This Research Article has been supervised by Nutritionist/Food Expert Anum Nazir).She is Lecturer in School of Nutritional sciences At University of Faisalabad).

Researcher And Writer


Supervised By Anum  Nazir 

Department of Nutritional Sciences

University Of Faisalabad,Pakistan



Background: Stress is an undeniable event of life which cannot be removed but can be managed to keep it under control and to reduce its recurrence. Chronic stress leads to depression and causes several issues for instance low mood and poor cognition which eventually affects an individual’s quality of life. Introduction: Depression is an emotional insecurity which affects an individual’s capacity to deal and perform the daily events. Depression leads to different diseases and complications. Each and every person suffers from depression in some part of their life which can be due to several factors that affect the cognition including poor diet, adverse life events, trauma etc. Mental illnesses are becoming more significant health issue among the universal stress diseases. An adequate diet is really important for proper cognitive functioning therefore treating depression, low mood and poor cognition with a natural food is more likely to control its symptoms and slows its recurrence. Banana is considered as a mood enhancer because it contains tryptophan therefore it was chosen to observe its effectiveness on depression. Objective: main aim was to review the effectiveness of tryptophan on cognition, to see the effect of a natural mood enhancer and to know the role of tryptophan in controlling several stress hormones. Review: tryptophan is abundantly available in banana, meat, dairy, cheese and also plant sources that provide essential amin acids. WHO recommends 4 mg/kg/day of tryptophan to maintain brain health. Tryptophan acts as a precursor for the production of neurotransmitter serotonin. Less tryptophan will lead to less synthesis of brain serotonin eventually leading towards irritability, phycological complications, low mood, poor cognition and depression. Tryptophan is a natural sedative and has direct effect on sleep. In depression, individual suffers from lack of sleep therefore tryptophan can be efficient in improving the quality of sleep. Conclusion: tryptophan has antidepressant properties therefore is able to manage depression and improve cognition. It enhances mood, induces sleep, improves memory and also plays role in controlling symptoms of other brain diseases.



Stress is an unavoidable event of life also impossible to completely eliminate from life. But it is necessary to keep it controlled. Acquaintance with chronic stress significantly weakens an individual’s ability to deal with every day liabilities productively plus affects normal body functioning thus greatly worsening mental and physical wellness. Uncontrolled stress impairs memory, attentiveness, concentration, and other characteristics of cognitive strength. Outcomes of uncontrolled stress are mental issues like depression, low mood and anxiety. Chronic stress also results in mental and physical depletion and also lack of motivation, incentive and energy. (Simoloka and Bhikha, 2016)


Depression is an emotional instability characterized by persistent intuition of sadness, pointlessness and guilt and also losing interest and happiness. Factors related to inheritance and environment, such as detrimental events in formative years are considered to assist in depression, however the basic mechanisms are not completely recognized. (Gross and Seroogy, 2020) It negatively affects an individual the way he eats, his diet and sleeping pattern, the way he perceives about himself, plus the way an individual think about different affairs. (Khan et al., 2006) Depression reduces an individual’s living standard, sense of wellbeing and enhances functional impairment. (Waterworth et al., 2015) This term ‘depression’ is used for both, as a diagnostic classification and subjective explanation of mood. Low mood commonly shows crankiness and disturbing behavioural disorders like offending behaviour, (Jane, 2013)

Link with genetics

Genetic factors have an impact on commencement of depression partially by varying the sensitiveness of human beings to the depression-provoking effect of distressing events of the life. (Kendler et al ., 2010) Depression is lot more heterogeneous also the involvement of environmental risk factors is greater than genetic factors. (Tadafumi, 2007)


Depression turned out as a significant public health issue proved by being at fourth position amongst the universal stress of diseases. Many assume that by 2020 it will take second position. 450 million individuals worldwide experience mental disorder and poor cognition. 340 million individuals above 18 years of age undergo depressive disorders which aids to higher suicidal rates. In developing nations 10–44% go through depression and mental illnesses, under 35% receive support and approximately 50.8 million individuals suffer from main depression. (Gadit and Mugford, 2007) A study suggested that cognitive disorders affiliated with mood swings is confined to a few patients with the most being psychologically normal. (Iverson et al ., 2011) Depression is a general, debilitating illness and a threat to life which is expected by WHO to become the second major cause of impotence by 2020. (Roiser et al., 2012)

