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Journal List > J Psychiatry Neurosci > v.32(6); Nov 2007

PMCID: PMC2077351
Copyright © 2007 Canadian Medical Association
How to increase serotonin in the human brain without drugs
Simon N. Young
Editor-in-chief, Journal of Psychiatry and Neuroscience, and Department of Psych
iatry, McGill University, Montréal, Que.
Medical subject headings: serotonin, exercise, phototherapy, food, depression, h
appiness
* Other Sections▼
o References

For the last 4 decades, the question of how to manipulate the serotonergic syste
m with drugs has been an important area of research in biological psychiatry, an
d this research has led to advances in the treatment of depression. Research on
the association between various polymorphisms and depression supports the idea t
hat serotonin plays a role, not only in the treatment of depression but also in
susceptibility to depression and suicide. The research focus here has been on po
lymorphisms of the serotonin transporter, but other serotonin-related genes may
also be involved.1–5 In the future, genetic research will make it possible to pred
ict with increasing accuracy who is susceptible to depression. Much less attenti
on has been given to how this information will be used for the benefit of indivi
duals with a serotonin-related susceptibility to depression, and little evidence
exists concerning strategies to prevent depression in those with such a suscept
ibility. Various studies have looked at early intervention in those with prodrom
al symptoms as well as at population strategies for preventing depression.6–11 Obv
iously, prevention is preferable to early intervention; moreover, although popul
ation strategies are important, they are ideally supplemented with preventive in
terventions that can be used over long periods of time in targeted individuals w
ho do not yet exhibit even nonclinical symptoms. Clearly, pharmacologic approach
es are not appropriate, and given the evidence for serotonin's role in the etiol
ogy and treatment of depression, nonpharmacologic methods of increasing serotoni
n are potential candidates to test for their ability to prevent depression.
Another reason for pursuing nonpharmacologic methods of increasing serotonin ari
ses from the increasing recognition that happiness and well-being are important,
both as factors protecting against mental and physical disorders and in their o
wn right.12–14 Conversely, negative moods are associated with negative outcomes. F
or example, the negative mood hostility is a risk factor for many disorders. For
the sake of brevity, hostility is discussed here mainly in relation to one of t
he biggest sources of mortality, coronary heart disease (CHD). A meta-analysis o
f 45 studies demonstrated that hostility is a risk factor for CHD and for all-ca
use mortality.15 More recent research confirms this. Hostility is associated not
only with the development of CHD but also with poorer survival in coronary arte
ry disease (CAD) patients.16 Hostility may lead to decreased social support and
social isolation,17 and low perceived social support is associated with greater
mortality in those with CAD.18 Effects are not just limited to CHD. For example,
the opposite of hostility, agreeableness, was a significant protective factor a
gainst mortality in a sample of older, frail participants.19
The constitution of the WHO states “Health is a state of complete physical, mental
and social well-being and not merely the absence of disease or infirmity.”20 This
may sound exaggerated but positive mood within the normal range is an important
predictor of health and longevity. In a classic study, those in the lowest quar
tile for positive emotions, rated from autobiographies written at a mean age of
22 years, died on average 10 years earlier than those in the highest quartile.21
Even taking into account possible confounders, other studies “found the same soli
d link between feeling good and living longer.”12 In a series of recent studies, n
egative emotions were associated with increased disability due to mental and phy
sical disorders,22 increased incidence of depression,23 increased suicide24 and
increased mortality25 up to 2 decades later. Positive emotions protected against
these outcomes. A recent review including meta-analyses assessed cross-sectiona
l, longitudinal and experimental studies and concluded that happiness is associa
ted with and precedes numerous successful outcomes.26 Mood may influence social
behaviour, and social support is one of the most studied psychosocial factors in
relation to health and disease.27 Low social support is associated with higher
levels of stress, depression, dysthymia and posttraumatic stress disorder and wi
th increased morbidity and mortality from a host of medical illnesses.27
Research confirms what might be intuitively expected, that positive emotions and
agreeableness foster congenial relationships with others.28,29 This in turn wil
l create the conditions for an increase in social support.
