Source:
NIH / National Institute Of Mental Health
Date:
2004-08-04
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Depression Traced To Overactive Brain Circuit
A brain imaging study by the NIH's National Institute of Mental Health
(NIMH) has found that an emotion-regulating brain circuit is overactive
in people prone to depression even when they are not depressed.
Researchers discovered the abnormality in brains of those whose
depressions relapsed when a key brain chemical messenger was
experimentally reduced. Even when in remission, most subjects with a
history of mood disorder experienced a temporary recurrence of symptoms
when their brains were experimentally sapped of tryptophan, the chemical
precursor of serotonin, the neurotransmitter that is boosted by
antidepressants.
Areas that show over-activity following tryptophan depletion in
depression patients in remission and thought to reflect a trait
dysfunction include emotion regulating circuitry involving the anterior
cingulate, thalamus, ventral striatum and orbitofrontal cortex. (Source:
NIMH Mood and Anxiety Disorders Program 2004)
Neither a placebo procedure in patients nor tryptophan depletion in
healthy volunteers triggered the mood and brain activity changes. Brain
scans revealed that a key emotion-processing circuit was overactive only
in patients in remission whether or not they had re-experienced
symptoms and not in controls. Since the abnormal activity did not
reflect mood state, the finding suggests that tryptophan depletion
unmasks an inborn trait associated with depression.
Alexander Neumeister, M.D., Dennis Charney, M.D., Wayne Drevets, M.D.,
NIMH Mood and Anxiety Disorders Program, and colleagues, report on their
positron emission tomography (PET) scan study in the August 2004
Archives of General Psychiatry.
The NIMH researchers and others had previously shown that omitting
tryptophan from a cocktail of several other essential amino acids washes
out the precursor chemical from the blood and brain, depleting serotonin
and often triggering symptoms in people with a history of depression
and even in healthy people from depression-prone families. This added to
evidence that a genetic predisposition that renders some people
vulnerable to inadequate serotonin activity may be at the root of the
mood disorder.
The researchers scanned subjects after their blood tryptophan levels
were reduced by about three-fourths, using a radioactive tracer (a form
of glucose, the brain's fuel) which reveals where the brain is active
during a particular experimental condition.
They randomly gave 27 unmedicated depressed patients-in-remission and 19
controls either pills containing seven essential amino acids, such as
lysine and valine, or identical-looking placebo pills. Subjects received
either the active pills or placebos in repeated trials over several days
in a blind, crossover design.
Sixteen (59 percent) of the patients experienced a transient return of
symptoms under tryptophan depletion; their mood lifted to normal by the
next day. Compared to controls, the patients showed increased brain
activity in a circuit coursing through the front and center of the brain
(orbitofrontal cortex, thalamus, anterior cingulate, and ventral
striatum) areas involved in regulating emotions and motivation that
have been implicated in previous studies of depression. Whereas previous
studies interpreted the circuit activation as a transient,
mood-dependent phenomenon, the new evidence suggests that circuit
over-activation is likely an underlying vulnerability trait, say the
researchers.
Because of its ability to unmask what appears to be a trait marker for
major depressive disorder, the researchers suggest that tryptophan
depletion may be a useful tool for studying the genetic basis of
depression.
"Since brain function appears to be disregulated even when patients are
in remission, they need to continue long-term treatment beyond the
symptomatic phase of their illness," noted Neumeister, who recently
moved to the Yale University psychiatry department.
Also participating in the research were: Drs. Allison Nugent, Tracy
Waldeck, Omer Bonne, Earl Bain and Marilla Geraci, David Luckenbaugh,
NIMH; Dr. Markus Schwarz, Munich University Hospital of Psychiatry, Dr.
Peter Herscovitch, NIH Clinical Center PET Department.
NIMH is part of the National Institutes of Health (NIH), the Federal
Government's primary agency for biomedical and behavioral research. NIH
is a component of the U.S. Department of Health and Human Services.
Editor's Note: The original news release can be found here.
------------------------------------------------------------------------
This story has been adapted from a news release issued by NIH / National
Institute Of Mental Health.
Tryptophan(Trp)is also important for sleep. Reduced sleep is a
problem for many on CR (either as reduced number of hours of sleep or
a broken sleep). Reduced sleep in itself might be a cause for
depression. Here is a new study [1] suggesting that in CR'ed rats
alpha lactoalbumin improved sleep.
Searching the net, I found that BiPro whey (I have no affiliation with
Daviscofoods) has the highest amount of Trp [2,3] of all whey
products. BiPro is whey protein isolate produced by the preferred
process of ion exchange.
Any comment? Any experience with the product/similar ones would be
appreciated.
TIA
1. Behav Brain Res. 2004 Jul 9;152(2):335-40. Related Articles,
Links
A tryptophan-rich protein diet efficiently restores sleep after food
deprivation in the rat.
Minet-Ringuet J, Le Ruyet PM, Tome D, Even PC.
UMR INRA/INA P-G, UMR physiologie de la nutrition et du comportement
alimentaire, Institut National Agronomique Paris-Grignon, 16 rue
Claude Bernard, 75231 Paris Cedex 05, France.
Sleep depends on the quantity and quality of the diet. Several studies
have shown that food deprivation results in a reduction in sleep
duration. It has also been demonstrated that in the newborn, the
supply of certain essential amino acids improves sleep through their
action on the synthesis of specific neurotransmitters. The aim of the
present study was to test if the quantity and/or quality of dietary
protein could improve the recovery of sleep during re-feeding after
caloric deprivation. Sleep parameters were compared in rats fed ad
libitum, food restricted during 4 days, or reefed isocalorically after
food restriction with three dietary regimens varying in terms of the
amount (14% versus 30%) or quality (milk protein or alpha-lactalbumin)
of protein. The results showed that sleep recovery, in particular
slow-wave sleep, was improved in rats re-fed with alpha-lactalbumin.
This result confirms the close relationship between feeding and sleep
and suggest that alpha-lactabumin could be used to improve sleep in
adult submitted to nutritional disturbances such as food restriction,
shift work, Ramadan. Copyright 2003 Elsevier B.V.
PMID: 15196801 [PubMed - in process]
2. http://www.daviscofoods.com/BiPRO/
3. http://www.findarticles.com/p/articles/mi_m3289/is_3_169/ai_61759509
For your pet, Bios (biochemicals.com) has pharmaceutical grade
tryptophan in capsules and powder.
"Arbor" <soowhat...@hotmail.com> wrote in message
news:9ffdc316.04090...@posting.google.com...