In short: Yes. More so: please do!

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Originating from China, scientific name camellia sinensis, most of us have, at one point or another, indulged ourselves in a cup.

Green tea has caffeine in it, as many other teas do, and which coffee is famous for. It’s freely available, not regulated, no amount of danger present. Doctors might as well hold it as less dangerous than coffee, for all of its caffeine content.

The consensus is that 300-500 mg of caffeine per day is not unhealthy.

Yet, green tea is largely therapeutic because of another chemical in it: theanine.

  • Caffeine and theanine content
    • Green tea, per cup
      • Caffeine
        • 30 – 50 mg 
      • Theanine
        • ~7.9 mg
    • Black tea, per cup
      • Caffeine
        • 25 – 110 mg
      • Theanine
        • ~24.2 mg
    • Coffee (no theanine), per cup
      • Caffeine
        • Instant
          • 27 – 173 mg
        • Brewed
          • 102 – 200 mg
        • Espresso
          • 240 -720 mg

The below essay goes over, in-depth, the remarkable utility of theanine.

*Though one may purchase theanine by itself, it is more healthy to consume it in its natural state within tea. The same goes for fish oil, Vitamin D, magnesium, and so on*

Image result for theanine parkinson's alzheimer's

On Theanine Improving Neurodegenerative and Mentally Ill Conditions



Millions of people drink it every day. It’s scientific name is camellia sinensis. It is green tea, which, along with coffee and other teas, naturally produces caffeine. (Boros, Jedlinszki & Csupor 2016) Yet while coffee is considered a mild stimulant, camellia sinensis is considered a relaxant. Experts have specified the compound in green tea that produces this effect: theanine, or, l-theanine – absent in coffee, present in green tea. After concluding proper experimentation on this substance, The United States Food & Drug Administration has determined theanine to be essentially harmless, or, Generally Recognized as Safe (GRAS). (NIH, 2017) Over the past several years, theanine has garnered more national attention. This is partly because other agents with depressant activity, such as alcohol or valium, can be extremely addictive and harmful. Addictive potential hasn’t been observed in theanine. It furthermore isn’t associated with any significant side effects. (NIH, 2017) According to preliminary studies, theanine may be quite medicinal.  Recent academic studies have found it to have a wide range of medical applications for theanine in the fields of neurological and mental illness.


Alzheimer’s Disease

The main manner that Alzheimer’s disease begins to destroy the brain, is with the amyloid β plaque and tangle accumulation, which first invades the hippocampus (the hippocampus being the major region associated with memory). (Pinel, 2013) An experiment, using mice, determined if l-theanine could inhibit cell death caused by this amyloid, and improve memory. After five weeks of treatment with theanine solution, scientists observed a significant prevention of neurotoxicity, corresponding with less memory and learning impairment. Furthermore, quantity of theanine and memory were highly, positively and significantly associated with each other (in a dose-dependent fashion). Theanine reduced amyloid beta levels and cell death in the cortexes and hippocampi of the mice, the former being crucial to our exercise of highly, human functions. It stopped Aβ extracellular kinase, mitogen-activated kinases, and nuclear factor. Damage to proteins and lipids were significantly lower than they otherwise would have been. The researchers conclude by stating that theanine has multiple beneficial effects on memory by the kinase and nuclear factor suppression, and oxidative damage. (Kim, Lee, Park, Choi, Ban, Park,  . . . Hong,  2009).


Parkinson’s Disease

Another experiment focused on Parkinson’s disease. The disease was simulated in-vitro using dopaminergic neurons. The toxins rotenone and dieldrin act to increase oxidative stress to the extent that there is an overabundance of free radicals, which damages, and can destroy, neurons and tissue. This effect happens in the nigrostriatal tract in those with parkinson’s disease. (Pinel, 2013) In the experiment, 500 micrometers of theanine were introduced one hour before the toxins were. Observed was a prevention of DNA damage and of cell death that these toxins otherwise cause. Furthermore theanine “significantly blocked” the manner by which these toxins prevent important kinases from functioning. Thirdly, theanine acted to increase BDNF and GDNF creation. The authors concluded that theanine could be studied as an anti-parkinsonian agent. (Cho, Kim,  Lee, Park, Kim, & Chun, 2008)