Several studies found an association between measures related to serotonin and m
ood in the normal range. Lower platelet serotonin2 receptor function was associa
ted with lower mood in one study,30 whereas better mood was associated with high
er blood serotonin levels in another.31 Two studies found that greater prolactin
release in response to fenfluramine was associated with more positive mood.32,3
3 The idea that these associations indicate a causal association between seroton
in function and mood within the normal range is consistent with a study demonstr
ating that, in healthy people with high trait irritability, tryptophan, relative
to placebo, decreased quarrelsome behaviours, increased agreeable behaviours an
d improved mood.34 Serotonin may be associated with physical health as well as m
ood. In otherwise healthy individuals, a low prolactin response to the serotonin
-releasing drug fenfluramine was associated with the metabolic syndrome, a risk
factor for heart disease,35 suggesting that low serotonin may predispose healthy
individuals to suboptimal physical as well as mental functioning.
Nonpharmacologic methods of raising brain serotonin may not only improve mood an
d social functioning of healthy people — a worthwhile objective even without addit
ional considerations — but would also make it possible to test the idea that incre
ases in brain serotonin may help protect against the onset of various mental and
physical disorders. Four strategies that are worth further investigation are di
scussed below.
The article by Perreau-Linck and colleagues36 (page 430 of this issue) provides
an initial lead about one possible strategy for raising brain serotonin. Using p
ositron emission tomography, they obtained a measure of serotonin synthesis in t
he brains of healthy participants who underwent positive, negative and neutral m
ood inductions. Reported levels of happiness were positively correlated and repo
rted levels of sadness were negatively correlated with serotonin synthesis in th
e right anterior cingulate cortex. The idea that alterations in thought, either
self-induced or due to psychotherapy, can alter brain metabolism is not new. Num
erous studies have demonstrated changes in blood flow in such circumstances. How
ever, reports related to specific transmitters are much less common. In one rece
nt study, meditation was reported to increase release of dopamine.37 The study b
y Perreau-Linck and colleagues36 is the first to report that self-induced change
s in mood can influence serotonin synthesis. This raises the possibility that th
e interaction between serotonin synthesis and mood may be 2-way, with serotonin
influencing mood and mood influencing serotonin. Obviously, more work is needed
to answer questions in this area. For example, is the improvement in mood associ
ated with psychotherapy accompanied by increases in serotonin synthesis? If more
precise information is obtained about the mental states that increase serotonin
synthesis, will this help to enhance therapy techniques?
Exposure to bright light is a second possible approach to increasing serotonin w
ithout drugs. Bright light is, of course, a standard treatment for seasonal depr
ession, but a few studies also suggest that it is an effective treatment for non
seasonal depression38 and also reduces depressed mood in women with premenstrual
dysphoric disorder39 and in pregnant women suffering from depression.40 The evi
dence relating these effects to serotonin is indirect. In human postmortem brain
, serotonin levels are higher in those who died in summer than in those who died
in winter.41 A similar conclusion came from a study on healthy volunteers, in w
hich serotonin synthesis was assessed by measurements of the serotonin metabolit
e 5-hydroxyindoleacetic acid (5-HIAA) in the venous outflow from the brain.42 Th
ere was also a positive correlation between serotonin synthesis and the hours of
sunlight on the day the measurements were made, independent of season. In rats,
serotonin is highest during the light part of the light–dark cycle, and this stat
e is driven by the photic cycle rather than the circadian rhythm.43,44 The exist
ence of a retinoraphe tract may help explain why, in experimental animals, neuro
nal firing rates, c-fos expression and the serotonin content in the raphe nuclei
are responsive to retinal light exposure.44–48 In humans, there is certainly an i
nteraction between bright light and the serotonin system. The mood-lowering effe
ct of acute tryptophan depletion in healthy women is completely blocked by carry
