Causes
Treatments/prevention
Mental
illness: caused in the brain, by neurotransmitters and
serotonin.
Mental
disorders: caused by a trauma (mostly during
childhood), not able to handle in a healty way, emotional growth stops at the
age of the trauma.
Future: treatments/prevention
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Food (diets)
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(Brainresearch)
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Vitamins
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(Technology)
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Exercise
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Light/color
Future: The perfect diet.
Superfood, raw food
What do the … /vitamins/minerals do with us?
Neurotransmitter
Transmittertreatments
Planning, afbeeldingen, idea’s, visuals,
Prevention by transmitters
Moodfood
monoamine neurotransmitter
dopamine, noradrenaline, adrenaline and serotonin
Monoamines are neurotransmitters and neuromodulators that include serotonin, dopamine, norepinephrine, and epinephrine.
Norepinephrine may be
related to alertness and energy as well as anxiety, attention, and interest in
life; [lack of] serotonin to anxiety, obsessions, and compulsions; and dopamine
to attention, motivation, pleasure, and reward, as well as interest in life.
Many variations of the
monoamine hypothesis involve the neurotransmitter serotonin, regulated by the serotonin
transporter, which assists the
modulation of feelings and behavior such as anxiety, anger, appetite, sexuality, sleep, mood, etc. People with depression may have
differences in serotonin transporter gene length.[33] People with both alleles that are long are less
likely to become depressed, while people with one short and one long or two
short alleles are more likely to develop depression.[34]
The functions of
serotonin are difficult to describe in a simple way. In some circumstances
serotonin seems to act as a signal of "repletion" or
"satisfaction". Thus, satiation after eating, and orgasm following
sex, both produce release of serotonin. In animals that have hierarchical
social structures, dominant individuals show higher levels of serotonin
metabolites than lower-status individuals. In the brain, serotonin exerts a
suppressive effect on both the reward
system and punishment system[clarification needed], and therefore is likely to reduce the intensity of
motivation whether aversive or appetitive.[citation needed]
Fructose malabsorption
has been associated with depression in young women. Their mood improved when
their intake of fructose was restricted. The mechanisms of these effects are
not well understood, but may involve low circulating levels of tryptophan, which is the precursor of serotonin.[35] à In fruit, increases the level of tryptophan, which
increases the level of serotonin
Catecholamine
epinephrine: adrenaline, nnorepinephrine: oradrenaline and dopamine
Serotonin is made in
the part of the brain that is called the Raphe Nuclei, a group of small nerve
cell nuclei in the upper brain stem, located directly at the mid-line of the
brain.
There is a powerful
interaction between the Raphe nuclei and the SCN, SCN is the control center for
the body's biological clock. In animal studies, this input has been shown to
modulate the ability of light to reset the timing of the biological clock: the
more serotonin, the stronger the effects of light. On the other hand, the
biological clock exerts a strong influence on the Raphe nuclei: serotonin
levels drop during sleep, and fall almost to nothing during REM (dreaming)
sleep.
The ventral tegmentum (or ventral tegmental area) is a small area in the basal midbrain which
is a critical part of the brain's reward system. It sends projections to the nucleus accumbens that use the neurotransmitter dopamine. Addictive drugs universally increase the effects of
dopamine in this system, whereas drugs that oppose dopamine produce anhedonia of the sort seen in depressed people.
Dopamine-enhancers such as cocaine often relieve the lack-of-pleasure in
depression, but the effects only last as long as a drug is present in the body:
that is, they temporarily alleviate one of the main symptoms, but do not help
to cure the disease. à Dopamine is created in the Ventral Tegmentum, basal
midbrain, critical part of the reward system.
Recent studies have
shown that Brodmann
area 25, also known as Subgenual cingulate is metabolically overactive in treatment-resistant depression.[42] This region is extremely rich in serotonin transporters and is considered as a governor for a vast network
involving areas like hypothalamus and brain
stem, which influences
changes in appetite and sleep; the amygdala and insula, which affect the mood and anxiety; the hippocampus, which plays an important role in memory formation;
and some parts of the frontal
cortex responsible for
self-esteem.[43][44] Thus disturbances in this area or a smaller than
normal size of this area contributes to depression. Deep Brain Stimulations of
this area have been successful in reducing its elevated activity and thus
curing depression in patients that could not be cured by anti-depressants.[45]
The anterior cingulate cortex is activated by negative experiences of many types,
and consistently shows higher levels of activity in depressed people than in
non-depressed people. The functions of the ACC are controversial, but one
proposal is that it mediates the conscious experience of suffering. Several
decades ago, trials were made of ablating parts of the ACC in an attempt to
relieve intolerable pain in patients who were terminally ill. These patients
reported that after the surgery, they could still perceive the physical
sensations of pain, but they no longer found them distressing. (The effects of
heroin and morphine are sometimes described in the same way.) Very recently,
clinical experiments were made in using deep
brain stimulation to
temporarily inactivate the ACC in severely depressed patients. This was not
effective in all cases, but in some patients very striking results were
achieved, with a perceptible lifting of mood immediately apparent to the patient
as soon as the stimulus was applied.
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