BDNF and GDNF are neurotrophins. These are peptide-chains that have many healthful functions. They facilitate the adaptive growth of new synaptic connections. They preserve neurons, contributing to their health and maintenance. They guide neurons to grow in certain manners. Otherwise, neurotrophins conduce to the efficiency and productive activity of the nervous system. Brain-derived neurotrophic factor is the most proliferant neurotrophin the human nervous system. (Stahl, 2013)


Cerebral Degeneration

One peer-reviewed, systematic review study of theanine literature determined that theanine is effective against cerebral degeneration, and particularly how theanine preserves survival of neurons significantly longer than they would normally die due to lack of oxygen. The cerebellum is the chief brain region involved with regulating motor movements. The author reviews many statistically rigorous studies which found theanine useful for cell survival and proliferation in the dentate gyrus part of the hippocampus; this is one of three regions of the hippocampus, perhaps most salient, as it chooses which phenomena of the tons of sensory inputs we get each day, to encode into longer-term memory. (Stahl, 2013) The author notes one particular study. 29 volunteers af average age 85 took 47.5mg of theanine for 12 months. Changes were documented on a monthly basis. The people taking theanine, as opposed to placebo or nothing, scored much better at the Hasegawa’s Dementia Scale-Revised (HDS-R) test. (Kakuda, 2011) These participants were of very old age, well past the average age death.


Mechanism of Action

They continue with pharmacodynamics of theanine. It is an antagonist at the AMPA and kainate receptor subunits, though has low affinity (a weak bond with these receptors). More important is how theanine inhibits excessive neuronal conversion of glutamine to glutamate. As glutamate is the main excitatory neurotransmitter in the brain, this leads to greater calmness. Theanine also can increase the calming neurotransmitter GABA. GABA is the main inhibitory neurotransmitter in the brain. (Breedlove & Wastson, 2016) It is also the way that minor tranquilizers work to calm people (examples include valium, ativan, klonopin, and xanax). More GABA leads to less glutamate-caused exocytosis and cell death. It is dangerous to withdraw from GABAergics without doctoral overseeing the process because the excess in glutamate can cause seizures, delirium tremens.  Experts have determined that theanine may also have a similar mechanism as memantine, which is used for Alzheimer’s disease. (Kakuda, 2011)

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Schizophrenia and Quality of Sleep

As for treatment of mental illness, rigorous evidence exists. Theanine was administered to people with schizophrenia. The experts in this study being by referencing that glutamatergic dysfunction is biologically tied to schizophrenia. A past study, they state, revealed that theanine can reduce symptoms of schizophrenia. Their goal is to evaluate, again, how theanine might affect chronic symptoms of schizophrenia, and to find out just how, chemically, this might work. 250 mg/day was added to antipsychotic usage. Positive and Negative Syndrome Scale (PANSS), Pittsburgh Sleep Quality Index scores and MRS results were scored before the experiment, and at its end, eight weeks later. After theanine was added, significant improvements in PANSS positive scale, Sleep Quality Index, and MRS, were documented. Conclusively, theanine has use for positive symptoms of schizophrenia, and quality of sleep. (Ota, Wakabayashi, Sato, Hori, Hattori, Teraishi, . . . Kunugi, 2015)

The study by Ota, Wakabayashi, Sato, Hori, Hattori, Teraishi, . . . Kunug is more valuable than it may seem. Sleep itself is a major factor in the realm of mental illness. Staying awake long enough will yield effects that mirror mental illness for the most hardy of us. If one can’t sleep, or has problems sleeping, then their health across the continuity of their being, will decrease. Oftentimes, people will not be able to sleep, however, and are treated with a hypnotic, whereas there is an underlying problem that is causing them not to sleep. Bipolar mania (or hypomania), depression, and anxiety, can all lead to insomnia. Theanine may be useful as a sleeping agent because of it calming down the limbic system, the tract in the brain dealing with reward and positive symptoms of schizophrenia. (Hooley, Mineka, Knock, & Butcher 2016) Much of the time, too, people state that they can’t sleep, though they practice very poor sleep hygiene. They watch tv in their bed right before sleep, and eat dinner an hour before they go to bed.