ing out the study in bright light (3000 lux) instead of dim light.49
Relatively few generations ago, most of the world population was involved in agr
iculture and was outdoors for much of the day. This would have resulted in high
levels of bright light exposure even in winter. Even on a cloudy day, the light
outside can be greater than 1000 lux, a level never normally achieved indoors. I
n a recent study carried out at around latitude 45° N, daily exposure to light gre
ater than 1000 lux averaged about 30 minutes in winter and only about 90 minutes
in summer50 among people working at least 30 hours weekly; weekends were includ
ed. In this group, summer bright light exposure was probably considerably less t
han the winter exposure of our agricultural ancestors. We may be living in a bri
ght light–deprived society. A large literature that is beyond the scope of this ed
itorial exists on the beneficial effect of bright light exposure in healthy indi
viduals. Lamps designed for the treatment of seasonal affective disorder, which
provide more lux than is ever achieved by normal indoor lighting, are readily av
ailable, although incorporating their use into a daily routine may be a challeng
e for some. However, other strategies, both personal and institutional, exist. “Li
ght cafes” pioneered in Scandinavia have come to the United Kingdom,51 and an Aust
rian village that receives no sunshine in the winter because of its surrounding
mountains is building a series of giant mirrors to reflect sunlight into the val
ley.52 Better use of daylight in buildings is an issue that architects are incre
asingly aware of. Working indoors does not have to be associated with suboptimal
exposure to bright light.
A third strategy that may raise brain serotonin is exercise. A comprehensive rev
iew of the relation between exercise and mood concluded that antidepressant and
anxiolytic effects have been clearly demonstrated.53 In the United Kingdom the N
ational Institute for Health and Clinical Excellence, which works on behalf of t
he National Health Service and makes recommendations on treatments according to
the best available evidence, has published a guide on the treatment of depressio
n.54 The guide recommends treating mild clinical depression with various strateg
ies, including exercise rather than antidepressants, because the risk–benefit rati
o is poor for antidepressant use in patients with mild depression. Exercise impr
oves mood in subclinical populations as well as in patients. The most consistent
effect is seen when regular exercisers undertake aerobic exercise at a level wi
th which they are familiar.53 However, some skepticism remains about the antidep
ressant effect of exercise, and the National Institute of Mental Health in the U
nited States is currently funding a clinical trial of the antidepressant effect
of exercise that is designed to overcome sources of potential bias and threats t
o internal and external validity that have limited previous research.55
Several lines of research suggest that exercise increases brain serotonin functi
on in the human brain. Post and colleagues56 measured biogenic amine metabolites
in cerebrospinal fluid (CSF) of patients with depression before and after they
increased their physical activity to simulate mania. Physical activity increased
5-HIAA, but it is not clear that this was due to increased serotonin turnover o
r to mixing of CSF from higher regions, which contain higher levels of 5-HIAA, w
ith lumbar CSF (or to a combination of both mechanisms). Nonetheless, this findi
ng stimulated many animal studies on the effects of exercise. For example, Chaou
loff and colleagues57 showed that exercise increased tryptophan and 5-HIAA in ra
t ventricles. More recent studies using intracerebral dialysis have shown that e
xercise increases extracellular serotonin and 5-HIAA in various brain areas, inc
luding the hippocampus and cortex (for example, see58–60). Two different mechanism
s may be involved in this effect. As reviewed by Jacobs and Fornal,61 motor acti
vity increases the firing rates of serotonin neurons, and this results in increa
sed release and synthesis of serotonin.62 In addition, there is an increase in t
he brain of the serotonin precursor tryptophan that persists after exercise.63
The largest body of work in humans looking at the effect of exercise on tryptoph
an availability to the brain is concerned with the hypothesis that fatigue durin
g exercise is associated with elevated brain tryptophan and serotonin synthesis.
