ADHD Coffee Paradox: Why Coffee Makes Me Sleepy [Explained]

Individuals with Attention-Deficit/Hyperactivity Disorder (ADHD) may experience paradoxical reactions to stimulants like caffeine, finding themselves feeling tired rather than energized. This counterintuitive effect can stem from several physiological and neurological mechanisms. Caffeine, a stimulant, primarily works by blocking adenosine receptors in the brain. Adenosine is a neurotransmitter that promotes relaxation and sleepiness. Blocking these receptors leads to increased alertness in most individuals. However, in people with ADHD, the baseline levels of dopamine and norepinephrine, neurotransmitters crucial for focus and attention, are often lower.

The paradoxical fatigue experienced is often attributed to how caffeine interacts with the already dysregulated neurotransmitter system in those with ADHD. Instead of simply stimulating, caffeine may, in some cases, lead to a calming effect, as it helps to normalize or regulate dopamine levels, potentially alleviating some of the cognitive overload associated with ADHD. This regulating effect can then manifest as a decrease in hyperactivity and a feeling of relaxation, which is interpreted as sleepiness. Additionally, the diuretic effect of caffeine can lead to dehydration, potentially exacerbating fatigue and cognitive difficulties. Historical context is limited regarding specific study of this phenomenon; research continues to explore the nuanced interplay between stimulants and ADHD brains.

Several factors contribute to this differing response. Individual metabolism, dosage, and the presence of comorbid conditions such as anxiety or sleep disorders all influence the effect of caffeine. Identifying the underlying cause of this unexpected reaction requires careful observation and consultation with healthcare professionals. Evaluating these individual factors and understanding how they interact can lead to a more tailored approach to managing ADHD symptoms and associated fatigue.

Strategies for Managing Caffeine’s Effects in ADHD

The following strategies aim to mitigate the counterintuitive effects of caffeine consumption in individuals with ADHD, focusing on optimizing energy levels and cognitive function.

Tip 1: Monitor Caffeine Intake: Diligently track caffeine consumption to identify potential correlations between dosage, timing, and subjective experiences of fatigue or alertness. Detailed records can aid in discerning optimal caffeine levels.

Tip 2: Consider Alternative Stimulants: Explore non-caffeinated alternatives to enhance focus and energy. These may include regular exercise, improved sleep hygiene, or specific dietary adjustments.

Tip 3: Evaluate Dehydration Levels: Assess hydration status, as caffeine’s diuretic effect can contribute to fatigue. Maintain adequate fluid intake throughout the day, particularly when consuming caffeinated beverages.

Tip 4: Time Caffeine Consumption Strategically: Experiment with the timing of caffeine intake, avoiding consumption close to bedtime to prevent sleep disruption. Determine if a small dose in the morning provides more consistent benefits.

Tip 5: Consult a Healthcare Professional: Seek guidance from a qualified healthcare provider experienced in ADHD. Medical professionals can provide individualized advice and assess potential interactions with existing medications.

Tip 6: Prioritize Consistent Sleep Schedule: Establishing a regular sleep-wake cycle can significantly improve energy levels and reduce the reliance on stimulants. This includes maintaining consistent sleep times, even on weekends.

Tip 7: Incorporate Mindfulness Techniques: Practice mindfulness and meditation to manage stress and improve focus. Reducing stress levels can minimize the need for caffeine as a coping mechanism.

Implementing these strategies can assist in regulating the impact of caffeine and optimizing energy levels, contributing to improved cognitive function and overall well-being.

These strategies represent a starting point for managing caffeine’s effects. The subsequent sections will address related considerations and further guidance.

1. Neurotransmitter Regulation

Dysregulation of neurotransmitter systems, particularly those involving dopamine and norepinephrine, forms a critical link to the paradoxical experience of caffeine-induced sleepiness in individuals with Attention-Deficit/Hyperactivity Disorder (ADHD). In typical neurological function, caffeine acts as a stimulant by blocking adenosine, thereby increasing neuronal activity. However, in ADHD, baseline levels of dopamine and norepinephrine are often lower than in neurotypical individuals. This pre-existing deficiency can result in an atypical response to caffeine. Instead of a stimulating effect, caffeine may contribute to a normalizing or regulating effect on these neurotransmitter levels. For example, a person with ADHD who is experiencing significant cognitive disorganization due to low dopamine might find that caffeine, rather than causing stimulation, helps to subtly increase dopamine to a more functional level, inadvertently reducing hyperactivity and leading to a perceived state of relaxation or sleepiness. The importance of understanding neurotransmitter regulation lies in its potential to explain the varied and often unexpected effects of stimulants on individuals with ADHD.