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Psychotic Disorders and Depression

Other experts explored antipsychotic and antidepressant potential. The researchers set out to find a mechanism for theanine in the brain of mice. They expressly state the purpose of their study as to independently analyze theanine as a possible medication for mental illness due to BDNF and action at the NMDA receptor. Mice were given 1 mg/kg or 10 mg/kg of theanine or saline, then were subjected to the OFT, FST, EMPR, and PPI. Western blot analysis then revealed that one theanine dose blocks effects of of MK-801 (as an aside, MK-801 simulates the positive and negative symptoms of schizophrenia by being a potent NMDA antagonist, similar in function to PCP and ketamine). Three weeks administration yielded statistically significant reduced immobility time in the FST, with an improved baseline from PPI. BDNF in the hippocampus increased. In the cortical region, theanine increased Ca intracellular concentration, blocked by NMDA antagonists. Thus, antipsychotic and antidepressant potential were found and noted. (Wakabayashi, Numakawa, Ninomiya, Chiba, & Kunugi, 2011).

It is thought that brain-derived neurotrophic factor (BDNF) may be the major peptide responsible for SSRIs and other antidepressants manifesting a euthymic mood, and that the region is does so is the hippocampus, which is one of the two brain regions that continues to grow after we reach adulthood. It takes weeks or even months for antidepressants to work sometimes because this activity only manifests after serotonin down-regulates. (Stahl, 2013)

Ca+2 floods the terminal button of a neuron in order for vesicles to fuse to the presynaptic membrane and release neurotransmitters. So, increasing this action in the cortical region leads to more brain activity in the prefrontal cortex, which is thought to be reduced, and responsible for the negative effects, of schizophrenia.(Stahl, 2013) So, Wakabayashi, Numakawa, Ninomiya, Chiba, & Kunugi could have explicitly claimed a decrease in negative symptoms, which is there are no medications currently approved for. (NIH, 2017)



Researchers probed any effects that theanine might have on clinical depression. Mice were exposed to an anxiety-provoking situation individually. Then they were exposed to an environment that causes cerebral atrophy, compromised learning, and clinical depression. When theanine was introduced, of 5 mg/kg, lifespan rose, less cerebral damage and ability to learn was presented, depression fell, and oxidative damage lowered. Theanine was a neuroprotectant and mood-elevator while exposed to a high-stress environment exposure. Thus, physical and mental benefits were shown in one study. (Unno, Fujitani, Takamori, Takabayashi, Maeda, Miyazaki, . . . Hoshino, 2011).

An an in-vivo experiment with human subjects diagnosed with clinical depression, detailed the addition of 250mg to their current medication regimen. Subjects were tested right before the study, four weeks later, and at the conclusion, after eight weeks total. At each of these three points in time, subjects were rigorously subjected to five different, empirically qualified tests: The Hamilton Depression Rating Scale, State-Trait Anxiety Inventory, Pittsburgh Sleep Quality Index, Stroop test, and Brief Assessment of Cognition in Schizophrenia. The researchers noted symptomatic improvements across these vectors. Depression and anxiety decreased. Sleep quality increased. Lastly, cognition presented itself as more sharp. The authors remark that more rigorous studies are called for. (Hidese, Ota, Wakabayashi, Noda, Ozawa, Okubo, & Kunugi, 2016)


Responses to Prospective Criticisms

It would have been perhaps more useful for the scientists of these papers, if there are multiple benefits of theanine, to point out if one benefit is due secondarily to another benefit, or if it’s separately cause independently by theanine. The latter might be more useful, broadly applicable, as there would possibly be two different conditions that theanine could directly treat, not one. This is why extraneous variables should be located and eliminated,  and it may be counterproductive to assess for several variables in one study. For instance, Hidese, Ota, Wakabayashi, Noda, Ozawa, Okubo, & Kunugi found less depression, less anxiety, greater quality of sleep, and more acute cognitive skills. It might be possible that quality of sleep lead to all of the others, in which case, the only concrete finding would be increased sleep. The authors may find a way to parse out these effects. So, firstly, in the case of sleep, perhaps lessening their sleep quality and assessing the other variables.

