Effects of oral 5-hydroxy-tryptophan on energy intake and macronutrient selection in non-insulin dependent diabetic patients Effects of 5-hydroxytryptophan on eating behavior and adherence to dietary prescriptions in obese adult subjects. The effects of tryptophan depletion on cognitive and affective processing in healthy volunteers Effect of different tryptophan sources on amino acids availability to the brain and mood in healthy volunteers Whey protein rich in alpha-lactalbumin increases the ratio of plasma tryptophan to the sum of the other large neutral amino acids and improves cognitive performance in stress-vulnerable subjects. Neural and behavioral responses to tryptophan depletion in unmedicated patients with remitted major depressive disorder and controls. Tryptophan and high-carbohydrate diets as adjuncts to smoking cessation therapy Tryptophan depletion reduces right inferior prefrontal activation during response inhibition in fast, event-related fMRI Effects of tryptophan depletion vs catecholamine depletion in patients with seasonal affective disorder in remission with light therapy. Reversal of the Kynurenine Pathway of Tryptophan Catabolism May Improve Depression in ART-Treated HIV-Infected Ugandans Impact of Experimentally Induced Serotonin Deficiency by Tryptophan Depletion on Sleep EEG in Healthy Subjects Tryptophan depletion in normal volunteers produces selective impairment in memory consolidation An index of 5-HT synthesis changes during early antidepressant treatment: α-[11C]methyl-l-tryptophan PET study Tryptophan Depletion Alters the Decision-Making of Healthy Volunteers through Altered Processing of Reward Cues The Effects of Acute Tryptophan Depletion on Neuropsychological Function Macronutrient intake, plasma large neutral amino acids and mood during weight-reducing diets Ingestion of branched-chain amino acids and tryptophan during sustained exercise in man: failure to affect performance.
OBJECTIVE : In obese patients , brain serotonergic stimulation via orally administered 5-hydroxy-tryptophan ( 5-HTP ) , the precursor of serotonin , causes decreased carbohydrate intake and weight loss . Since diabetes mellitus is associated with depressed brain serotonin , hyperphagia and carbohydrate craving , we hypothesized that in diabetic patients , orally administered 5-HTP stimulates brain serotonergic activity and thus normalizes eating behaviour . To test this hypothesis , we investigated whether in diabetic patients : 1 ) predicted brain serotonin concentrations are depressed as a result of decreased availability of the precursor , tryptophan ; and 2 ) oral 5-HTP is effective in reducing energy and carbohydrate intake . SUBJECTS AND METHODS : 25 overweight non-insulin dependent diabetic out patients were enrolled in a double-blind , placebo-controlled study , and r and omized to receive either 5-HTP ( 750 mg/d ) or placebo for two consecutive weeks , during which no dietary restriction was prescribed . Energy intake and eating behaviour , as expressed by macronutrient selection , were evaluated using a daily diet diary . Plasma amino acid concentrations and body weight , as well as serum glucose , insulin and glycosylated haemoglobin were assessed . RESULTS : 20 patients ( nine from the 5-HTP group and 11 from the Placebo group ) completed the study . Brain tryptophan availability in diabetic patients was significantly reduced when compared to a group of healthy controls . Patients receiving 5-HTP significantly decreased their daily energy intake , by reducing carbohydrate and fat intake , and reduced their body weight . CONCLUSIONS : These data confirm the role of the serotonergic system in reducing energy intake , by predominantly inhibiting carbohydrate intake , and suggest that 5-HTP may be safely utilized to improve the compliance to dietary prescriptions in non-insulin dependent diabetes mellitus Changes in plasma amino acid levels by affecting the availability of neurotransmitter amino acid precursors within the brain may influence eating behavior ( Wurtman et al. , 1981 ; Fernstrom , 1983 ) . Among the different neuro-transmitter systems , a number of theoretical and experimental data support the role played by serotonin in the regulation of eating habits ( Lytle , 1977 ; Li et al. , 1983 ) . Rather recently , R.J. Wurtman et al. ( 1981 ) have shown that the serotonergic system plays an important role also in the selection of macronutrients , especially in obese people consuming preferentially carbohydrate-rich foods . Moreover , a “ normalization ” of such aberrant behavior was obtained by pharmacologically enhancing brain serotonin synthesis ( J.J. Wurtman et al. , 1981 ) . A significant reduction in food intake has been reported by Blundell and Leshem ( 1975 ) in hyperphagic obese rats by administration of tion of 5-hydroxytryptophan ( 5-HTP ) . Previous experiences from this laboratory in a group of obese adult female subjects have shown that the oral administration of 5-HTP caused the onset of typical anorexia-related symptoms , decreased food intake and promoted weight loss in the