A large body of evidence supports the idea that exercise, including exercise to
fatigue, is associated with an increase in plasma tryptophan and a decrease in
the plasma level of the branched chain amino acids (BCAAs) leucine, isoleucine a
nd valine (see64,65 for reviews). The BCAAs inhibit tryptophan transport into th
e brain.66 Because of the increase in plasma tryptophan and decrease in BCAA, th
ere is a substantial increase in tryptophan availability to the brain. Tryptopha
n is an effective mild hypnotic,67 a fact that stimulated the hypothesis that it
may be involved in fatigue. A full discussion of this topic is not within the s
cope of this editorial; however, it is notable that several clinical trials of B
CAA investigated whether it was possible to counter fatigue by lowering brain tr
yptophan, with results that provided little support for the hypothesis. Further,
exercise results in an increase in the plasma ratio of tryptophan to the BCAAs
before the onset of fatigue.64,65 The conclusion of these studies is that, in hu
mans, a rise in precursor availability should increase serotonin synthesis durin
g and after exercise and that this is not related to fatigue, although it may be
related to improved mood. Whether motor activity increases the firing rate of s
erotonin neurons in humans, as in animals, is not known. However, it is clear th
at aerobic exercise can improve mood.
As with exposure to bright light, there has been a large change in the level of
vigorous physical exercise experienced since humans were hunter-gatherers or eng
aged primarily in agriculture.68 Lambert68 argued that the decline in vigorous p
hysical exercise and, in particular, in effort-based rewards may contribute to t
he high level of depression in today's society. The effect of exercise on seroto
nin suggests that the exercise itself, not the rewards that stem from exercise,
may be important. If trials of exercise to prevent depression are successful, th
en prevention of depression can be added to the numerous other benefits of exerc
ise.
The fourth factor that could play a role in raising brain serotonin is diet. Acc
ording to some evidence, tryptophan, which increases brain serotonin in humans a
s in experimental animals,69 is an effective antidepressant in mild-to-moderate
depression.67,70 Further, in healthy people with high trait irritability, it inc
reases agreeableness, decreases quarrelsomeness and improves mood.34 However, wh
ether tryptophan should be considered primarily as a drug or a dietary component
is a matter of some dispute. In the United States, it is classified as a dietar
y component, but Canada and some European countries classify it as a drug. Treat
ing tryptophan as a drug is reasonable because, first, there is normally no situ
ation in which purified tryptophan is needed for dietary reasons, and second, pu
rified tryptophan and foods containing tryptophan have different effects on brai
n serotonin. Although purified tryptophan increases brain serotonin, foods conta
ining tryptophan do not.71 This is because tryptophan is transported into the br
ain by a transport system that is active toward all the large neutral amino acid
s and tryptophan is the least abundant amino acid in protein. There is competiti
on between the various amino acids for the transport system, so after the ingest
ion of a meal containing protein, the rise in the plasma level of the other larg
e neutral amino acids will prevent the rise in plasma tryptophan from increasing
brain tryptophan. The idea, common in popular culture, that a high-protein food
such as turkey will raise brain tryptophan and serotonin is, unfortunately, fal
se. Another popular myth that is widespread on the Internet is that bananas impr
ove mood because of their serotonin content. Although it is true that bananas co
ntain serotonin, it does not cross the blood–brain barrier.
α-L ct lbumin, minor constituent of milk, is one protein th t cont ins rel tivel
y more tryptoph n th n most proteins. Acute ingestion of α-l ct lbumin by hum ns c
n improve mood nd cognition in some circumst nces, presum bly owing to incre s
ed serotonin.72,73 Enh ncing the tryptoph n content of the diet chronic lly with
α-l ct lbumin is prob bly not pr ctic l. However, incre sing the tryptoph n conte
nt of the diet rel tive to th t of the other mino cids is something th t possi
bly occurred in the p st nd could occur g in in the future. Kerem nd colle gu
es74 studied the tryptoph n content of both wild chickpe s nd the domestic ted
chickpe s th t were bred from them in the Ne r E st in neolithic times. The me n
protein content (per mg dry seed) w s simil r for 73 cultiv rs nd 15 wild v ri
eties. In the cultiv ted group, however, the tryptoph n content w s lmost twice
th t of the wild seeds. Interestingly, the gre ter p rt of the incre se w s due
to n incre se in the free tryptoph n content (i.e., not p rt of the protein).