There aren’t many manners that can serve as contradictory to these findings. This research is not to state that theanine is a medicine for mental illness; that is only something that a doctor can really say, if anyone. In the United States, it takes about a decade of testing, four different stages of testing, and hundreds of millions of dollars, simply to have a medication approved for use. (NIH, 2017) Firstly, extraneous and confounding variables are nullified in real clinical trials of a substance, as I’m sure environment plays a role in the effects. Also, given that theanine isn’t a medication, one is never sure just how much theanine they’re taking, as it’s not mandated to be of a specific purity by the Food and Drug Administration. One’s specific dosage, therefore, would not be known, and the dosage would oscillate, too, even if taken as supplement form. So, without specific and standard guidelines and access to a known and constant mg amount, it can’t act as a medication – when one receives a medication, they know how much they’re getting, by threat of governmental action. And it means a lot to take a standard dose. I suppose that there are as-needed medications, such as benzodiazepines, to be taken when needed; but even then, we would know how much we’re taking, and so would be able to forsee what kind of effects it has. There aren’t any congregations of websites that offer opinions and specific information about theanine, as there are with pharmaceutical medications – sometimes it helps to talk to others who’ve taken, or are taking, the same medicine.

And yet, a thorough examination of multiple databases yields that theanine has little to no potential at causing significant harm, reflected by its GRAS status. The study of theanine has essentially no conflict-of-interest because it’s freely available at a very accessible price. The US pharmaceutical block largely thrives on patents for new substances. One can’t patent green tea or theanine, as it is in green tea. Our economy is very capitalist-driven.

Studies on theanine in pill form may pose a bit of a conflict of interest, as theanine but theanine is still readily available via green tea. One study, conducted by a known theanine vendor, Suntheanine, has been disqualified. If people are loathe to use theanine because of the lack of government ascertaining its use, there is no risk related to a trial. No studies or anecdotes state that it acts against any pharmaceutical agent. Again, as it is GRAS, there is no real addiction potential. If one’s doctor does not know what theanine is, and states that their patient shouldn’t use it, green tea is different. Dr. Dauria, Dr. Gerson, Dr. Feinstein, and Dr. Breggin all have stated that green tea is safe. That said, studies cited focused on theanine itself, not green tea, not theanine and caffeine, nor any other mixture. One would expect that, if either green tea of theanine were to be dangerous, theanine would be found as such – similarly, in several South American countries, chewing coca lead is a cultural norm similar to out drinking coffee, but pure cocaine is very dangerous and unhealthy.



Caffeine can be found in coffee, and in various teas. Green tea somewhat differs in that it also produces theanine, a chemical deemed entirely safe to use, and which is responsible for its acute relaxing effects. Recently, statistically rigorous studies in theanine have found it to allay both neurodegenerative, and mental illnesses. The former includes Parkinson’s disease, Alzheimer’s disease, and cerebral degeneration. As for mental illness, improvement was found in positive symptoms of schizophrenia and the quality of sleep in those with schizophrenia, the positive symptoms and depression that accompanies schizophrenia, clinical depression, protectant against severe stress, anxiety, sleep quality, and cognition. Hopefully, in the years to come, theanine, or, green tea, will be inaugurated as having significant medical virtue. As for now, having a cup or two of green tea won’t hurt.




Hooley, J. M., Mineka, S., M., Knock, M. K., Butcher, J. N. (2016). Abnormal Psychology, Global Edition. Essex, England: Pearson International.


Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical application (4th ed.). Cambridge: Cambridge University Press.


Unno, K., Fujitani, K., Takamori, N., Takabayashi, F., Maeda, K., Miyazaki, H., . . . Hoshino, M. (2011). Theanine intake improves the shortened lifespan, cognitive dysfunction and behavioural depression that are induced by chronic psychosocial stress in mice. Free Radical Research, 45(8), 966-974. doi:10.3109/10715762.2011.566869


Hidese, S., Ota, M., Wakabayashi, C., Noda, T., Ozawa, H., Okubo, T., & Kunugi, H. (2016). Effects of chronic l-theanine administration in patients with major depressive disorder: an open-label study. Acta Neuropsychiatrica, 29(02), 72-79. doi:10.1017/neu.2016.33


Wakabayashi, C., Numakawa, T., Ninomiya, M., Chiba, S., & Kunugi, H. (2011). Behavioral and molecular evidence for psychotropic effects in l-theanine. Neuroscience Research, 71. doi:10.1016/j.neures.2011.07.858


Ota, M., Wakabayashi, C., Sato, N., Hori, H., Hattori, K., Teraishi, T., . . . Kunugi, H. (2015). Effect of l-theanine on glutamatergic function in patients with schizophrenia. Acta Neuropsychiatrica, 27(05), 291-296. doi:10.1017/neu.2015.22


Kakuda, T. (2011). Neuroprotective effects of theanine and its preventive effects on cognitive dysfunction. Pharmacological Research, 64(2), 162-168. doi:10.1016/j.phrs.2011.03.010


