The Ortho Molecular Answer
Home | · | About | · | Credentials | · | History | · | FAQ | · | Testimonials | · | Contact |
What's New | · | Podcasts | · | Illnesses | · | Case Studies | · | Articles | · | Resources | · | Supplements |
Depression - Phenylalanine for Endogenous Depression
Phenylalanine for Endogenous
Depression
I. A. Yaryura-Tobias, B. Heller, H. Spatz, and E.
Fischer
Orthomolecular Psychiatry
Vol. 3, Number 2, 1973
I. A. Yaryura-Tobias, B. Heller, H. Spatz, and E.
Fischer
It has been shown that the urinary elimination of phenylethylamine (PEA) is
usually decreased in endogenous depression (Fischer et al., 1968; Fischer et
al., 1972) and the 2-PEA is also present in the human brain (Mosnaim et al.,
1973). PEA is also to antagonize almost completely the reserpine effect in
pretreated rats (Fischer et al., 1972,Mosnaim and Sabelli, 1971). Replacing PEA
by its precursor, phenylalanine, it was observed that the levorotatory form had
little effect in antagonizing rats pretreated with reserpine; a better effect
was observed with the racemic form (d-1) while greatest efficacy was obtained
with d-phenylalanine. These results are in agreement with the increase of PEA in
the rat brain, after the administration of the racemic form, l-form and d-form,
the latter being the best (Mosnaim et al., 1973; Fischer et al., 1973).
Based
upon that information, PEA was administered to patients suffering from
endogenous depression, but severe cephaleas forced us to discontinue the study
(Mosnaim et al., 1973). This preliminary report consisted of 15 patients, eight
females and seven males, with ages ranging from 36 to 72 (x= 50.66), onset of
illness ranging from 2 to 45 years (x= 16.73), and the duration of the last
period of depression ranging from six days to 520 days (x= 130.40). Target
symptoms were early morning depression, with later evening improvement,
anorexia, irregular sleep, suicidal ideation or attempt, lack of drive, feeling
of hopelessness and helplessness. The intensity was rather severe in most cases.
Patients were divided in two groups - Group A (Dr. Yaryura-Tobias' patients) (N
= 6) received d-I phenylalanine in 100 mg capsules b.i.d., and Group B (Dr.
Heller's patients) (N = 9) received d-phenylalanine in 100 mg capsules b.i.d.
Before treatment, PEA levels in urine were measured in six patients of Group A
and found to be low in five cases (x= 34_/24 hours) and normal in a psychotic
patient with depression (209 _/24 hours). Duration of treatment was two weeks.
Improvement, if any, was usually reported and observed within the first five
days of treatment. In Group A, three cases improved out of six, and in Group B,
seven cases improved out of nine.
In the positive cases, no further
medication was needed. In those who required additional therapy, it seemed that
phenylalanine (d or d-l form) enhanced the clinical action of tricyclic
antidepressants. Although the experimental trial was very short in duration and
the amount of drug given was small, it seems that some form of endogenous
depression responded well to phenylalanine therapy, mainly with the
dextrorotatory form. The psychotic patient with depression worsened his
psychosis. In three cases, mild cephalea was reported. No toxic effects were
observed.
It is postulated that the better response obtained by the use
of d-phenylalanine over d-l phenylalanine is due to higher specificity of the
hydroxylase that converts the I form into dihydroxyphenylalanine where
d-phenylalanine would follow only the phenylethylamine
pathway.