absence of any dietary restriction ( Ceci et al. , 1989 ) . The aim of the present study was to confirm these data in a longer study period and to verify whether the adherence to dietary prescriptions could be improved by oral administration of 5-HTP Abstract Rationale . Cognitive impairment is a common feature of depressive illness . While accumulating evidence suggests that brain serotonin ( 5-HT ) pathways play an important role in the neurobiology of depression , the extent to which altered 5-HT function is responsible for the associated changes in cognition and emotion remains unclear . Objective . The present study examined the effects of acute dietary depletion of tryptophan ( TRP ) on cognitive and affective processing in healthy volunteers and explored the putative role of 5-HT in the neuropsychology of depression . Methods . We administered computerised cognitive tests to healthy control participants following ingestion of TRP-free and nutritionally balanced amino acid drinks in a double-blind , placebo-controlled , crossover design . Results . The TRP-free amino acid mixture significantly lowered plasma total and free TRP concentrations relative to baseline values and produced selective deficits similar to those observed previously in cases of clinical depression . In particular , TRP depletion increased response times for happy but not sad targets in an affective go/no-go task and slowed responding in a visual discrimination and reversal learning task . These deficits were not due to a global sedative effect , as planning ability was unimpaired . Conclusions . The present data indicate that serotonergic factors may be more involved in the disrupted inhibitory and emotional processing characteristic of depression than in other aspects of executive function , such as planning ability . These findings support the recent proposal that serotonergic manipulation may have greater effects on tasks mediated by frontal circuitry that includes the orbitofrontal cortex than by dorsolateral prefrontal cortex circuitry Rationale Reduced brain serotonin function is acknowledged as a vulnerability factor for affective disturbances . Since the production of serotonin is limited by the availability of its plasma dietary amino acid precursor tryptophan ( TRP ) , the beneficial effects of tryptophan-rich alpha-lactalbumin whey protein ( ALAC ) have recently been studied . The effects of ALAC remain rather modest , and alternative protein sources of tryptophan may be more effective . Objectives We tested whether hydrolyzed protein ( HPROT ) has greater effects on the plasma TRP/large neutral amino acids ( LNAA ) ratio and mood than intact ALAC protein in healthy volunteers . Material s and methods In a double-blind , r and omized cross-over study , plasma amino acids and mood were repeatedly measured in 18 healthy subjects before and after intake of  ALAC and HPROT as well as after placebo protein , pure tryptophan , and a tryptophan-containing synthetic peptide . Except for the placebo protein , all interventions contained 0.8 g TRP . Results Significantly faster and greater increases in plasma TRP/LNAA were found after HPROT than after ALAC . In addition , the effects of HPROT on plasma TRP/LNAA were comparable with the effects of the tryptophan-containing synthetic peptide and even exceeded the effect of pure tryptophan . Sixty minutes after intake , mood was improved only following intake of HPROT and pure tryptophan , whereas longer-lasting mood effects were only found after intake of HPROT . Conclusions The use of a tryptophan-rich hydrolyzed protein source may be more adequate to increase brain tryptophan and 5-HT function compared with intact alpha-lactalbumin protein or pure tryptophan BACKGROUND Cognitive performance often declines under chronic stress exposure . The negative effect of chronic stress on performance may be mediated by reduced brain serotonin function . The uptake of the serotonin precursor tryptophan into the brain depends on nutrients that influence the availability of tryptophan by changing the ratio of plasma tryptophan to the sum of the other large neutral amino acids ( Trp-LNAA ratio ) . In addition , a diet-induced increase in tryptophan may increase brain serotonergic activity levels and improve cognitive performance , particularly in high stress-vulnerable subjects . OBJECTIVE We tested whether alpha-lactalbumin , a whey protein with a high tryptophan content , would increase the plasma Trp-LNAA ratio and improve cognitive performance in high stress- vulnerable subjects . DESIGN Twenty-three high stress-vulnerable subjects and 29 low stress-vulnerable subjects participated in a double-blind , placebo-controlled , crossover study . All subjects conducted a  memory-scanning task after the intake of a diet enriched with either alpha-lactalbumin ( alpha-lactalbumin diet ) or sodium caseinate ( control diet ) . Blood sample s were taken to measure the effect of dietary manipulation on the plasma Trp-LNAA ratio . RESULTS A significantly greater increase in the plasma Trp-LNAA ratio after consumption of