In cultiv ted chickpe s, lmost two-thirds of the tryptoph n w s in the free for
m. Kerem nd colle gues74 rgue th t there w s prob bly selection for seeds with
higher tryptoph n content. This is pl usible, given nother ex mple of n e r
ly str tegy to incre se the v il ble tryptoph n content of n import nt food so
urce. Pell gr is disorder c used by ni cin deficiency, usu lly owing to pover
ty nd diet relying he vily on corn (m ize), which h s low level of ni cin
nd its precursor tryptoph n. Cultures in the Americ s th t relied gre tly on cor
n used lk li during its processing (e.g., boiling the corn in lime when m king
tortill s). This enh nced the nutrition l qu lity of the corn by incre sing the
bio v il bility of both ni cin nd tryptoph n, pr ctice th t prevented pell gr
.75 The Europe ns tr nsported corn round the world but did not tr nsport the t
r dition l lk li-processing methods, thereby c using epidemics of pell gr in p
st centuries. Breeding corn with higher tryptoph n content w s shown in the 1
980s to prevent pell gr 76; presum bly, it lso r ised br in serotonin. In rec
ent issue of N ture Biotechnology, Morris nd S nds77 rgue th t pl nt breeders
should be focusing more on nutrition th n on yield. They sk, “Could consumption o
f tryptoph n-rich foods pl y role in reducing the prev lence of depression nd
ggression in society?” Cross-n tion l studies h ve reported positive ssoci ti
on between corn consumption nd homicide r tes78 nd neg tive ssoci tion betw
een diet ry tryptoph n nd suicide r tes.79 Although the ide behind such studie
s is interesting, ny c us l ttribution must rem in specul tive, given the poss
ible confounds. Nonetheless, the possibility th t the ment l he lth of popul t
ion could be improved by incre sing the diet ry int ke of tryptoph n rel tive to
the diet ry int ke of other mino cids rem ins n interesting ide th t should
be explored.
The prim ry purpose of this editori l is to point out th t ph rm cologic str teg
ies re not the only ones worthy of study when devising str tegies to incre se b
r in serotonin function. The effect of nonph rm cologic interventions on br in s
erotonin nd the implic tions of incre sed serotonin for mood nd beh viour need
to be studied more. The mount of money nd effort put into rese rch on drugs t
h t lter serotonin is very much gre ter th n th t put into non-ph rm cologic me
thods. The m gnitude of the discrep ncy is prob bly neither in tune with the wis
hes of the public nor optim l for progress in the prevention nd tre tment of me
nt l disorders.
Footnotes
Competing interests: None decl red.
Correspondence to: Dr. Simon N. Young, Dep rtment of Psychi try, McGill Universi
ty, 1033 Pine Ave. W., Montré l QC H3A 1A1; f x 514 398-4370; Simon.Young@mcgill.c

* Other Sections▼
o References
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Articles from Journ l of Psychi try & Neuroscience : JPN re provided here court
esy of
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PubMed rticles by these uthors
* Young, S.
PubMed rel ted rticles
* Serotonin met bolism of nim l model of depression.
Adv Exp Med Biol. 1981; 133:603-25.
[Adv Exp Med Biol. 1981]
* Se son l ch nges in the levels nd the turnover of br in serotonin nd nor
dren line in the Europe n h mster kept under const nt environment.
Experienti . 1978 Aug 15; 34(8):1032-3.