Identifying poor cognition and low mood can be complicated. Even though globally agreed diagnosis for depression in adolescents and adults is considered to be same with irritability being a notable feature. Another significant difference among adolescents in comparison with adults is the recurrence of psychological issues. This makes the diagnosis difficult for health care practitioners. (Jane, 2013)


Diet and depression


Lately diet has appeared as critical for cognition as it turns out for other diseases. (Zainuddin and Thuret, 2012) Nutrition is increasingly being recognized as an important amendable threat for depression and anxiety related disorders. In 2009, a study concluded that individuals who opted for healthy eating habits had a lower risk of poor cognition and depression over 10 years of monitoring. A research published subsequently demonstrated that individuals had a less chance of establishing depression if they consumed “whole food” and were at greater risk if they consumed “processed food”. (Jacka and Berk, 2013) In general there was favorable connection between healthy eating habits or consuming high-quality foods and less events of depression. Likewise, a relationship was present between inadequate nutrition and intake of poor-quality foods and low mood and poor cognition. (khalid et al., 2016) Brain requires an adequate nutrition for numerous aspects of its functioning. (Bodnar and Wisner, 2005) Learning and remembering abilities and also mood can be affected by diet during development and as well as in adulthood. Certainly, numerous epidemiological researches have proposed an association between cognitive problems and diet where inverse relationship between the type of diet and general mental disorders, anxiety, low mood and depression have been defined and indicated in adults. (Zainuddin and Thuret, 2012)




A natural solution to manage stress is through diet. Banana must be eaten for relieving stress. Banana contains tryptophan which helps to boost mood and promote sleep by preventing stress and depression. (Simoloka and Bhikha, 2016)


Several evidences show that reduced tryptophan and a triggered tryptophan catabolite (TRYCAT) pathway are involved in depression and poor cognition. (Roomruangwong et al., 2016) Tryptophan is an essential amino acid which should be taken from diet. Along with protein synthesis it also functions as a substrate for bioactive components with essential physiological roles. (Takada et al., 2018) Serotonin (5-hydroxytryptamine, 5-HT) malfunction is linked with pathophysiology of poor cognition. Tryptophan hydroxylase (TPH), the flow restricting enzyme in biosynthesis of 5-HT, is considered to have vital role in several cognitive problems including depression. (Chen et al., 2017) Dietary cure with tryptophan rich hydrolyzed protein has favorable impacts on cognition and physiological pressure for both high cognitive reactivity and lower cognitive reactivity individuals. Hydrolyzed protein can be a better nutritional method for raising brain tryptophan and serotonin. (Firk and Markus, 2009).

Tryptophan depicts a key component for cognitive functioning because it acts as a precursor thus important for the formation of serotonin, a neurotransmitter. In clinical situations, low levels of tryptophan resulting from higher catabolic rate of tryptophan are frequent and are associated with depressive mood frequently. (Strasser et al., 2016)


Modifying central serotonin function resulting from acute tryptophan depletion (ATD) has granted the fundamental understandings that cognitive roles are affected by tryptophan and serotonin. It might be anticipated that serotonergic stimulation from tryptophan could provoke positive behavioural changes as it has notable effects on cognition, sleep and mood. It is assumed that the impact of tryptophan loading on execution or performance maybe reliant on the beginning of the serotonin system of an individual. Tryptophan loading resulted in memory improvements in populations where primary serotonergic disorders are recognized. Likewise, tryptophan loading emerges to be more efficient in enhancing mood in susceptible subjects plus enhances sleep in individuals with any sleep disturbances. (Silber and Schmitt, 2010) A tryptophan and antioxidant rich diet have a beneficial effect on cognition and mood. (Strasser et al., 2016)




