Abstract
Depression is characterized by sadness, purposelessness, irritability, and impaired body functions.
Depression causes severe symptoms for several weeks, and dysthymia, which may cause chronic, low-grade symptoms. Treatment of
depression involves psychotherapy, medications, or phototherapy. Clinical and experimental evidence indicates that an appropriate
diet can reduce symptoms of
depression.
The neurotransmitter, serotonin (5-HT), synthesized in the brain, plays
an important role in mood alleviation, satiety, and sleep regulation.
Although certain fruits and vegetables are rich in 5-HT, it is not
easily accessible to the CNS due to blood brain barrier. However the
serotonin precursor, tryptophan, can readily pass through the blood
brain barrier. Tryptophan is converted to 5-HT by tryptophan hydroxylase
and 5-HTP decarboxylase, respectively, in the presence of pyridoxal
phosphate, derived from vitamin B(6). Hence diets poor in tryptophan may
induce
depression as this essential amino acid is not naturally abundant even in protein-rich foods. Tryptophan-rich
diet is important in patients susceptible to
depression such as certain females during pre and postmenstrual phase, post-traumatic stress
disorder,
chronic pain, cancer, epilepsy, Parkinson's disease, Alzheimer's
disease, schizophrenia, and drug addiction. Carbohydrate-rich
diet
triggers insulin response to enhance the bioavailability of tryptophan
in the CNS which is responsible for increased craving of carbohydrate
diets. Although serotonin reuptake inhibitors (SSRIs) are prescribed to
obese patients with
depressive
symptoms, these agents are incapable of precisely regulating the CNS
serotonin and may cause life-threatening adverse effects in the presence
of monoamine oxidase inhibitors. However, CNS serotonin synthesis can
be controlled by proper intake of tryptophan-rich
diet. This report highlights the clinical significance of tryptophan-rich
diet and vitamin B(6) to boost
serotonergic neurotransmission in
depression observed in various neurodegenerative diseases. However pharmacological interventions to modulate
serotonergic neurotransmission in
depression, remains clinically significant.
Depression may involve several other molecular mechanisms as discussed briefly in this report.
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