Further complicating the issue is the potential for other neurotransmitter pathways to be affected. Caffeine can indirectly influence serotonin levels, and altered serotonin activity can impact mood and sleep patterns. Moreover, the individual’s genetic predisposition, pre-existing conditions, and concurrent medications can interact with caffeine, modulating its effects on neurotransmitter release and receptor sensitivity. Consider the practical application of this knowledge: By understanding the role of neurotransmitter regulation, healthcare professionals can better predict and manage the effects of caffeine and other stimulants in patients with ADHD, potentially tailoring treatment plans to address specific neurotransmitter imbalances. For instance, some individuals might respond better to medications that directly target dopamine or norepinephrine, while others might benefit from non-pharmacological interventions aimed at regulating neurotransmitter function, such as behavioral therapy or dietary modifications.

In summary, the connection between neurotransmitter regulation and the paradoxical sleepiness experienced by some individuals with ADHD after caffeine consumption involves a complex interplay of neurological factors. Low baseline levels of key neurotransmitters, the modulating effects of caffeine on these systems, and individual variations in metabolism and genetics all contribute to this phenomenon. Recognizing the central role of neurotransmitter regulation is crucial for developing personalized strategies to manage ADHD symptoms and mitigate the adverse effects of stimulants. Challenges remain in fully elucidating the exact mechanisms involved, highlighting the need for ongoing research in this area. The insights gained can significantly improve the quality of life for individuals with ADHD by enabling more effective and targeted interventions.

2. Adenosine Receptor Blockade

Adenosine receptor blockade, a primary mechanism of caffeine action, holds significant relevance in understanding why some individuals with Attention-Deficit/Hyperactivity Disorder (ADHD) experience fatigue after consuming caffeine. Adenosine, a nucleoside, functions as a neuromodulator, promoting relaxation and sleepiness by binding to adenosine receptors throughout the brain. Caffeine, structurally similar to adenosine, competitively binds to these receptors, preventing adenosine from exerting its usual inhibitory effects on neuronal activity. This blockade typically leads to increased alertness and reduced fatigue. However, in ADHD, this process may not unfold as expected. The already dysregulated neurochemical environment in ADHD brains can cause an alternative response to the sudden prevention of adenosine signaling.

In some individuals with ADHD, the blockade of adenosine receptors, rather than triggering stimulation, may lead to a paradoxical calming effect. When adenosine is prevented from binding, other neurotransmitter systems, such as dopamine and norepinephrine, may be indirectly affected. If the individual’s system is already deficient in these stimulatory neurotransmitters, the forced hyperactivity of the adenosine-blocked system could lead to a compensatory downregulation or a sense of being overwhelmed, translating to perceived fatigue or sleepiness. Consider the practical implications: A student with ADHD preparing for an exam may consume caffeine to stay alert, only to find themselves feeling more tired and less focused after an initial brief period of stimulation. This highlights the importance of understanding the individualized response to caffeine, considering the underlying neurochemical profile, and adjusting dosage or seeking alternative strategies for maintaining focus.

The interplay between adenosine receptor blockade and the complex neurobiology of ADHD necessitates careful consideration. While caffeine effectively blocks adenosine, the resulting cascade of neurochemical events can vary significantly. Factors such as individual metabolism, pre-existing conditions, and concurrent medications can influence the outcome. This variability underscores the challenges in predicting the effects of caffeine and the need for personalized approaches to managing ADHD symptoms. Understanding this connection allows for more informed decision-making regarding caffeine consumption, optimizing the potential benefits while minimizing the risk of paradoxical fatigue. Further research is needed to fully elucidate the nuances of these interactions, paving the way for more targeted interventions.