  • Effectiveness of tryptophan on mood and cognition


  • To know the effect of natural mood enhancer on mood and improve cognitive ability


  • To know the role of tryptophan in controlling stress hormones which leads to low mood and poor cognition hence depression




Symptoms of depression and poor cognition


Emotional Perception: Emotional disorder is the crucial problem of depressive symptomatology and cognitive disorders engage with the emotional tone of stimulus material. Emotional processing biases are seeming interactively in numerous domains of cognitive functioning, involving insight, attention, remembrance, and feedback processing. Reduction in the identification of facial sentiments have been stated constantly in depression. (Roiser et al., 2012)


Emotional Attention: patients with depression tend to take more time to designate the color of undesirable emotional words while in an emotional assignment, depressed patients also including initial episode-depressed teenagers, responded lately to happy goals. Few studies have proposed that depressed individuals fail to show a partiality toward optimistic emotional material, however such a partiality is noticeably constant in healthy volunteers. (Roiser et al., 2012)

Emotional Memory: Depression is related to negative favoritisms in recalling tasks. Some studies discovered that depressed individuals tend to favorably recall negative stimuli. (Roiser et al., 2012)

Reward and Punishment Processing: It is anticipated that depressed individuals might show exaggerated reactions to adverse performance feedback. (Roiser et al., 2012).

Benefits of tryptophan


Tryptophan is a crucial plant-derived amino acid which is required for the synthesis of proteins. After ingestion, it is transformed into bioactive metabolites like kynurenine, serotonin, niacin, melatonin. Tryptophan helps in diagnosis and alleviation of multiple diseases. Dietary tryptophan along with its metabolites contribute in different therapies for cognitive function, depression, multiple sclerosis, autism, sleep, cardiovascular diseases, chronic kidney diseases, social function, chronic kidney disease, inflammatory bowel disease and microbial infections. Tryptophan also facilitates the diagnosis of conditions for example human cataracts, renal cell carcinoma, colon neoplasms and prognosticating diabetic nephropathy. (Mendel, 2018)


Sources and recommendation


The rate of formation of tryptophan in the brain rely on dietary precursors available since brain is unable to synthesize without them. (parker and brotchie, 2011). Ingestion pf pure tryptophan along with intake of carbohydrate or even by consumption of tryptophan rich alpha-lactalbumin protein. These dietary factors can increase the blood concentrations of tryptophan as compared to other amino acids giving tryptophan greater access into the brain. (Markus et al., 2008) Dietary sources include animal sources meat and meat product, eggs, fish, milk products and cheese provide all the essential and required amino acids, and consuming plant-based foods will also supply essential amino acids. Recommendation by The World Health Organization is 4 mg/kg/day for adults. Almost 0.5g of tryptophan is a part of western diet, out of which 2–3% is involved in production of central serotonin. the availability of tryptophan to the CNS is said to be depending upon two factors: the concentration of free versus bound tryptophan in the blood and second, the osmolarity of large neutral amino acids (LNAA) – which include tyrosine, phenylalanine, leucine, isoleucine and valine. These compete with tryptophan (bound and free) for the uptake by the carrier for transportation beyond the blood–brain barrier. (parker and brotchie, 2011)


Tryptophan Depletion


Initial research intending to reduce central tryptophan hired the irreversible tryptophan hydroxylase inhibitor, which diminishes serotonin by discontinuing the rate-limiting step in its formation. An alternate to inhibit the enzyme responsible for synthesis of serotonin is to reduce tryptophan from the brain. Rapid nutritional depletion of tryptophan permits the examination of the consequence of reduced tryptophan levels. The intake of a diet containing more neutral amino acids however lacking tryptophan results in an acute lowering of blood serum tryptophan. This happens because the exclusion of tryptophan from the diet act as a stimulus for liver to synthesize protein by using accessible plasma tryptophan. This result has been noted experimentally in mice, rats and humans. Moreover, the enormous neutral amino acids from the diet race with tryptophan for transfer throughout the blood brain barrier and therefore limit the access of tryptophan across the brain. This depletes both tryptophan and serotonin, centrally. Studies on rodents have revealed that the acute tryptophan depletion diminished tryptophan levels in the brain nearly up to 70% and also decreases central serotonin. In human acute depletion of tryptophan impedes serotonin


synthesis plus reduces cerebrospinal fluid concentrate of tryptophan, 5-hydroxyindoleacetic acid and the main serotonin metabolite. (Jenkins et al., 2016)