the alpha-lactalbumin diet than after the control diet ( P = 0.0001 ) was observed ; memory scanning improved significantly only in the high stress-vulnerable subjects ( P = 0.019 ) . CONCLUSION Because an increase in the plasma Trp-LNAA ratio is considered to be an indirect indication of increased brain serotonin function , the results suggest that dietary protein rich in alpha-lactalbumin improves cognitive performance in stress-vulnerable subjects via increased brain tryptophan and serotonin activities CONTEXT An instructive paradigm for investigating the relationship between brain serotonin function and major depressive disorder ( MDD ) is the response to tryptophan depletion ( TD ) induced by oral loading with all essential amino acids except the serotonin precursor tryptophan . OBJECTIVE To determine whether serotonin dysfunction represents a trait abnormality in MDD in the context of specific neural circuitry abnormalities involved in the pathogenesis of MDD . DESIGN R and omized double-blind crossover study . SETTING Outpatient clinic . PARTICIPANTS Twenty-seven medication-free patients with remitted MDD ( 18 women and 9 men ; mean + /- SD age , 39.8 + /- 12.7 years ) and 19 controls ( 10 women and 9 men ; mean + /- SD age , 34.4 + /- 11.5 years ) . INTERVENTIONS We induced TD by administering capsules containing an amino acid mixture without tryptophan . Sham depletion used identical capsules containing hydrous lactose . Fluorodeoxyglucose F 18 positron emission tomography studies were performed 6 hours after TD . Magnetic resonance images were obtained for all participants . MAIN OUTCOME MEASURES Quantitative positron emission tomography of regional cerebral glucose utilization to study the neural effects of sham depletion and TD . Behavioral assessment s used a modified ( 24-item ) version of the Hamilton Depression Rating Scale . RESULTS Tryptophan depletion induced a transient return of depressive symptoms in patients with remitted MDD but not in controls ( P<.001 ) . Compared with sham depletion , TD was associated with an increase in regional cerebral glucose utilization in the orbitofrontal cortex , medial thalamus , anterior and posterior cingulate cortices , and ventral striatum in patients with remitted MDD but not in controls . CONCLUSION The pattern of TD-induced regional cerebral glucose utilization changes in patients with remitted MDD suggests that TD unmasks a disease-specific , serotonin system-related trait dysfunction and identifies a circuit that probably plays a key role in the pathogenesis of MDD Treatments that reduce the immediate effects of smoking withdrawal have potential for helping smokers quit . Serotonin-enhancing substances , such as tryptophan and high-carbohydrate diets , have been used in clinical disorders to relieve negative affect , a classic symptom of cigarette withdrawal . This research project investigated the use of tryptophan ( 50 mg/kg/day ) and high-carbohydrate diets , together with more traditional smoking cessation treatment techniques , to ameliorate the  smoking withdrawal syndrome  and to improve abstinence rates .  Subjects were r and omly assigned to receive either tryptophan ( n=16 ) or placebo ( n=15 ) . St and ard smoking cessation treatment was identical for the experimental and control groups and consisted of four 2-hr weekly sessions of multicomponent group therapy .  Smoking behavior , symptoms of nicotine withdrawal , and negative affect were assessed during a 2-week withdrawal period . Tryptophan-treated subjects who could not fully abstain were able to smoke fewer daily cigarettes . Reported anxiety and other withdrawal symptoms were lower in the tryptophan group compared with control subjects . These data suggest that serotonin-enhancing substances show promise for use as an adjunct to existing smoking cessation programs Rationale and objective In animal and human studies , the neurotransmitter serotonin ( 5-hydroxytryptamine ; 5-HT ) has been implicated in mediating impulsiveness and aggression . To test the hypothesis that 5-HT modulates neuro-cognitive brain activation during inhibitory control , we examined the effect of acute tryptophan depletion ( ATD ) , a dietary challenge , which has been shown to decrease 5-HT synthesis in the brain , on functional brain activation during a go/no-go task . Methods Nine healthy , right-h and ed volunteers performed a rapid , event-related go/no-go task in two functional magnetic resonance imaging ( fMRI ) scanning sessions , 5 h after either a tryptophan-free or a balanced amino acid drink in a double-blind , sham depletion-controlled , counterbalanced , crossover design . The task required subjects to selectively execute or inhibit a motor response . Tryptophan depletion significantly lowered total plasma tryptophan concentration by 80 % , but did not significantly alter inhibitory performance or mood ratings . Results ATD significantly reduced right orbito-inferior prefrontal activation during the no-go condition , and increased activation in superior and medial temporal cortices . Conclusions These findings