3. Paradoxical Calming Effect

The paradoxical calming effect, where a stimulant induces relaxation rather than stimulation, represents a key component in understanding the phenomenon of feeling sleepy after caffeine consumption in individuals with Attention-Deficit/Hyperactivity Disorder (ADHD). This effect arises due to the atypical neurochemical environment prevalent in ADHD brains. Caffeine’s primary action, the blockade of adenosine receptors, often leads to increased dopamine release. However, in individuals with ADHD, who frequently exhibit lower baseline dopamine levels, this increase can help to normalize dopamine activity towards a more optimal range. This normalization, rather than causing hyperactivity, may reduce cognitive overload and induce a sense of calm, which can be misinterpreted as sleepiness. Consider, for instance, an individual with ADHD who reports increased focus and reduced impulsivity after consuming coffee. While alertness is not increased, the stabilization of dopamine can diminish hyperactivity, leading to a subdued, relaxed state.

The practical significance of understanding this paradoxical effect lies in its implications for managing ADHD symptoms. Traditional stimulants, such as methylphenidate and amphetamine, also aim to increase dopamine levels. Recognizing that caffeine can similarly modulate neurotransmitter activity, albeit to a lesser extent, highlights the importance of careful self-monitoring. Individuals with ADHD can use this awareness to fine-tune their caffeine intake, potentially leveraging it as a mild regulator of dopamine activity. However, consistency and moderation are crucial. Excessive caffeine consumption can lead to a subsequent crash or increased anxiety, offsetting any initial calming benefits. The paradoxical calming effect further complicates the treatment landscape, as it implies that not all stimulants will elicit the same response in every individual with ADHD. Tailoring treatment strategies to individual neurochemical profiles is paramount.

In summary, the paradoxical calming effect associated with caffeine consumption in ADHD results from the modulation of neurotransmitter systems, primarily dopamine, toward a more balanced state. While seemingly counterintuitive, this phenomenon can help to explain why some individuals with ADHD experience sleepiness or relaxation after consuming a stimulant. Recognizing the potential for this effect can inform strategies for managing ADHD symptoms and optimizing caffeine intake, though careful consideration of individual responses and moderation remain essential. Challenges persist in fully elucidating the specific mechanisms underlying this paradoxical effect, underscoring the need for further research.

4. Individual Metabolism

Individual metabolism plays a critical role in modulating the effects of caffeine, thereby influencing why some individuals with Attention-Deficit/Hyperactivity Disorder (ADHD) experience sleepiness after consuming it. The rate at which the body processes and eliminates caffeine varies significantly among individuals, impacting the duration and intensity of its effects.

• CYP1A2 Enzyme Activity

  The cytochrome P450 1A2 (CYP1A2) enzyme is primarily responsible for metabolizing caffeine in the liver. Individuals with lower CYP1A2 activity process caffeine more slowly, leading to elevated levels of caffeine in the bloodstream for an extended period. This prolonged exposure can result in an overstimulation followed by a subsequent “crash,” contributing to fatigue. For example, if a person with slow caffeine metabolism consumes a moderate amount of coffee in the morning, they may experience a period of heightened alertness followed by a noticeable dip in energy levels later in the day. This dip can manifest as sleepiness or lethargy.

• Genetic Variations

  Genetic polymorphisms in the CYP1A2 gene influence the enzyme’s activity. Certain genetic variants are associated with faster or slower caffeine metabolism. Individuals with genetic predispositions for slow caffeine metabolism may be more likely to experience the paradoxical sleepiness effect. For example, a person with a specific CYP1A2 genetic variant may find that even small amounts of caffeine induce drowsiness rather than alertness, regardless of the time of day it is consumed. This can be attributed to the prolonged presence of caffeine in their system, leading to neurochemical imbalances over time.

• Liver Function

  Liver function, including overall health and the presence of liver diseases, directly affects caffeine metabolism. Impaired liver function can reduce the rate at which caffeine is broken down, resulting in higher blood concentrations and prolonged effects. In individuals with liver conditions, the typical stimulating effects of caffeine may be overshadowed by the subsequent fatigue and energy slump. For instance, a person with a history of liver disease may experience increased sleepiness after consuming caffeine, as their body struggles to metabolize the stimulant efficiently.

• Drug Interactions

  Certain medications can inhibit CYP1A2 enzyme activity, altering caffeine metabolism and potentially leading to increased fatigue. Drugs such as fluvoxamine and cimetidine are known to slow down caffeine metabolism. For example, if a person with ADHD taking fluvoxamine consumes caffeine, the drug interaction may prolong caffeine’s half-life, leading to an extended period of alertness followed by a more pronounced and prolonged episode of fatigue. This interaction highlights the significance of considering potential drug interactions when assessing the effects of caffeine on individuals with ADHD.