Tryptophan Supplementation and Cognition


Tryptophan-rich dietary proteins increase tryptophan accessibility to the mind and therefore possibly boost serotonin synthesis. Clinical researchers have come to the conclusion that acute tryptophan supplementation enhanced consecutive reaction times and mental visual memory, whereas positive facial recognition memory was improved by chronic supplementation (14 days). Furthermore, elderly patients who were going through mild cognitive impairment were given a 12-week diet of docosahexaenoic acid phospholipids along with tryptophan plus melatonin. They indicated improvements in cognition and mood (Jenkins et al., 2016)


Tryptophan and serotonin relation


Tryptophan synthesizes serotonin in a 2-step reaction. Firstly, an enzyme tryptophan- 5-hydroxylase hydrolysis amino acid into 5-hydroxytryptophan and then 5-hydroxytryptophan is decarboxylated by an enzyme aromatic L-amino acid decarboxylase resulting in serotonin. The primary step is rate limiting and therefore tryptophan hydroxylation regulates the complete rate of serotonin synthesis. Studies shows that physiologic and pharmaceutical rises in brain tryptophan concentrations speedily stimulate serotonin formation. Serotonin synthesis in a rat brain would be stimulated by tryptophan dose as little as 12.5 mg/kg, a very little dose, signifying that the trail is quite delicate to modifications in precursor provision. The brain experiences great variations in brain Tryptophan concentrations, for example can happen after the consumption of meal that directly affect serotonin synthesis. (John, 2012)


Tryptophan, Sleep, Mood and Cognition


Tryptophan has direct effect on sleep, it induces sleep and decreases wakefulness. Thus, improving quality of sleep which is associated with an enhancement of mood, cognitive measures, better morning alertness and also brain actions. Patients suffering from depression also suffer from poor quality of sleep, sometimes antidepressant treatment also worsen sleep inadequacy with insomnia plus decreases overall sleep time. In depression, the consequence of tryptophan reduction on sleep has mainly focused on remitted patients who were consuming antidepressants thus resulted in less sleep and REM, representing that depleting tryptophan did not modify the side effects of antidepressant. In patients with obsessive compulsive disorder, tryptophan depletion encouraged the worsening of the continuity of sleep however no fluctuations of REM. (Jenkins et al., 2016)


Effects of tryptophan on sleep


To check the effect, five healthy and normal volunteers were consecutively given L- tryptophan for almost ten nights which resulted in an upsurge in non- rapid-eye-movement nap (non-R.E.M.) while they displayed a decrease in R.E.M. sleep. Seven individuals with insomnia received L-tryptophan dose for 5 or 10 successive nights and resulted in improvement in total sleep plus non-R.E.M. sleep. Inhibiting synthesis of serotonin decreases R.E.M. sleep and raising serotonin to enhance R.E.M. sleep by administration of 5-hydroxytryptophan it seems that L-tryptophan creates its snooze effects by a non- serotonin mechanism. Moreover, it was supported by a finding of improved non- R.E.M. sleep and less R.E.M. sleep when administered in the company of a drug p-chlorophenylalanine, which blocks the transformation of tryptophan to serotonin. (John, 2012).