Cho, H., Kim, S., Lee, S., Park, J. A., Kim, S., & Chun, H. S. (2008). Protective effect of the green tea component, l-theanine on environmental toxins-induced neuronal cell death. NeuroToxicology, 29(4), 656-662. doi:10.1016/j.neuro.2008.03.004


Kim, T. I., Lee, Y. K., Park, S. G., Choi, I. S., Ban, J. O., Park, H. K., . . . Hong, J. T. (2009). L-Theanine, an amino acid in green tea, attenuates β-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction in oxidative damage and inactivation of ERK/p38 kinase and NF-κB pathways. Free Radical Biology and Medicine, 47(11), 1601-1610. doi:10.1016/j.freeradbiomed.2009.09.008


Rappa, L., & Viola, J. (2012). Condensed Psychopharmacology 2013: A Pocket Reference for Psychiatry and Psychotropic Medications. Ft. Lauderdale, FL: RXPSYCH LLC.


Breedlove, S. M., & Watson, N. V. (2016). Behavioral Neuroscience. Sunderland,

Massachusetts: Sinauer Associates.

Pinel, P. J. (2013). Biopsychology. New York: Pearson.


National Institute of Health (2017). NIH. Retrieved from





  • In-vitro


          1. Studies performed within a cell culture


  • In-vivo


          1. Studies performed in a living organism


  • Amyloid β


          1. The main part of the amyloid plaques, spanning 10’s of linked amino acids, that destroy the brain beset with the neurodegenerative Alzheimer’s Disease


  • Ischemia


          1. When an organ is cut off from the blood supply that allows it to function


  • open-field test (OFT)


          1. An experiment design measuring the activity of rats or mice, including willingness to explore new territory, and relatedly, level of anxiety, given a substance or being genetically altered


  • forced swim test (FST)


          1. This test is run with mice, which are put in a tank of liquid without escape, to evaluate the potential antidepressant activity of a compound based on when they give up, or being genetically altered, compared to placebo


  • elevated plus-maze test (EPMT)


          1. Yet another test, involving mice or rats, that assesses the anti-anxiety potential of various chemicals, or being genetically altered, by putting them in open, elevated, and novel territory


  • prepulse inhibition (PPI) of acoustic startle


          1. A behavioral phenomena test during which a weak stimulus has been conditioned with a strong stimulus immediately proceeding it, leaving the subjects (rats or mice) to no longer express such a strong reaction at the strong stimuli.


  • western blot analysis


          1. Called immunoblotting, allows the detection of protein in a much greater mix of cells or tissue


  • BDNF and related proteins


          1. Neurotrophic factors. These are peptides in the nervous system that tend to the health of neurons and glia via a wide range of actions. BDNF, the most prominent human neurotrophic factor, is said to become more proliferate as one succeeds with antidepressant treatment.


  • Hippocampus


          1. The part of the brain, variously stated to be part of the basal ganglia, limbic system, or telencephalon, that is most salient in terms of memory. Specifically, the dentate gyrus is responsible with encoding and storing the most salient memories – picking which memories are most important


  • Hasegawa’s Dementia Scale-Revised (HDS-R)


          1. A test for the presence of dementia


  • Excitotoxicity


          1. Stimulation to the point of toxicity


  • Hamilton Depression Rating Scale


          1. A test for the presence of clinically significant depression


  • State-Trait Anxiety Inventory


          1. A test for the presence of clinically significant anxiety


  • Pittsburgh Sleep Quality Index


          1. A test for the presence of clinically significant sleep abnormality


  • Stroop test


          1. A test for the clinically significant lack of directed attention


  • Brief Assessment of Cognition in Schizophrenia


          1.  A test for cognitive attributes that most strongly are consequential in prognosis of treatment for someone with schizophrenia


  • Cerebral cortex


          1. Composing the outermost brain layer, divided into the frontal, temporal, parietal, and occipital lobes.


  • MK-801


          1. An NMDA antagonist, most well-situated to chemically simulate schizophrenia in mice and rats


  • NMDA N-methyl-D-aspartate


          1. The receptor that is blocked as part of how NMDA works


  • GABA (gamma-aminobutyric acid)


          1. The main inhibitory neurotransmitter in the body


  • AMPA (Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid )
        1. An ionotropic receptor