might not really notice much of a beneficial or therapeutic effect from your caffeine consumption. This is because in persons with a high tolerance to caffeine, adenosine receptors are upregulated – making it tougher for caffeine to block adenosine.
Moreover, it’s thought that CYP1A2 receptors may become more efficient at metabolizing caffeine as an adaptation to chronic and/or high-dose administration. Improved efficiency of caffeine metabolism may minimize the magnitude of its effect and make it more difficult to notice when caffeine actually “kicks in.”
If you have zero or low tolerance to caffeine as a result of infrequent consumption, you’ll be more likely to notice a stronger neurophysiologic effect from its consumption – compared to a person with high tolerance. For this reason, persons without tolerance (or low tolerance) should have an easier time noticing exactly when caffeine takes effect.
Misc. user-specific variables
User-specific variables might also impact the rate at which caffeine takes effect (or is perceived as taking effect) following administration. A person’s age, body composition, liver function, and preexisting medical status could impact caffeine’s onset of action. Moreover, a person’s level of self-awareness might determine how quickly and/or effectively they’re able to notice caffeine taking effect.
Age: Research suggests that caffeine metabolism is reduced by around 33% in elderly persons (ages 65 to 70) compared to adults below the age of 65. Evidence also suggests that the volume of caffeine distribution is significantly reduced in elderly users.
If you’re over the age of 65, you might notice caffeine “kicking in” at a slower rate than it did when you were younger – but its effect (relative to the dose) might be stronger due to a reduction in metabolism.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/22924488
- Source: http://www.ncbi.nlm.nih.gov/pubmed/6886969
Body composition: It’s possible that, to a slight extent, individual body composition may affect the pharmacokinetics of caffeine. The dosage of caffeine administered relative to height, weight, body fat, and/or muscle mass – may impact caffeine distribution and onset of action.
Perhaps someone who is tall with substantial body fat will exhibit different systemic distribution of caffeine and an altered onset of action – compared to someone with minimal body fat and substantial lean mass.
Liver function: The liver function of a caffeine user may influence how quickly caffeine is metabolized and reaches peak plasma concentrations. Individuals with preexisting liver impairment (i.e. hepatic dysfunction) may metabolize caffeine slower than the general population and exhibit elevated peak plasma concentrations.
Studies have documented that the half-life of caffeine can increase up to 168 hours in persons with liver impairment. If your liver function is impaired, expect caffeine to take effect at a slower rate – but exert a more potent, noticeable, and longer-lasting effect.
Medical status: If you have preexisting medical conditions and/or are pregnant, realize that your current medical status could influence the pharmacokinetics of caffeine and the rate at which it takes effect (following ingestion). As was already mentioned, persons with preexisting hepatic impairment tend to exhibit delayed onset of caffeine action with a longer duration of effect than healthy individuals (devoid of hepatic dysfunction).
Other medical conditions like neurodegenerative disorders might interfere with one’s ability to notice or consciously detect the onset of caffeine’s action, whereas anxiety disorders might enhance one’s ability to detect caffeine “kicking in.” Moreover, realize that medications used to treat medical conditions may affect caffeine’s onset of action.
Self-awareness: The self-awareness of a caffeine user could impact how rapidly he/she is able to notice its effect after administration. Even if caffeine “kicks in” or takes effect within 15 minutes of consumption, someone with low self-awareness may not notice this early action – and might only perceive caffeine working after it reaches peak plasma concentrations. On the other hand, someone with high self-awareness may notice caffeine working in the earliest moments of its action.
Duration of caffeine use
The total amount of time over which you’ve been regularly consuming caffeine will likely influence neurophysiologic tolerance [relative to its dose], the magnitude of its effect, and how quickly you notice it “kicking in.” In most cases, caffeine-naïve individuals (persons with no history of caffeine use), short-term caffeine users, and/or infrequent caffeine consumers – will experience a stronger response to caffeine [relative to its dose] due to lower preexisting neurophysiologic tolerance.