provide neuro-functional evidence of a serotonergic modulation of right inferior prefrontal during inhibitory motor control . The increased engagement of temporal brain regions may reflect compensatory mechanisms BACKGROUND Although hypotheses about the therapeutic mechanism of action of light therapy have focused on serotonergic mechanisms , the potential role , if any , of catecholaminergic pathways has not been fully explored . METHODS Sixteen patients with seasonal affective disorder who had responded to a st and ard regimen of daily 10000-lux light therapy  were enrolled in a double-blind , placebo-controlled , r and omized crossover study . We compared the effects of tryptophan depletion with catecholamine depletion and sham depletion . Ingestion of a tryptophan-free amino acid beverage plus amino acid capsules was used to deplete tryptophan . Administration of the tyrosine hydroxylase inhibitor alpha-methyl-paratyrosine was used to deplete catecholamines . Diphenhydramine hydrochloride was used as an active placebo during sham depletion . The effects of these interventions were evaluated with measures of depression , plasma tryptophan levels , and plasma catecholamine metabolites . RESULTS Tryptophan depletion significantly decreased plasma total and free tryptophan levels . Catecholamine depletion significantly decreased plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels . Both tryptophan depletion and catecholamine depletion , compared with sham depletion , induced a robust increase ( P<.001 , repeated- measures analysis of variance ) in depressive symptoms as measured with the Hamilton Depression Rating Scale , Seasonal Affective Disorder Version . CONCLUSIONS The beneficial effects of light therapy in the treatment of seasonal affective disorder are reversed by both tryptophan depletion and catecholamine depletion . These findings confirm previous work showing that serotonin plays an important role in the mechanism of action of light therapy and provide new evidence that brain catecholaminergic systems may also be involved Background : Major depressive disorder is highly prevalent among HIV-infected persons , and depression symptom severity improves during the course of HIV antiretroviral therapy ( ART ) . The potential biologic pathways explaining these phenomena remain unclear . We investigated the extent to which ART-mediated suppression of the kynurenine pathway of tryptophan catabolism ( via indoleamine 2,3-dioxygenase-1 and potentially other sources ) may correlate with improvements in depression symptom severity in this setting . Method : We used the first year of data from the Ug and a AIDS Rural Treatment Outcomes Study , a prospect i ve cohort of 504 HIV-infected individuals initiating their first ART regimen in rural Ug and a. We fitted r and om-effects regression models to estimate the associations between plasma tryptophan , plasma kynurenine , dietary diversity , and self-reported depression symptom severity . Results : Greater depressive symptoms were associated with both lower plasma tryptophan and higher plasma kynurenine/tryptophan ( KT ) ratio over 12-month follow-up . In multivariable-adjusted models , declines in KT ratio and increases in plasma tryptophan levels partially explained ART-mediated improvements in depressive symptom severity . The association between KT ratio and depression symptom severity was stronger among persons with protein-deficient diets than among those with protein-rich diets . Conclusions : Indoleamine 2,3-dioxygenase-1-mediated tryptophan catabolism may contribute to depression symptom severity among HIV-infected individuals , particularly among those with poor dietary protein intake . ART-mediated improvements in depressive symptom severity may also be at least partially mediated by immunologic mechanisms . Interventions to reduce immune activation , and dietary protein supplementation , may be promising strategies to further reduce depression in this setting The tryptophan depletion test is a research strategy to investigate the functional consequences of decreasing the brain serotonin metabolism . Because serotonin is involved in sleep regulation and the regulation of affective states , we studied the acute polysomnographic effects of tryptophan depletion and expected to induce similar changes of sleep EEG as observed in depressed patients . A total of 12 healthy subjects ( mean age 34 ± 3 years ) had eight polysomnograms  , divided in two blocks of 4 consecutive nights . After one adaptation and 1 baseline night , subjects received a low-protein diet on day 3 and 4 until midday . On day 4 at 18.00 h , they drank an amino acid mixture either devoid of tryptophan or containing 2.3 g of tryptophan ( placebo control ) in r and omized and double-blind order , result ing in an 85 % decrease ( tryptophan depletion ) and a 144 % increase ( placebo control ) of serum tryptophan at 22.00 h. After tryptophan depletion but not placebo , significant effects on sleep EEG were observed in terms of decreased non-rapid eye movement ( non-REM ) stage 2 , increase of