These facets of individual metabolism underscore the complex interaction between caffeine and the neurobiology of ADHD. Understanding these factors allows for more tailored approaches to managing caffeine consumption, optimizing potential benefits while minimizing the risk of paradoxical fatigue. For example, individuals with slower caffeine metabolism might benefit from consuming smaller doses or avoiding caffeine altogether to prevent adverse effects. Identifying individual metabolic profiles and adjusting caffeine consumption accordingly can contribute to improved cognitive function and overall well-being.

5. Dosage Sensitivity

Dosage sensitivity, the degree to which an individual responds to varying amounts of a substance, is a crucial determinant in understanding the paradoxical reaction of sleepiness after caffeine consumption in individuals with Attention-Deficit/Hyperactivity Disorder (ADHD). This sensitivity stems from the intricate interplay between caffeine’s pharmacological effects and the unique neurobiological characteristics associated with ADHD.

• Threshold Effect

  A threshold effect refers to a specific dose level below which a substance elicits no noticeable response. In the context of caffeine and ADHD, individuals may exhibit a higher or lower threshold. A lower threshold implies a more pronounced reaction even to minimal doses, potentially triggering fatigue rather than alertness. For example, an individual with ADHD might find that even a small cup of coffee leads to a subsequent feeling of lethargy and reduced focus, whereas another individual may require a significantly higher dose to experience any noticeable effects. This difference underscores the variability in individual responsiveness to caffeine.

• Optimal Dosage Range

  The optimal dosage range represents the amount of a substance that produces the desired therapeutic effects without causing adverse reactions. For caffeine, this range differs substantially among individuals with ADHD. Some might experience enhanced focus and reduced impulsivity within a narrow dosage window, while exceeding this range triggers anxiety, restlessness, and eventual fatigue. Consider a scenario where an individual consumes a standardized energy drink. They might initially experience improved concentration, but as the caffeine wears off, they could encounter heightened irritability and increased sleepiness. Finding and maintaining this optimal range is critical for harnessing the benefits of caffeine without precipitating adverse outcomes.

• Tolerance Development

  Tolerance development involves a reduced response to a substance after repeated exposure, necessitating higher doses to achieve the same effect. In individuals with ADHD, tolerance to caffeine can develop rapidly, leading to increased consumption to maintain the desired level of alertness. This increased consumption may eventually result in chronic overstimulation, dysregulation of neurotransmitter systems, and a paradoxical increase in fatigue. For instance, someone who initially benefited from a single cup of coffee may find that they require multiple cups to achieve the same level of focus, ultimately leading to a state of exhaustion and diminished cognitive performance.

• Individual Variability

  Individual variability encompasses the range of factors that contribute to differences in response to a substance. This includes genetic factors, metabolism, concurrent medications, and pre-existing conditions. Individuals with ADHD exhibit a wide spectrum of responses to caffeine, with some experiencing predominantly positive effects, some experiencing negative effects, and others experiencing a mixed response. An example of this variability is observed when comparing two individuals with ADHD consuming the same dose of caffeine: One may report improved attention and energy, while the other reports heightened anxiety and fatigue. Understanding this inherent variability is crucial for managing caffeine consumption and tailoring treatment strategies to individual needs.

The interplay between these facets of dosage sensitivity highlights the complexity of caffeine’s effects on individuals with ADHD. Recognizing the threshold effect, identifying the optimal dosage range, managing tolerance development, and accounting for individual variability are all essential for understanding why caffeine can paradoxically induce sleepiness in this population. Strategies for managing caffeine intake must be highly individualized to account for these diverse factors and optimize the potential benefits while minimizing adverse consequences.

6. Comorbid Conditions

Comorbid conditions, or co-occurring disorders, significantly influence the effects of caffeine in individuals with Attention-Deficit/Hyperactivity Disorder (ADHD), often contributing to the paradoxical experience of sleepiness. These co-existing conditions can alter neurochemical pathways and physiological responses, thereby modifying the typical stimulant effects of caffeine.

