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Chapter 4 Serotonin, Emotional Buffering and Light
What tryptophan depletion tells us
Serotonin (5-hydroxytryptamine) is made from the essential amino acid tryptophan. Researchers cannot measure serotonin directly in a living human brain, so they often lower it temporarily with an experimental method: acute tryptophan depletion. In the laboratory, participants drink a mixture containing large amounts of other amino acids but no tryptophan; within hours blood tryptophan falls sharply and the brain has less raw material for serotonin. A control group drinks a balanced mixture containing tryptophan.
Evidence
Cools, Roberts and Robbins reviewed such studies: lowering serotonin changes the processing of punishment and negative information, affects some forms of impulse control, and does so more clearly in people who are already vulnerable. They proposed that serotonin helps regulate emotional and behavioural control, especially processes related to aversive predictions, rather than simply corresponding to good or bad mood (Cools et al. 2008).
Evidence
In an ultimatum game, Crockett and colleagues found that after tryptophan depletion participants rejected more unfair offers, while their judgements of how fair the offers were, and their mood, did not change (Crockett et al. 2008).
These experiments show that serotonin is involved in responses to unfavourable signals: with lowered serotonin, people respond more readily to unfairness with punishment. They do not show that more serotonin is always better, nor that everyday low mood is caused by too little serotonin.
Note
Corrected on checking. The popular claim that depression is caused by a lack of serotonin lacks consistent evidence. A systematic umbrella review by Moncrieff and colleagues examined research on serotonin and its metabolites, receptors, the serotonin transporter, tryptophan depletion and genetics, and concluded that there is no consistent evidence that depression is caused by lowered serotonin activity (Moncrieff et al. 2023). The review has itself been criticised by some psychiatrists, but it is a reminder not to equate a neurotransmitter with a mood. Whether antidepressants work is a separate question that this book does not address; please consult a doctor about any medication. Tryptophan depletion is an experimental procedure carried out with ethical approval and medical supervision, not something to try on oneself.
There is one direct human measurement linking light and serotonin.
Evidence
Lambert and colleagues sampled blood from the internal jugular vein of healthy men and measured a serotonin metabolite to estimate the turnover of serotonin in the brain. Turnover was lowest in winter and correlated positively with the hours of bright sunlight on the day of measurement (Lambert et al. 2002).
Another kind of light-sensitive cell in the eye
Besides the rods and cones used for vision, the retina contains a small population of intrinsically photosensitive retinal ganglion cells (ipRGCs). They contain melanopsin, are most sensitive to blue-green light, respond slowly and persistently, and project mainly to the suprachiasmatic nucleus of the hypothalamus, the master circadian clock.
Evidence
Berson, Dunn and Takao showed in rats that retinal ganglion cells projecting to the suprachiasmatic nucleus are themselves light-sensitive, even when their synaptic input from rods and cones is blocked (Berson et al. 2002).
The intrinsic period of the human circadian clock averages about 24.2 hours, slightly longer than a day (Czeisler et al. 1999). Without correction by light, the clock would drift a little later each day. Light acts differently at different times:
Evidence
Khalsa and colleagues gave single 6.7-hour pulses of bright light at different biological times and measured the human phase response curve: light before the minimum of core body temperature shifts the clock later (a delay), and light after it shifts the clock earlier (an advance) (Khalsa et al. 2003). Zeitzer and colleagues found that the resetting of the clock and the suppression of melatonin by night-time light reach half their maximum at about 100 lux and approach saturation at about 550 lux (Zeitzer et al. 2000). Gooley and colleagues found that ordinary room light (about 200 lux) before bedtime, compared with dim light, delayed the onset of melatonin and shortened its duration (Gooley et al. 2011).
Evidence
Wright and colleagues had participants camp outdoors for a week in summer, exposed only to natural light and no electric light. After camping, the time at which their melatonin began to rise was on average about two hours earlier, closer to sunset (Wright et al. 2013).
A phase model
Calculation
A simplified phase model of the human circadian clock. The state is the clock time of the core-body-temperature minimum (CBTmin); the intrinsic period is 24.2 hours; light before CBTmin delays the clock and light after it advances the clock (a sinusoidal phase response curve); the effect of light saturates with illuminance (half-saturation about 100 lux). Four daily light plans are compared after 90 days, and the evening dim-light melatonin onset (DLMO) is estimated as about 7 hours before CBTmin.