wake % , and of rapid eye movement ( REM ) density compared with baseline . REM latency was not altered , however the first and second REM period interval were significantly shorter after tryptophan depletion . This study underlines the impact of the serotonergic system on sleep maintenance and on REM sleep . © 1998 American College of Abstract Serotonin ( 5-hydroxytryptamine ; 5-HT ) circuits may play a role in cognitive performance , particularly in learning and memory . Cognitive impairment is often seen in depressed patients , in whom 5-HT turnover in the brain is thought to be lowered . A possible human pharmacological model to study the involvement of the serotonergic system in cognitive impairment is to reduce central 5-HT synthesis through L-tryptophan depletion in healthy subjects . In this study , the cognitive effects of tryptophan depletion were assessed and whether genetically or developmentally determined vulnerability factors were predictive of the cognitive impairment induced by tryptophan depletion . Sixteen healthy volunteers with a positive family history of depression and 11 without were given 100 g of an amino acid mixture with or without tryptophan , according to a double-blind , cross-over design . Tryptophan depletion specifically impaired long-term memory performance in all subjects : delayed recall performance , recognition sensitivity , and recognition reaction times were significantly impaired after tryptophan depletion relative to placebo . Short-term memory and perceptual and psychomotor functions were unchanged . There were no differences between groups with a positive and a negative family history for depression . On the basis of these results , it is concluded that tryptophan depletion specifically impairs long-term memory formation , presumably as a result of an acute decrease in 5-HT turnover in the brain The antidepressant selective serotonin transporter inhibitors ( SSRIs ) are clinical ly active after a delay of several weeks . Indeed , the rapid increase of serotonin ( 5-HT ) caused by SSRIs , stimulates the 5-HT(1A ) autoreceptors , which exert a negative feedback on the 5-HT neurotransmission . Only when autoreceptors are desensitized , can SSRIs exert their therapeutic activity . The 5-HT(1A ) receptor antagonist pindolol has been used to accelerate the clinical effects of antidepressant by preventing the negative feedback . Using the alpha-[(11)C]methyl-L-tryptophan/positron emission tomography ( PET ) , the goal of the present double-blind , r and omized study was to compare the changes in alpha-[(11)C]methyl-L-tryptophan trapping , an index of serotonin synthesis , in patients suffering from unipolar depression treated with the SSRI citalopram ( 20 mg/day ) plus placebo versus patients treated with citalopram plus pindol ( 7.5 mg/day ) .  PET and Hamilton depression rating scale ( HDRS-17 ) were performed at baseline , and after 10 and 24 days of antidepressant treatment . Results show that the combination citalopram plus pindol , compared to citalopram alone shows a more rapid and greater increase of an index of 5-HT synthesis in prefrontal cortex ( BA 9 ) . This research is the first human PET study demonstrating that , after 24 days , the combination SSRIs plus pindolol produces a greater increase of the metabolism of serotonin in the prefrontal cortex , an area associated to depressive symptoms While accumulating evidence suggests that effective real-life decision-making depends upon the functioning of the orbitofrontal cortex , much less is known about the involvement of the monoamine neurotransmitter systems and , in particular , serotonin . In the present study , we explored the impact of depleting the serotonin precursor , tryptophan , on human decision-making . Eighteen healthy volunteers consumed an amino-acid drink containing tryptophan and 18 healthy volunteers consumed an amino-acid drink without tryptophan , before choosing between simultaneously presented gambles , differing in the magnitude of expected gains ( ie reward ) , the magnitude of expected losses ( ie punishment ) , and the probabilities with which these outcomes were delivered . Volunteers also chose between gambles probing identified non-nomative biases in human decision-making , namely , risk-aversion when choosing between gains and risk-seeking when choosing between losses . Tryptophan-depleted volunteers showed reduced discrimination between magnitudes of expected gains associated with different choices . There was little evidence that tryptophan depletion was associated with altered discrimination between the magnitudes of expected losses , or altered discrimination between the relative probabilities with which these positive or negative outcomes were delivered . Risk-averse and risk-seeking biases were also unchanged . These results suggest that serotonin mediates decision-making in healthy volunteers by modulating the processing of reward cues , perhaps represented within the orbitofrontal cortex . It is possible that such a change in the cognition mediating human choice is one mechanism