Miloni Shah
Caffeine is the most widely used drug globally (Meredith et al., 2013). It is found in coffee, energy drinks, supplements, chocolate drinks, and certain sports food (Cappelletti et al., 2015). The increase in advertisements about energy drinks over the past few years has increased the use of caffeine among young adults. Literacy around the benefits of caffeine has also seen simultaneous growth (Cappelletti et al.). However, there is little awareness of the dangers of caffeine, especially its neuro-psychological effects. This blog will give a brief overview of these effects, with a special emphasis on Caffeine Use Disorder.
It is known that caffeine is a psychostimulant. It affects neurotransmitter release and activates certain neuronal pathways (Cappelletti et al., 2015). Higher consumption is associated with preventing memory loss in Alzheimer’s and motor symptoms in Parkinson’s disease (Cappelletti et al.). It increases alertness, attention, energy, sociability, and reaction time, effects that resemble drug effects of other stimulants like cocaine and d-amphetamine (Meredith et al., 2013). Caffeine consumption does not directly cause the enhancement of cognitive functions. Rather, it provides relief from withdrawal symptoms which leads to such cognitive benefits (Cappelletti et al.).
Caffeine’s effect on the nervous system is responsible for its physio-cognitive benefits. Caffeine is an antagonist of adenosine which is an inhibitory neurotransmitter that promotes sleep and inhibits arousal. It blocks two types of adenosine receptors: A1 and A2A. A1 receptors are primarily responsible for inducing sleep (Basheer et al., 2004). One cup of coffee is enough to block adenosine receptors. Dopamine, noradrenaline, and glutamate are released in higher concentrations consequently. Dopamine is implicated in feeling pleasure and movement regulation (Olguin et al., 2016). Glutamate is essential for healthy brain functioning (Zhou and Danbolt, 2014). The cerebrum, cerebellum, hippocampus, and thalamic nuclei have the highest concentration of A1 receptors. A2A receptors are found in the basal ganglia. Its inhibition is elemental in making caffeine a psychostimulant (Cappelletti et al., 2015). It regulates oxygen levels and blood flow. In smaller amounts, caffeine stimulates physical activity and cognitive function. However, in higher doses- above 600 mg or 4 to 7 cups a day- it acts like an anxiogenic drug meaning that it induces anxiety (Cappelletti et al.).
The same mechanism which makes the drug desirable is also responsible for its negative effects. The inhibition of A1, A2A, and A2B receptors in blood vessels leads to a decrease in blood flow in the heart muscle. This is because adenosine usually induces vasodilation. As an antagonist, caffeine impedes this action. As a result, caffeine has negative implications on the cardiovascular system. Tachycardia and arrhythmias are linked with the consumption of high doses. Additionally, increased levels of noradrenaline, a neurotransmitter that regulates physiological responses to stress, lead to a rise in blood pressure in men with normal and high blood pressure. It should be noted that not all heart-related conditions are associated with caffeine. For example, coronary artery disease, myocardial infarction, and strokes have nothing to do with caffeine consumption (Cappelletti et al., 2015).
Besides the physiological impacts of a high caffeine intake, the DSM V records caffeine’s capacity to induce distress. The World Health Organisation and the American Psychiatric Association classify caffeine dependence as a clinical disorder in the ICD 10 and DSM V respectively. According to DSM V, Caffeine Use Disorder has three critical diagnostic criteria :
1) Persistent desire or unsuccessful efforts to cut down or control caffeine use,
2) Continued caffeine use despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by caffeine,
3) Characteristic caffeine withdrawal syndrome or caffeine use to relieve or avoid withdrawal symptoms (Meredith et al., 2013).
The difference between use and abuse should be noted. It is common and even healthy to consume some amounts of caffeine on a daily basis. However, when there is an insatiable urge to consume it despite being aware of its negative effects on health, normal consumption becomes caffeine abuse. It translates to dependence when an individual builds up a tolerance for the substance due to chronic use. Dependence and abuse are both accounted for in Caffeine Use Disorder. The disorder is measured on a scale of mild to severe based on the severity of the symptoms (Cappelletti et al., 2015). Approximately 9% of the general population in the USA is diagnosed with Caffeine Use Disorder. Caffeine is an addictive substance because of the way in which the inhibition of adenosine alters the amount of dopamine released in the nucleus accumbens shell of the brain. This is why many people become dependent on it and are affected by the disorder. Genotype partially influences an individual’s vulnerability to the disorder. Twin studies show that tolerance levels, caffeine use, and withdrawal capacities are 35% to 77% heritable. This is similar to the heritability of nicotine and alcohol markers (Meredith et al., 2013).
Many regular consumers try to abstain from consumption altogether but fail most of the time. They experience withdrawal symptoms that interfere with their daily functioning. These include symptoms like migraines, intense cravings, anxiety, lesser concentration, and inability to stay awake. 7% of the general population in the USA who tried to temporarily abstain and 24% who tried to stop permanently continued consuming high amounts of caffeine despite the risks associated with it to avoid withdrawal symptoms. They required caffeine to function normally (Meredith et al., 2013).
Further research is required to study the clinical significance of Caffeine Use Disorder in different populations. Since comorbidity between non-drug psychiatric disorders and drug dependence disorders are common, further research is required to study the relationship of the same vis a vis Caffeine Use Disorder. Current research is limited as it is descriptive. High consumption of caffeine is common among those diagnosed with Schizophrenia. It also has the potential to aggravate certain conditions like anxiety. Caffeine dependence is linked with major depression, panic disorder, and adult antisocial disorder. This is all that is known. However, the predictive nature of Caffeine Use Disorder in relation to other psychiatric conditions is yet to be explored (Meredith et al., 2013) Moreover, the negative psychological effects of high consumption of caffeine should be disseminated. Though the consequences of abusing the drug are not as severe as those of other drugs, spreading awareness could help avert potential problems.
References
Basheer, R., Strecker, R. E., Thakkar, M. M., & McCarley, R. W. (2004). Adenosine and Sleep–Wake Regulation. Progress in Neurobiology, 73(6), 379–396. https://doi.org/10.1016/j.pneurobio.2004.06.004
Cappelletti, S., Daria, P., Sani, G., & Aromatario, M. (2015). Caffeine: Cognitive and Physical Performance Enhancer or Psychoactive Drug? Current Neuropharmacology, 13(1), 71–88. https://doi.org/10.2174/1570159x13666141210215655
Juárez Olguín, H., Calderón Guzmán, D., Hernández García, E., & Barragán Mejía, G. (2016). The Role of Dopamine and its Dysfunction as a Consequence of Oxidative Stress. Oxidative Medicine and Cellular Longevity, 2016, 1–13. https://doi.org/10.1155/2016/9730467
Meredith, S. E., Juliano, L. M., Hughes, J. R., & Griffiths, R. R. (2013). Caffeine Use Disorder: A Comprehensive Review and Research Agenda. Journal of Caffeine Research, 3(3), 114–130. https://doi.org/10.1089/jcr.2013.0016
Zhou, Y., & Danbolt, N. C. (2014). Glutamate as a Neurotransmitter in the Healthy Brain. Journal of Neural Transmission, 121(8), 799–817. https://doi.org/10.1007/s00702-014-1180-8
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