Side effects of tryptophan treatment


Concerning side effects of Tryptophan treatment, studies were conducted and when tryptophan was provided alone no side effects were reported and were reported in few individuals. Side effects included dry mouth, dizziness, tremor, mild nausea. (John, 2012)


Side effects with an antidepressant drug


When tryptophan was managed with an antidepressant drug, side effects due to tryptophan collectively with a tricyclic antidepressant (TCAD) blockers of presynaptic transmitter reuptake were not present or were negligible. When Tryptophan was supplemented to a MAOI, resulting side effects were infrequent-mild (muscle twitching, drowsiness and ataxia) and more prominent like hyperreflexia, nausea, drowsiness. Similar symptoms of side effects were also distinguished in nonpsychiatric patients who were receiving an MAOI and Tryptophan however were not noted when participants got the exact same dosages of Tryptophan alone. (John, 2012)


Role of tryptophan in dementia


Current research has revealed that depression that recurrently accompanies plus precedes the movement ailments of Parkinson’s disease is mainly of the less functioning of serotonin nerves therefore tryptophan can be a suitable aid to L- Dopa/ deprenyl handling of Parkinson’s. In the later phases of Alzheimer’s, intensified irritability and gratuitous aggression regularly escort to the mental deterioration. Supplemental tryptophan might enhance the activity of serotonergic neurons thus reducing anger and also aggression. (James, 2002)


Tryptophan depletion and its intimation for psychiatry


Tryptophan depletion results in decrease in plasma tryptophan and thus serotonin synthesis and its release. Its effects in healthy volunteers are affected by the features of the individuals and include low mood, poor cognition, memory impairment and upsurge in aggression. Tryptophan depletion in patients with depression and panic disorders result in relapse of symptoms in those patients who responses to antidepressants predominantly serotonergic agents. (Bell et al., 2001)



This review concluded that tryptophan which is an essential amino acid (plant-derived) is effective in managing depression and poor cognition because of its antidepressant properties. Tryptophan is a precursor for the synthesis of serotonin, a key hormone which helps in stabilizing our mood and feelings of well-being thus overall control an individual’s mood. Tryptophan is a natural sedative

which induces sleep, improve sleep continuity and also improves memory and cognition. It also assists in controlling symptoms of different brain diseases.




  1. Bell, C., Abrams, J., & Nutt, D. (2001). Tryptophan depletion and its implications for psychiatry. The British Journal of Psychiatry, 178(5), 399-405.
  2. Bodnar, L. M., & Wisner, K. L. (2005). Nutrition and depression: implications for improving mental health among childbearing-aged women. Biological psychiatry, 58(9), 679-685.


  1. Chen, Y., Xu, H., Zhu, M., Liu, K., Lin, B., Luo, R., … & Li, M. (2017). Stress inhibits tryptophan hydroxylase expression in a rat model of depression. Oncotarget, 8(38), 63247.
  2. Fernstrom, J. D. (2012). Effects and side effects associated with the non-nutritional use of tryptophan by humans. The Journal of nutrition, 142(12), 2236S-2244S.
  3. Firk, C., & Markus, C. R. (2009). Mood and cortisol responses following tryptophan-rich hydrolyzed protein and acute stress in healthy subjects with high and low cognitive reactivity to depression. Clinical Nutrition, 28(3), 266-271.
  4. Friedman, M. (2018). Analysis, nutrition, and health benefits of tryptophan. International Journal of Tryptophan Research, 11, 1178646918802282.
  5. Gadit, A. A. M., & Mugford, G. (2007). Prevalence of depression among households in three capital cities of Pakistan: need to revise the mental health policy. Plos one, 2(2).
  6. Gross, C., & Seroogy, K. B. (2020). Neuroprotective roles of neurotrophic factors in depression. In Neuroprotection in Autism, Schizophrenia and Alzheimer’s Disease (pp. 125-144). Academic Press.


  1. Iverson, G. L., Brooks, B. L., Langenecker, S. A., & Young, A. H. (2011). Identifying a cognitive impairment subgroup in adults with mood disorders. Journal of affective disorders, 132(3), 360-367.
  2. Jacka, F. N., & Berk, M. (2013). Depression, diet and exercise. The Medical Journal of Australia, 199(6), S21-S23.
  3. Jenkins, T. A., Nguyen, J. C., Polglaze, K. E., & Bertrand, P. P. (2016). Influence of tryptophan and serotonin on mood and cognition with a possible role of the gut-brain axis. Nutrients, 8(1), 56.