Lower neurophysiologic tolerance tends to yield a greater magnitude of effect [relative to caffeine dose], making it seem as though caffeine is “kicking in” or exerting a noticeable effect – at a fast pace. That said, persons who’ve been consuming caffeine frequently for a long-term will experience a less significant response to caffeine [relative to its dose] due to higher preexisting neurophysiologic tolerance.
High neurophysiologic tolerance tends to reduce the magnitude of caffeine’s effect [relative to its dose], making it seem as though caffeine is “kicking in” or exerting a noticeable effect – at a slower rate. Nevertheless, it is reasonable to suspect that some individuals may need to administer caffeine regularly for a moderate and/or long-term before it begins working or facilitating therapeutic benefit in the management of certain medical conditions like major depressive disorder.
In other words, although caffeine will “kick in” on the very first day of administration – it might not exert a therapeutic effect until it’s been consistently administered for a duration of weeks (or months). For example, research by Pechlivanova, Tchekalarova, Alova, et al. (2012) documented that oral administration of caffeine (8 mg/kg) alleviated symptoms of depression and anxiety in Wistar rats – when administered for a period of 6 weeks.
The antidepressant and anxiolytic effect facilitated by long-term (6-week) caffeine ingestion in the rats was attributable to CNS adaptations that required time to emerge, most notably: increased dopamine and increased serotonin signaling in the hippocampus. If caffeine would’ve only been administered for a day and/or sporadically throughout the 6-week period, the therapeutic effects probably wouldn’t have occurred.
Another study by Sallaberry, Nunes, Costa, et al. (2013) reported that chronic caffeine administration modulates concentrations of BDNF (brain-derived neurotrophic factor) in rats. Specifically, chronic caffeine administration: mitigated age-related memory deficits; increased BDNF levels in the hippocampus; upregulated proBDNF and CREB; and reduced TrkB expression – in the rats.
Although the aforementioned studies involved animal models, it’s fair to speculate that similar beneficial or therapeutic CNS adaptations might only occur in humans after regular, long-term caffeine ingestion. Until these adaptations occur, it may not seem as though caffeine is “working” or helping manage symptoms of your medical condition.
- Source: https://www.ncbi.nlm.nih.gov/pubmed/22841916
- Source: https://www.ncbi.nlm.nih.gov/pubmed/22785384
Why caffeine should “kick in” rapidly (Reasons)
- Efficient pharmacokinetics: Research suggests that, in most humans, approximately 99% of caffeine is absorbed within 45 minutes of administration. Plasma concentrations will peak within 15 and 120 minutes following oral ingestion. The variance in time to attain peak plasma concentrations is related to: gastric emptying rate and dietary intake. Following absorption, caffeine: reversibly binds to plasma proteins; is distributed within intracellular tissue water; and crosses the blood-brain-barrier to exert a psychoactive effect.
- Immediate action in CNS & PNS: The onset of caffeine’s action is relatively rapid for most people. Once caffeine is distributed throughout the peripheral and central nervous system, it modulates: adenosine receptor activation; sympathetic nervous system activation; hormone production; neural connectivity; the activation of brain regions; neuroelectrical activity (i.e. brain waves); and cerebral blood flow. Due to the culmination of aforestated effects, most people notice caffeine taking effect quickly after administration.
- Placebo-like confound: Although caffeine is a potent psychoactive substance that usually takes effect quickly after administration, we must consider that a placebo-like effect may partly (or fully) account for rapid responses to caffeine. Having a strong expectation or belief that caffeine will “kick in” rapidly – may alter neurophysiology in ways that would be consistent with a placebo-like effect. Neurophysiologic alterations from a placebo-like effect may synergize with the actual effects of caffeine to induce a quicker onset of caffeine action and/or more noticeable reaction.