• Anxiety Disorders

  Anxiety disorders frequently co-occur with ADHD, influencing how individuals respond to stimulants. Caffeine, known to exacerbate anxiety symptoms in susceptible individuals, can trigger heightened physiological arousal, leading to a feeling of being overwhelmed. This overstimulation can paradoxically result in fatigue as the body attempts to compensate for the increased stress. For instance, an individual with both ADHD and generalized anxiety disorder may consume coffee to enhance focus, only to experience increased heart rate, nervousness, and eventual exhaustion. The anxiety-induced stress response depletes energy reserves, contributing to a state of fatigue rather than alertness.

• Sleep Disorders

  Sleep disorders, such as insomnia and sleep apnea, are commonly observed in individuals with ADHD. Caffeine’s disruption of sleep patterns can further exacerbate these pre-existing sleep disturbances. While caffeine might initially provide a temporary boost in alertness, it can interfere with the ability to fall asleep or maintain restful sleep, leading to chronic sleep deprivation. An individual with ADHD and insomnia might rely on caffeine to stay awake during the day, but the resulting sleep loss compounds their fatigue, creating a cycle of dependence and diminished cognitive function. Chronic sleep deprivation further dysregulates neurotransmitter systems, contributing to the paradoxical fatigue experienced after caffeine consumption.

• Mood Disorders

  Mood disorders, including depression and bipolar disorder, often co-exist with ADHD, influencing the effects of caffeine. In individuals with depression, caffeine’s stimulating effects might be blunted, or the subsequent “crash” can worsen depressive symptoms. Caffeine can also interact with mood-stabilizing medications, altering their efficacy or leading to adverse effects. For example, an individual with ADHD and depression might consume caffeine in an attempt to improve energy levels, only to experience a worsening of their depressive symptoms and increased fatigue. The interaction between caffeine and mood-related neurochemical pathways can contribute to the paradoxical fatigue experienced in this population.

• Substance Use Disorders

  Substance use disorders frequently co-occur with ADHD, further complicating the effects of caffeine. Individuals with a history of substance abuse may exhibit altered sensitivity to stimulants, including caffeine, due to changes in neurotransmitter systems and receptor function. Caffeine may be used as a substitute for other substances or as a coping mechanism, leading to increased consumption and potential adverse effects. An individual with ADHD and a history of stimulant abuse might consume excessive amounts of caffeine, resulting in a state of overstimulation followed by profound fatigue. The altered neurochemical responses and compensatory mechanisms associated with substance use disorders can influence how caffeine impacts energy levels and cognitive function.

The presence of comorbid conditions significantly alters the effects of caffeine in individuals with ADHD, often contributing to the paradoxical experience of sleepiness. The interplay between these co-existing disorders and caffeine’s pharmacological effects necessitates careful consideration. Understanding these interactions is essential for developing tailored strategies to manage caffeine consumption and optimize treatment outcomes in individuals with ADHD and co-occurring conditions.

7. Dehydration Impact

Dehydration significantly influences the effects of caffeine, potentially contributing to the paradoxical experience of sleepiness in individuals with Attention-Deficit/Hyperactivity Disorder (ADHD). The diuretic properties of caffeine can exacerbate fluid loss, impacting physiological functions and potentially overriding the stimulant effects.

• Increased Fluid Loss

  Caffeine acts as a mild diuretic, increasing urine production and promoting fluid loss from the body. This diuretic effect can lead to dehydration if fluid intake does not compensate for the increased excretion. For example, an individual with ADHD consuming multiple caffeinated beverages throughout the day may experience significant fluid depletion. This fluid loss can contribute to reduced blood volume and impaired delivery of oxygen and nutrients to the brain, potentially resulting in fatigue.

• Electrolyte Imbalance

  Dehydration can lead to an imbalance of electrolytes, such as sodium, potassium, and magnesium, which are essential for proper nerve and muscle function. Electrolyte imbalances can disrupt neuronal signaling and contribute to feelings of fatigue and cognitive impairment. Consider an individual with ADHD who exercises while consuming caffeine. The combined effects of sweating and caffeine-induced diuresis can result in significant electrolyte loss, leading to muscle weakness, fatigue, and impaired concentration. These symptoms can overshadow any potential benefits from caffeine.