  1. Kato, T. (2007). Molecular genetics of bipolar disorder and depression. Psychiatry and clinical neurosciences, 61(1), 3-19.
  2. Kendler, K. S., Kessler, R. C., Walters, E. E., MacLean, C., Neale, M. C., Heath, A. C., & Eaves, L. J. (2010). Stressful life events, genetic liability, and onset of an episode of major depression in women. Focus, 8(3), 459-470.


  1. Khalid, S., Williams, C. M., & Reynolds, S. A. (2016). Is there an association between diet and depression in children and adolescents? A systematic review. British journal of nutrition, 116(12), 2097-2108.
    1. Khan, M. S., Mahmood, S., Badshah, A., Ali, S. U., & Jamal, Y. (2006). Prevalence of depression, anxiety and their associated factors among medical students in Karachi, Pakistan. Journal-Pakistan Medical Association, 56(12), 583.


    1. Markus, C. R., Firk, C., Gerhardt, C., Kloek, J., & Smolders, G. F. (2008). Effect of different tryptophan sources on amino acids availability to the brain and mood in healthy volunteers. Psychopharmacology, 201(1), 107-114.
    2. Parker, G., & Brotchie, H. (2011). Mood effects of the amino acids tryptophan and tyrosine: ‘Food for Thought’III. Acta Psychiatrica Scandinavica, 124(6), 417-426.
    3. Roberts, J. (2013). Low mood and depression in adolescence: clinical update. Br J Gen Pract, 63(610), 273-274.
    4. Roiser, J. P., Elliott, R., & Sahakian, B. J. (2012). Cognitive mechanisms of treatment in depression. Neuropsychopharmacology, 37(1), 117-136.
    5. Roomruangwong, C., Kanchanatawan, B., Sirivichayakul, S., Anderson, G., Carvalho, A. F., Duleu, S., … & Maes, M. (2016). IgA/IgM responses to tryptophan and tryptophan catabolites (TRYCATs) are significantly associated with premenstrual syndrome or physio-somatic symptoms at the end of term, while lowered IgA responses to anthranilic acid are associated with perinatal depression. Molecular Neurobiol.[Epub ahead of print]. doi, 10.
    6. Silber, B. Y., & Schmitt, J. A. J. (2010). Effects of tryptophan loading on human cognition, mood, and sleep. Neuroscience & Biobehavioral Reviews, 34(3), 387-407.
    7. Simoloka, A., & Bhikha, R. (2016). Reducing stress naturally.


    1. South, J. (2002). L-Tryptophan-nature’s answer to Prozac. International Antiaging Systems, 6.
    2. Strasser, B., Gostner, J. M., & Fuchs, D. (2016). Mood, food, and cognition: role of tryptophan and serotonin. Current Opinion in Clinical Nutrition & Metabolic Care, 19(1), 55-61.


    1. Takada, A., Shimizu, F., & Masuda, J. (2018). Measurement of Plasma Tryptophan Metabolites: Clinical and Experimental Application for Depression and Stress States Assessment. Melatonin—Molecular Biology, Clinical and Pharmaceutical Approaches, IntechOpen, London, 143-160.
    2. Waterworth, S., Arroll, B., Raphael, D., Parsons, J., & Gott, M. (2015). A qualitative study of nurses’ clinical ‐experience in recognising low mood and depression in older patients with multiple long term conditions. Journal of clinical nursing, 24(17-18), 2562-2570.


    1. Wyatt, R., Kupfer, D., Sjoerdsma, A., Engelman, K., Fram, D., & Snyder, F. (1970). Effects of L-tryptophan (a natural sedative) on human sleep. The lancet, 296(7678), 842-846.


    Zainuddin, M. S. A., & Thuret, S. (2012). Nutrition, adult hippocampal neurogenesis and mental health. British medical bulletin, 103(1), 89-114


Leave a Comment