# A simplified phase model of the human circadian clock under daily light (cross-disciplinary
# simplification; real models such as Kronauer's are limit-cycle oscillators).
# State: clock time of the core-body-temperature minimum (CBTmin). Intrinsic period 24.2 h
# (Czeisler et al. 1999), so without light the clock drifts 0.2 h later each day.
# Light shortly before CBTmin delays the clock, light shortly after advances it (Khalsa et al. 2003);
# the response saturates with illuminance (half-maximal near 100 lux, Zeitzer et al. 2000).
import math
TAU = 24.2
def prc(hours_after_cbtmin):
x = (hours_after_cbtmin + 12) % 24 - 12 # wrap to -12..+12 h
return 0.6 * math.sin(math.pi * x / 12) # h of advance (+) per hour of saturating light
def drive(lux):
return lux / (lux + 100.0)
def settle(schedule, days=90):
"""schedule: list of (start hour, end hour, lux) of light at the eye, repeated daily."""
cbt = 4.0 # start: CBTmin at 04:00
for _ in range(days):
shift = 0.0
for start, end, lux in schedule:
h = start
while h < end:
shift += 0.25 * drive(lux) * prc(h + 0.125 - cbt)
h += 0.25
cbt = (cbt + (TAU - 24) - shift) % 24 # advance moves CBTmin earlier
return cbt
def clock(h):
h %= 24
return f"{int(h):02d}:{int(round(60 * (h % 1))) % 60:02d}"
indoor = [(7, 23, 150)]
plans = {
"indoor light only, 07:00-23:00 at 150 lux": indoor,
"plus 30 min outdoors after waking (10,000 lux)": [(7, 7.5, 10000), (7.5, 23, 150)],
"plus bright room 21:00-24:00 (500 lux)": [(7, 21, 150), (21, 24, 500)],
"both: morning outdoors, dim evening (20 lux)": [(7, 7.5, 10000), (7.5, 21, 150), (21, 23, 20)],
}
print("light plan CBTmin estimated DLMO (CBTmin - 7 h)")
for name, sched in plans.items():
c = settle(sched)
print(f"{name:46s} {clock(c)} {clock(c - 7)}")
# light plan CBTmin estimated DLMO (CBTmin - 7 h)
# indoor light only, 07:00-23:00 at 150 lux 03:19 20:19
# plus 30 min outdoors after waking (10,000 lux) 03:09 20:09
# plus bright room 21:00-24:00 (500 lux) 04:35 21:35
# both: morning outdoors, dim evening (20 lux) 02:23 19:23In this model, adding 30 minutes of outdoor morning light alone advances the clock by only about 10 minutes, because a full day of indoor light already supplies much of the “daytime” signal; three hours of bright indoor light in the evening delays the clock by more than an hour; and outdoor morning light together with dark evenings advances it by about an hour. This agrees in direction with Wright’s camping study: what matters is not only more light in the morning but also less light at night. The model’s numbers should not be taken as predictions: the real phase response curve is not a sine wave, and people differ widely.
Note
Morning outdoor light does not mean looking at the sun: being outdoors, looking naturally around at the sky and ground, is enough. Outdoor illuminance on an overcast day is usually still more than ten times that indoors. Never look directly at the sun. People with eye disease, those taking photosensitising medicines and those with bipolar disorder should consult a doctor before deliberately increasing their light exposure. This book does not discuss melatonin supplements and gives no doses.
Hypothesis · not established
Not established. In adults who go to bed late, spending at least 20 minutes outdoors within an hour of getting up and dimming indoor lighting to below 30 lux in the two hours before bed, every day for two weeks, will advance the onset of salivary melatonin by at least 30 minutes. If, in a randomised trial, the upper limit of the 95 % confidence interval for the difference in DLMO change between intervention and control groups is below 30 minutes, the hypothesis is refuted.
Summary
Serotonin helps regulate responses to negative signals, but “serotonin = calm” and “low serotonin = depression” are both too simple. Light is one of the few inputs a person can change at will: through ipRGCs it corrects the phase of the circadian clock, and in one human measurement brain serotonin turnover was higher on sunny days. The next chapter turns to a system that can be moved even more directly by intention: breathing and heart rate.
References
Fan, Y. (2026). Dynamical Systems of Neurotransmitters and Endocrinology: Dopamine Reward Prediction Error, Serotonergic Homeostasis, HPA-Axis Allostatic Load and the Challenge Hypothesis, Read Beside East Asian Classics of Mind Regulation [神经递质与内分泌的动力系统] (Version 1.0.0). 5D Library. https://doi.org/10.5281/zenodo.23738782 · Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0).