• Reduced Cerebral Blood Flow

  Dehydration can reduce cerebral blood flow, impairing the delivery of oxygen and glucose to the brain. Reduced cerebral blood flow can negatively impact cognitive function, attention, and energy levels. For instance, a student with ADHD preparing for an exam might consume caffeine to enhance focus but, due to dehydration, experiences impaired cognitive performance and increased fatigue. This effect underscores the importance of maintaining adequate hydration for optimal brain function, especially when consuming caffeine.

• Exacerbated ADHD Symptoms

  The symptoms of dehydration, such as fatigue, impaired concentration, and irritability, can mimic or exacerbate the symptoms of ADHD. This overlap can make it difficult to distinguish between the effects of dehydration and the underlying symptoms of ADHD. For example, an individual with ADHD who experiences dehydration may find that their inattentiveness and impulsivity worsen, leading to a further reliance on caffeine to compensate. This cycle can exacerbate both the dehydration and the ADHD symptoms, contributing to chronic fatigue.

The connection between dehydration and the paradoxical sleepiness experienced by some individuals with ADHD after caffeine consumption involves complex physiological interactions. The diuretic effect of caffeine, electrolyte imbalances, reduced cerebral blood flow, and exacerbation of ADHD symptoms all contribute to this phenomenon. Maintaining adequate hydration is crucial for mitigating these effects and optimizing the potential benefits of caffeine while minimizing the risk of adverse consequences.

Frequently Asked Questions

The following frequently asked questions address common concerns regarding the paradoxical effects of caffeine on individuals with Attention-Deficit/Hyperactivity Disorder (ADHD). The information provided aims to offer clarity on this complex topic.

Question 1: Is it common for caffeine to induce sleepiness in individuals with ADHD?

The experience of sleepiness after caffeine consumption, while paradoxical, is a recognized phenomenon among some individuals with ADHD. This response is not universal but occurs due to the complex interplay between caffeine and the neurochemical imbalances characteristic of ADHD.

Question 2: What are the primary reasons caffeine might cause fatigue in those with ADHD?

The primary reasons include the normalization of dopamine levels, blockade of adenosine receptors leading to a calming effect, individual metabolic variations, potential exacerbation of dehydration, and the presence of comorbid conditions such as anxiety or sleep disorders.

Question 3: How does caffeine affect dopamine levels in the ADHD brain?

Caffeine can increase dopamine release, which, in individuals with lower baseline dopamine levels typical of ADHD, may lead to a normalizing effect. This normalization can reduce cognitive overload and induce a state of calm, perceived as sleepiness.

Question 4: Can the dosage of caffeine influence its effect on individuals with ADHD?

Dosage significantly influences caffeine’s effects. A lower dose may provide a subtle regulating effect, while higher doses can lead to overstimulation followed by a subsequent “crash,” potentially exacerbating fatigue.

Question 5: Are there specific strategies to mitigate the fatigue-inducing effects of caffeine?

Strategies include monitoring caffeine intake, considering alternative stimulants, evaluating dehydration levels, timing caffeine consumption strategically, and consulting with a healthcare professional to address individualized needs.

Question 6: How do comorbid conditions affect caffeine’s impact on individuals with ADHD?

Comorbid conditions such as anxiety disorders, sleep disorders, and mood disorders can alter the response to caffeine. These conditions can either exacerbate the stimulant effects or contribute to increased fatigue due to physiological and neurochemical interactions.

Understanding the multifaceted reasons behind caffeine’s paradoxical effects is crucial for individuals with ADHD to manage their energy levels and cognitive function effectively.

The subsequent sections will explore alternative strategies for managing energy levels and improving focus in individuals with ADHD.

Conclusion

The preceding exploration has elucidated the multifaceted reasons why individuals with Attention-Deficit/Hyperactivity Disorder (ADHD) may experience sleepiness after caffeine consumption. Key factors identified include the normalization of dopamine levels, adenosine receptor blockade, individual metabolic variations, the impact of dehydration, and the presence of comorbid conditions. The paradoxical response underscores the complexity of caffeine’s interaction with the neurobiological characteristics of ADHD.

Recognizing the potential for caffeine to induce fatigue rather than stimulation is crucial for effective self-management. A comprehensive understanding of individual responses, combined with informed strategies for mitigating adverse effects, offers a path towards optimizing energy levels and cognitive function. Continued research is essential to further unravel the nuanced mechanisms involved and to develop more targeted interventions tailored to the specific needs of individuals with ADHD experiencing this counterintuitive reaction.