- Co-administered substances: If you’re using medications and/or supplements with caffeine, there’s a chance that these agents might slightly expedite the rate at which caffeine “kicks in” – and/or the rate at which you’re able to perceive caffeine “kicking in.” For example, if you’re already under the influence of a stimulant, you might have an easier time noticing when caffeine takes effect due to the fact that the stimulants increase focus and self-awareness.
Why caffeine may not “kick in” right away (Reasons)
- Abnormal pharmacokinetics: Though most caffeine users should notice an effect within 10 to 20 minutes of ingestion, a subset of the population may exhibit abnormal caffeine pharmacokinetics. In other words, the absorption, metabolism, and distribution of caffeine may appear abnormal in certain people – possibly accounting for delays in caffeine’s onset of action. Abnormal pharmacokinetics may be attributable to co-administered substances, medical conditions, and/or body composition.
- Caffeine format: The format of caffeine administered can impact how quickly it takes effect. Sublingual and intravenous administration of caffeine tends to yield a faster onset of action than ingestion of caffeine via a beverage. Furthermore, administration of encapsulated caffeine (i.e. a caffeine capsule) may yield a slower onset of action than a caffeinated beverage. If you’re using caffeine capsules for your caffeine fix, this may explain why caffeine doesn’t “kick in” as quickly as other formats.
- Co-administered substances: Using medications and/or supplements may delay caffeine’s onset of action – or your ability to perceive caffeine taking effect. Agents that interact with CYP1A2 enzymes in the liver may alter caffeine’s pharmacokinetics and postpone its onset of action. Additionally, some co-administered substances may oppose caffeine’s neurochemical action – making it difficult to notice caffeine working. Consumption of food prior to ingesting caffeine may also delay its onset of action – especially if the meal is large and/or contains substantial fiber.
- Medical conditions: As was already mentioned, certain medical conditions may alter the rate at which caffeine takes effect or “kicks in” – as well as its potency of effect. Other medical conditions may interfere with one’s ability to notice caffeine working – even while they’re under its influence. If you have a medical condition that alters caffeine pharmacokinetics, caffeine pharmacodynamics, or your self-awareness – this might explain why you aren’t noticing the effect of caffeine rapidly after ingestion.
- Lack of CNS adaptation: If you’re consuming caffeine in effort to attenuate symptoms of a medical condition (e.g. major depression, dementia, etc.), evidence suggests that caffeine may necessitate administration over a duration of weeks before it noticeably counteracts unwanted symptoms. More specifically, various adaptations [in response to caffeine] will need to emerge throughout the CNS (central nervous system) before symptoms will improve. In order to attain many of these CNS adaptations, caffeine needs to be administered consistently for a reasonable duration (e.g. weeks). For this reason, if you don’t notice caffeine working (or managing your medical symptoms) immediately – understand that it may eventually begin facilitating a therapeutic effect after several weeks.
Why caffeine might not work well (or work at all)…
If you’re a healthy adult, you should notice the effect of caffeine within minutes of administration. People who are unable to notice caffeine taking effect usually: are using an inadequate dose; have a high neurophysiologic tolerance; and/or are rapid metabolizers. In other words, if you’re using a very tiny dose of caffeine; you have a high tolerance; and/or you’re a rapid metabolizer – you might not notice any effect from your caffeine consumption.
- Inadequate caffeine dose: A subset of individuals who don’t notice caffeine working (or taking effect) may be ingesting too low of a caffeine dose (relative to their tolerance and caffeine metabolism). If you take a couple small sips of green tea, you won’t be ingesting much caffeine – and you may not even notice that you’re under its influence. On the other hand, if you rapidly consume (i.e. chug) an entire 16-ounce energy drink – you’re very likely to notice caffeine taking effect. For this reason, if you have trouble noticing when caffeine “kicks in,” realize that inadequate dosing may be the reason.