[Experienti . 1978]
* On the role of serotonin in sleep regul tion nd depression. A comment ry
on "Neurobiologic l b ses for the rel tion between sleep nd depression" (J. Adr
ien).
Sleep Med Rev. 2003 Feb; 7(1):101-2; uthor reply 103-5.
[Sleep Med Rev. 2003]
* Review[Dyn mic ch nges of br in serotonergic nd dop minergic ctivities d
uring development of nxious depression: experiment l study]
Usp Fiziol N uk. 2004 Oct-Dec; 35(4):19-40.
[Usp Fiziol N uk. 2004]
* ReviewIndole mines in depression nd suicide.
Prog Br in Res. 1986; 65:59-71.
[Prog Br in Res. 1986]
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* Met - n lysis supports ssoci tion between serotonin tr nsporter (5-HTT)
nd suicid l beh vior.
Mol Psychi try. 2007 J n; 12(1):47-54.
[Mol Psychi try. 2007]
* ReviewImplic tions of genetic rese rch on the role of the serotonin in dep
ression: emph sis on the serotonin type 1A receptor nd the serotonin tr nsporte
r.
Psychoph rm cology (Berl). 2004 Aug; 174(4):512-24.
[Psychoph rm cology (Berl). 2004]
* ReviewA system tic review of ssoci tion studies investig ting genes codin
g for serotonin receptors nd the serotonin tr nsporter: II. Suicid l beh vior.
Mol Psychi try. 2003 Jul; 8(7):646-53.
[Mol Psychi try. 2003]
* ReviewA system tic review of ssoci tion studies investig ting genes codin
g for serotonin receptors nd the serotonin tr nsporter: I. Affective disorders.
Mol Psychi try. 2003 Jun; 8(6):574-91.
[Mol Psychi try. 2003]
* Tryptoph n hydroxyl se-2 gene v ri tion influences person lity tr its nd
disorders rel ted to emotion l dysregul tion.
Int J Neuropsychoph rm col. 2007 Jun; 10(3):309-20.
[Int J Neuropsychoph rm col. 2007]
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* H ppiness.
BMJ. 2005 Dec 24; 331(7531):1489-90.
[BMJ. 2005]
* A met - n lytic review of rese rch on hostility nd physic l he lth.
Psychol Bull. 1996 M r; 119(2):322-48.
[Psychol Bull. 1996]
* Hostility s predictor of surviv l in p tients with coron ry rtery dise
se.
Psychosom Med. 2004 Sep-Oct; 66(5):629-32.
[Psychosom Med. 2004]
* Ch r cteristics of soci lly isol ted p tients with coron ry rtery dise se
who re t elev ted risk for mort lity.
Psychosom Med. 2001 M r-Apr; 63(2):267-72.
[Psychosom Med. 2001]
* Perceived soci l support s predictor of mort lity in coron ry p tients:
effects of smoking, sedent ry beh vior, nd depressive symptoms.
Psychosom Med. 2005 J n-Feb; 67(1):40-5.
[Psychosom Med. 2005]
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* Positive emotions in e rly life nd longevity: findings from the nun study
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J Pers Soc Psychol. 2001 M y; 80(5):804-13.
[J Pers Soc Psychol. 2001]
* H ppiness.
BMJ. 2005 Dec 24; 331(7531):1489-90.
[BMJ. 2005]
* Life diss tisf ction nd subsequent work dis bility in n 11-ye r follow-u
p.
Psychol Med. 2004 Feb; 34(2):221-8.
[Psychol Med. 2004]
* Life s tisf ction nd depression in 15-ye r follow-up of he lthy dults.
Soc Psychi try Psychi tr Epidemiol. 2004 Dec; 39(12):994-9.
[Soc Psychi try Psychi tr Epidemiol. 2004]
* Self-reported h ppiness in life nd suicide in ensuing 20 ye rs.
Soc Psychi try Psychi tr Epidemiol. 2003 M y; 38(5):244-8.