associated with the onset and maintenance of anhedonia and lowered mood in psychiatric illness Serotonin ( 5-HT , 5-hydroxytryptamine ) may have an important role in the maintenance of normal neuropsychological functioning . The method of acute tryptophan depletion ( ATD ) provides a pharmacological challenge by which central 5-HT levels can be temporarily decreased and effects on learning , memory and mood examined . Twenty healthy male volunteers were recruited to take part in this within-subject , double-blind , crossover study . Neuropsychological function was evaluated 4 - 6 h after ingestion of a control or 52 g tryptophan ( TRP ) depleting amino-acid drink . ATD significantly lowered levels of plasma total and free TRP ( p < 0.001 ) , but this did not affect mood or performance on tests of verbal and visuo-spatial learning and memory , attention or executive function . These results contradict previous findings ; however , the degree of disruption of central 5-HT levels result ing from the use of the 52 g amino-acid protocol may be an important factor in explaining the lack of effect . By utilizing more specific probes of individual 5-HT receptor subtypes , future studies can fully explore the role of 5-HT in neuropsychological functioning and may eluci date the factors determining vulnerability to the effects of serotonergic dysfunction Influence of diet composition on mood during weight-reducing diets was studied in healthy young women of normal weight . A broad range of macronutrient intake was achieved by means of divergent dietary instructions for the composition of a 1,000 kcal per day diet adhered to for six weeks . Global mood during the last three weeks of the diet was significantly better in the “ vegetarian ” than in the “ mixed ” diet group . During this time a significant correlation was observed between relative carbohydrate intake and global mood ( r=−0.74 ; p<0.01 ) and between the ratio of plasma tryptophan to other large neutral amino acids ( a predictor of tryptophan flow into brain ) and global mood ( r=− 0.52 ; p<0.05 ) . Results suggest that group differences are related to differences in carbohydrate intake . It is hypothesized that impairment of central serotonergic function due to reduced tryptophan availability can prompt mood deterioration in situations of relatively low carbohydrate intake 1 . An increased uptake of tryptophan in the brain may increase serotoninergic activity and recently has been suggested to be a cause of fatigue during prolonged exercise . The present study , therefore , investigates whether ingestion of tryptophan or the competing branched-chain amino acids ( BCAAs ) affect performance .  Ten endurance-trained male athletes were studied during cycle exercise at 70 - 75 % maximal power output , while ingesting , ad r and om and double-blind , drinks that contained 6 % sucrose ( control ) or 6 % sucrose supplemented with ( 1 ) tryptophan ( 3 g l-1 ) , ( 2 ) a low dose of BCAA ( 6 g l-1 ) or ( 3 ) a high dose of BCAA ( 18 g l-1 ) . 2 . These treatments greatly increased the plasma concentration of the respective amino acids . Using the kinetic parameters of transport of human brain capillaries , BCAA supplements were estimated to reduce brain tryptophan uptake at exhaustion by 8 - 12 % , while tryptophan ingestion caused a 7- to 20-fold increase . Exercise time to exhaustion was not different between treatments ( 122 + /- 3 min ) . 3 . The data suggest that manipulation of tryptophan supply to the brain either has no additional effect upon serotoninergic activity during prolonged exhaustive exercise or that manipulation of serotoninergic activity functionally does not contribute to mechanisms of fatigue
Graphical abstract Excessive dieting‐induced nutritional deficiency of tryptophan : Effects on behavior and efficacy of antipsychotic and antidepressant medication .
& NA ; A growing body of evidence suggests that our diet is an important contributing factor in the development , management and prevention of a number of psychiatric illnesses .
Tryptophan , an essential amino acid , is the sole precursor of neurotransmitter 5‐hydroxytryptamine ( 5‐HT ; serotonin ) .
Administration of tryptophan can boost serotonin neurotransmission to produce therapeutically important effects in serotonin deficiency disorders .
Anorexia nervosa ( AN ) an eating disorder associated with high levels of psychiatric comorbidity including psychosis , hyperactivity , depression and anxiety has highest lethality of all psychiatric illnesses .
Evidence suggests that excessive dieting and food restriction can decrease brain tryptophan and serotonin in AN patients to precipitate depression , psychosis and hyperactivity .
There are currently no FDA approved pharmacological treatments available for AN patients ; antidepressants and antipsychotics , largely used to treat associated psychiatric comorbidities are also not very effective .
The aim of this non‐ systematic review article is to evaluate and document a potential importance of tryptophan supplementation in improving therapeutics in AN patients .