Depression for
Health Care Professionals
Perspective
The “monoamine theory”
of depression states that increased
synaptic levels of monoamines can
improve depression symptoms and has been
a cornerstone of medicine for almost 30
years. The monoamines include serotonin,
dopamine, norepinephrine, and
epinephrine. In general, two types of
depression have been recognized in the
treatment of patients for
many years:
-
Exogenous depression
-
Endogenous depression
Exogenous depression is a term used to
describe depression triggered by
external sources – i.e. social losses
and problems.
Endogenous
depression
is a term used to describe depression
that is more likely inherited and
chemical in nature. Hence, it can happen
for no apparent reason.
In caring for
thousands of patients, it has become
apparent that grouping depressed
patients into two groups is not
adequate. Patients who present with
depression should be classified into one
of four groups:
-
Exogenous depression
-
Limited endogenous
depression,
(where the duration of symptoms is
less than six months).
-
Chronic endogenous
depression,
(where the duration of symptoms is
greater than six months).
-
Depressive bipolar
disorder.
The implications for treatment of each of these
four depression categories will be
discussed, as well as why long-term
management of each category differs
significantly.
Depression for
Health Care Professionals: DEPRESSION
DIAGNOSTIC CRITERIA
DSM-IV, the diagnostic
manual from American Psychiatric
Association, criteria
The episode of depression
has lasted at least two weeks with at
least five of the following 9 symptoms
present:
-
1.
Feeling depressed, sad,
blue, or tearful.
-
2.
Loss of interest or
pleasure in things previously enjoyed.
-
3.
Appetite is much less or
much greater than usual with weight loss
or gain.
-
4.
Trouble sleeping or
sleeping too much.
-
5.
Others notice agitation,
restlessness, or slowing down.
-
6.
Chronically tired and
have no energy.
-
7.
Feelings of worthlessness
or excessive guilt about things done or
not done.
-
8.
Trouble concentrating,
thinking clearly, or making decisions.
-
9.
Suicidal thoughts.
Depression for
Health Care Professionals:
DRUGS DEPLETE
NEUROTRANSMITTERS
Antidepressant drugs
do not increase the number of
neurotransmitter molecules in the
central nervous system (brain). They
work by moving neurotransmitter
molecules from one place to another. In
the process, neurotransmitter molecules
are exposed to enzymes that break them
down at a more frequent rate, which
leads to depletion of neurotransmitters
with long-term use of antidepressant
drugs.
Monoamine
neurotransmitters do not cross the blood
brain barrier. The only way to increase
CNS neurotransmitter levels and to
prevent neurotransmitter depletion when
using antidepressant drugs is to provide
proper amounts of amino acid precursors.
The precursors are able to cross the
blood brain barrier, which allows them
to be synthesized into new
neurotransmitters.
Drugs that work with
neurotransmitters, such as
antidepressants, are ineffective if
there are not enough neurotransmitters.
When anti-depressant drugs deplete
neurotransmitter levels, the drugs
appear to quit working and the patient’s
symptoms return.
Depression for
Health Care Professionals:
DEPRESSION TREATMENT PROTOCOL
Baseline neurotransmitter testing is of
no value in treatment of depression
those that have attempted to use
baseline testing philosophy (which is
not supported by science) have
established that very few patient
achieve relief of depression symptoms.
The NeuroResearch Clinics treatment
protocol through data base statistical
analysis has established three dosing
levels of 5-HTP, tyrosine, and cysteine
with cofactors for treatment of
depression. The patient is simply
started on level 1 nutrient dosing then
if there is no response in one week the
patient is increased to level 2 dosing.
After one week on level 2 dosing if the
symptoms of depression have not resolved
the patient with depression is increased
to level 3 dosing. If there is no
response on level 3 dosing urinary
neurotransmitter testing should obtained and
the nutrient dosing is adjusted as
guided by neurotransmitter testing until
the symptoms of depression have resolved
or the urinary serotonin and dopamine
are in the phase 3 therapeutic range.
Approximately 80% of patients can
achieve complete relief of symptoms
without the need for urinary
neurotransmitter testing of serotonin
and dopamine.
Depression for
Health Care Professionals: DEPRESSION
TREATMENT CONSIDERATIONS
Ø
If the patient is taking
antidepressant medications at the start
of amino acid therapy, continue the
medications until the patient’s symptoms
are under control. At that point, if
desired, you can slowly decrease the
antidepressant daily dosing. Most
patients are eventually able to
completely cease taking their
antidepressant medications.
Ø Patients
taking antidepressants without amino
acid supplementation, who report the
medication has quit working (as evident
by the return of their symptoms) should
start the level 1 amino acid dosing
along with the antidepressant. In most
patients, if this is done within the
first 2 to 4 weeks after the drug quits
working, amino acid therapy will
typically provide relief of symptoms
within a day or two.