[Soc Psychi try Psychi tr Epidemiol. 2003]
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* ReviewPerson lity development: st bility nd ch nge.
Annu Rev Psychol. 2005; 56():453-84.
[Annu Rev Psychol. 2005]
* ReviewPositive psychology in clinic l pr ctice.
Annu Rev Clin Psychol. 2005; 1():629-51.
[Annu Rev Clin Psychol. 2005]
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* Correl tions for serotonin levels nd me sures of mood in nonclinic l s
mple.
Psychol Rep. 2000 Dec; 87(3 Pt 1):707-16.
[Psychol Rep. 2000]
* Associ tions between whole-blood serotonin nd subjective mood in he lthy
m le volunteers.
Biol Psychol. 2006 Feb; 71(2):171-4.
[Biol Psychol. 2006]
* Serotonergic function in the centr l nervous system is ssoci ted with d i
ly r tings of positive mood.
Psychi try Res. 2004 Nov 30; 129(1):11-9.
[Psychi try Res. 2004]
* Soci l beh viour nd mood in everyd y life: the effects of tryptoph n in q
u rrelsome individu ls.
J Psychi try Neurosci. 2006 Jul; 31(4):253-62.
[J Psychi try Neurosci. 2006]
* Low centr l nervous system serotonergic responsivity is ssoci ted with th
e met bolic syndrome nd physic l in ctivity.
J Clin Endocrinol Met b. 2004 J n; 89(1):266-71.
[J Clin Endocrinol Met b. 2004]
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* Incre sed dop mine tone during medit tion-induced ch nge of consciousness.
Br in Res Cogn Br in Res. 2002 Apr; 13(2):255-9.
[Br in Res Cogn Br in Res. 2002]
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* The effic cy of light ther py in the tre tment of mood disorders: review
nd met - n lysis of the evidence.
Am J Psychi try. 2005 Apr; 162(4):656-62.
[Am J Psychi try. 2005]
* A controlled study of light ther py in women with l te lute l ph se dyspho
ric disorder.
Psychi try Res. 1999 Jun 30; 86(3):185-92.
[Psychi try Res. 1999]
* R ndomized clinic l tri l of bright light ther py for ntep rtum depressio
n: prelimin ry findings.
J Clin Psychi try. 2004 M r; 65(3):421-5.
[J Clin Psychi try. 2004]
* ReviewSe son l nd circ di n mono mine v ri tions in hum n br ins ex mined
post mortem.
Act Psychi tr Sc nd Suppl. 1980; 280():75-85.
[Act Psychi tr Sc nd Suppl. 1980]
* Effect of sunlight nd se son on serotonin turnover in the br in.
L ncet. 2002 Dec 7; 360(9348):1840-2.
[L ncet. 2002]
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* Austri n wom n sues doctor nd hospit l for sterilising her without consen
t.
BMJ. 2005 Nov 19; 331(7526):1162.
[BMJ. 2005]
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* ReviewEffects of physic l exercise on nxiety, depression, nd sensitivity
to stress: unifying theory.
Clin Psychol Rev. 2001 Feb; 21(1):33-61.
[Clin Psychol Rev. 2001]
* TREAD: TRe tment with Exercise Augment tion for Depression: study r tion l
e nd design.
Clin Tri ls. 2006; 3(3):291-305.
[Clin Tri ls. 2006]
See more rticles cited in this p r gr ph
* ReviewSimul ted beh vior st tes: n ppro ch to specificity in psychobiolo
gic l rese rch.
Biol Psychi try. 1973 Dec; 7(3):237-54.
[Biol Psychi try. 1973]
* Effects of conditioned running on pl sm , liver nd br in tryptoph n nd o
n br in 5-hydroxytrypt mine met bolism of the r t.
Br J Ph rm col. 1985 Sep; 86(1):33-41.