- High caffeine tolerance: Individuals with high tolerance to caffeine (or substances with similar pharmacodynamics) might not really notice much of any effect after caffeine consumption as a result of the tolerance. Tolerance to caffeine is associated with upregulation of adenosine receptors – making it more difficult for caffeine to induce a stimulatory effect. For this reason, if you’ve developed a high tolerance to caffeine, you may have a difficult time noticing when it “kicks in” and/or provides a stimulatory effect.
- Rapid caffeine metabolism: If you express the “A/A” genotype of rs762551, you’re a fast metabolizer of caffeine via the CYP1A2 enzyme. Fast metabolizers will exhibit lower peak plasma concentrations of caffeine and eliminate caffeine from systemic circulation at a faster pace than slower metabolizers. For this reason, if you happen to be a fast metabolizer of caffeine (based on your genes), it may be difficult to notice caffeine “kicking in” – especially if consumed slowly (e.g. sipping green tea over a 1-hour period). Other factors like foods (e.g. broccoli) and smoking can further expedite caffeine metabolism and elimination, making it more difficult to notice its effect.
How long does it take for caffeine to work for me?
After drinking green tea, coffee, or an energy drink – I’ll usually notice caffeine “kicking in” or taking effect within 15 to 20 minutes of ingestion. The effect will be more substantial if I drink my caffeinated beverage quickly – as opposed to slowly sipping over a long period of time (such as while writing).
If I eat a large meal prior to drinking caffeine, it may take slightly more time for me to notice an effect – than if ingested on an empty stomach. This is probably due to the fact that a large meal prior to caffeine consumption delays absorption and extends the time needed for caffeine to peak in the plasma.
Of all the times in my life that I’ve ingested caffeine, the only time I didn’t notice caffeine “kicking in” rapidly was when I administered a caffeine capsule. I’m not exactly sure about the caffeine capsule formatting (e.g. delayed release, extended-release, etc.) – but it didn’t take effect for at least 45 minutes after ingestion.
That said, it’s possible that this capsule could’ve interacted with another supplement that I administered that day – possibly delaying its onset. In any regard, my experience is consistent with the literature such that caffeine tends to take effect rapidly after ingestion of a caffeinated beverage, but slower with the administration of a caffeine capsule.
Moreover, I should mention that my genetic data indicate that I’m a rapid caffeine metabolizer (due to expressing the “A/A” genotype of rs762551). I also should note that I have generally high anxiety and self-awareness, and carry a variant of the ADORA2A gene that’s associated with caffeine-induced anxiety – all of which may enable me to easily detect caffeine’s onset of action.
How long does it take for you to notice caffeine “kicking in?”
If you’re a regular caffeine consumer, leave a comment below mentioning approximately how much time it normally takes for you to notice caffeine “kicking in” after administration. Mention the specific format of caffeine you consume (e.g. coffee, NoDoz, etc.); the total dosage of caffeine that you consume (e.g. 100 mg); the rate of your consumption (e.g. slowly sip over a 20-minute span); and your level of tolerance to caffeine.
Additionally, if you happen to know your rs762551 genotype (e.g. A/A; A/C; C/C) and/or ADORA2A gene variants – share this information in the comments. Also note whether you have any preexisting medical conditions and/or use substances (e.g. medications, supplements, illicit drugs) that might: interfere with your ability to notice caffeine working and/or minimize the neurophysiologic effect facilitated by caffeine.
Do you notice caffeine “kicking in” at a different rate when consumed after eating a large meal and/or fibrous foods? In the event that you’ve been using caffeine to attenuate symptoms of a medical condition (e.g. major depression), and it turned out to be helpful, how long did it take for you to attain therapeutic benefit?
In summary, most people will notice caffeine “kicking in” within 10 to 20 minutes of consuming a caffeinated beverage like coffee. That said, the rate at which caffeine takes effect is subject to interindividual variation and may require significantly more time (e.g. up to 120 minutes) to exert a noticeable effect in a subset of users.