[Br J Ph rm col. 1985]
* In vivo me surement of extr cellul r serotonin in the ventr l hippoc mpus
during tre dmill running.
Beh v Ph rm col. 1996 J n; 7(1):101-104.
[Beh v Ph rm col. 1996]
* Site-dependent effects of n cute intensive exercise on extr cellul r 5-H
T nd 5-HIAA levels in r t br in.
Neurosci Lett. 2001 M r 30; 301(2):143-6.
[Neurosci Lett. 2001]
* ReviewActivity of serotonergic neurons in beh ving nim ls.
Neuropsychoph rm cology. 1999 Aug; 21(2 Suppl):9S-15S.
[Neuropsychoph rm cology. 1999]
See more rticles cited in this p r gr ph
* ReviewSerotonin nd centr l nervous system f tigue: nutrition l consider t
ions.
Am J Clin Nutr. 2000 Aug; 72(2 Suppl):573S-8S.
[Am J Clin Nutr. 2000]
* ReviewAmino cids nd centr l f tigue.
Amino Acids. 2001; 20(1):25-34.
[Amino Acids. 2001]
* ReviewBlood-br in b rrier tr nsport of nutrients.
Nutr Rev. 1986 M y; 44 Suppl():15-25.
[Nutr Rev. 1986]
See more rticles cited in this p r gr ph
* ReviewRising r tes of depression in tod y's society: consider tion of the
roles of effort-b sed rew rds nd enh nced resilience in d y-to-d y functioning.
Neurosci Biobeh v Rev. 2006; 30(4):497-510.
[Neurosci Biobeh v Rev. 2006]
See more rticles cited in this p r gr ph
* Effect of tryptoph n dministr tion on tryptoph n, 5-hydroxyindole cetic
cid nd indole cetic cid in hum n lumb r nd cistern l cerebrospin l fluid.
J Neurol Neurosurg Psychi try. 1981 Apr; 44(4):323-8.
[J Neurol Neurosurg Psychi try. 1981]
* The tre tment of depression in gener l pr ctice: comp rison of L-tryptop
h n, mitriptyline, nd combin tion of L-tryptoph n nd mitriptyline with pl
cebo.
Psychol Med. 1982 Nov; 12(4):741-51.
[Psychol Med. 1982]
* Soci l beh viour nd mood in everyd y life: the effects of tryptoph n in q
u rrelsome individu ls.
J Psychi try Neurosci. 2006 Jul; 31(4):253-62.
[J Psychi try Neurosci. 2006]
* Precursor control of neurotr nsmitter synthesis.
Ph rm col Rev. 1980 Dec; 32(4):315-35.
[Ph rm col Rev. 1980]
See more rticles cited in this p r gr ph
* Diet rich in lph -l ct lbumin improves memory in unmedic ted recovered de
pressed p tients nd m tched controls.
J Psychoph rm col. 2006 Jul; 20(4):526-35.
[J Psychoph rm col. 2006]
* Whey protein rich in lph -l ct lbumin incre ses the r tio of pl sm trypt
oph n to the sum of the other l rge neutr l mino cids nd improves cognitive p
erform nce in stress-vulner ble subjects.
Am J Clin Nutr. 2002 Jun; 75(6):1051-6.
[Am J Clin Nutr. 2002]
* Tr dition l m ize processing techniques in the new world.
Science. 1974 M y 17; 184(4138):765-73.
[Science. 1974]
* The breeder's dilemm --yield or nutrition?
N t Biotechnol. 2006 Sep; 24(9):1078-80.
[N t Biotechnol. 2006]
* Diet ry tryptoph n int ke nd suicide r te in industri lized n tions.
J Affect Disord. 2007 M r; 98(3):259-62.
[J Affect Disord. 2007]
See more rticles cited in this p r gr ph
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Hostility s predictor of surviv l in p tients with coron ry rtery dise se.
Psychosom Med. 2004 Sep-Oct; 66(5):629-32.

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