Ø Properly
used amino acids allow drugs that work
with neurotransmitters to function
optimally; it can also bring out the
side effects of the drugs. This can be
confusing to the caregiver. If a
patient is taking an antidepressant and
experiences an unusual side effect a few
days after starting amino acid therapy,
there is a tendency to blame the amino
acids for the side effects. In most
cases, the side effect is actually due
to the prescription drug. As amino acid
therapy increases the number of
neurotransmitters available, the
prescription drugs begin to function. As
the function of the prescription drug
improves, the possibility of a
prescription drug side effect occurring
increases. Therefore, side effects
typically need to be managed as a
prescription drug side effect. We have
developed an in-depth side effect
profile of amino acids. If your patient
is taking prescription drugs with amino
acids and develops an unusual side
effect, call us because we can help
identify the problem.
Ø
Patients need to be seen
weekly (every 7 days) until relief of
symptoms is obtained.
Ø
It takes 3 to 5 days for
the full effect of starting or changing
an amino acid dose to occur. When your
patient returns, ask about the previous
day, rather than the entire week. It is
more indicative of changes that have
occurred in the system.
Ø
If during treatment the
patient’s depression becomes worse, this
is a “paradoxical reaction.” It
indicates a need to increase the amino
acid dosing to the next level.
Depression is one of the diseases that
stands out as displaying a paradoxical
reaction in patients. Increasing the
amino acid dosing will lead to relief of
the paradoxical reaction in 1 or 2 days.
Ø
Obtain a urinary
neurotransmitter test if the patient
does not responded to the level 3 dosing
after one week. Testing should continue
until serotonin and dopamine levels are
in the phase 3 therapeutic response or
until symptoms resolve.
Since 2005, we
have researched and monitored depression
results. We have observed that when
dosing protocols are properly followed,
virtually 100% of patients experience
relief of their depression symptoms.
THE FOUR TYPES OF DEPRESSION
Depression for
Health Care Professionals:
DEPRESSIVE BIPOLAR
DISORDER
A patient presents in
clinic with symptoms that allow you to
diagnose depression under the DSM IV
guidelines. There is no history of manic
or hypomanic episodes and treatment is
started.
You have taken the
patient to the level 3 amino acid dosing
and there is still no relief of
symptoms. Then, you obtain a urinary
neurotransmitter test and follow the
recommendations for the amino acid
dosing changes until serotonin and
dopamine levels are in the phase 3
therapeutic range, but still there is no
relief of symptoms.
In 98% of patients,
relief of symptoms will occur either
before or once serotonin and dopamine
levels are in the phase 3 therapeutic
range. The remaining 2% of patients will
continue to suffer from symptoms of
depression. This leads to the question,
what is occurring in the remaining 2% of
patients who have not obtained relief?
The answer is that they are suffering
from depressive bipolar disorder.
Typically, to make the diagnosis, you
need to have a manic or hypomanic
episode in the past. However, with these
patients, the manic cycling may be very
infrequent and may have gone unnoticed.
For example, the patient may have had a
hypomanic episode for two weeks, four
years ago. Such cycling is difficult to
pick up on.
Once the depressed
patient’s urinary serotonin and dopamine
levels are in the therapeutic range and
the phase 3 response with no relief of
symptoms, you will need to continue
amino acid therapy and start a mood
stabilizing drug (possibilities include
- Lithium 300 mg twice a day, Depakote
500 mg twice a day or Lamictil 100 mg
per day).
Most depressive bipolar
patients only find complete relief of
symptoms with balanced amino acids and
the starting dose of one of the above
mood stabilizing drugs. In the past 5
years, there have only been 3 patients
that continued to experience depression
after starting a mood stabilizing drug
while continuing amino acid therapy. In
these 3 patients, they needed to have
their amino acid dosing left in place
and the mood stabilizing drug adjusted
to higher levels (just as occurs in any
bipolar patient not responding to
treatment).
The
diagnosis of depressive bipolar is
clearly evident and easy to make when
the patient is using balanced serotonin
and dopamine amino acid precursors (as
indicated by the phase 3 therapeutic
response) with no relief of symptoms.
The typical depressive
bipolar patient identified through this
method has the following history prior
to amino acid therapy and a bipolar mood
stabilizing drug:
Ø
Many years with a history
of depression, it is not unusual to have
a history of 30 to 40 years of
depression.
Ø
Has seen many doctors
looking for relief of symptoms.
Ø
Has been on almost every
antidepressant drug known.
Ø
May be taking multiple
antidepressants when initially seen.
Virtually all of these
patients are on antidepressant
medication when they seek treatment.
Once their symptoms are under control,
which usually occurs one week after
starting a bipolar mood stabilizing
drug, they may be on a significant
number of pills each day. Many patients,
even though they do not need all of
their prescription drugs, do not want to
give up any of their pills because it is
the first time in their life that they
have been symptom-free. For these
patients, I simply leave them on the
prescription drugs with the amino acids
and wait about three months. After three
months of doing well, I usually suggest
making a small cut back on the dose of
one of their antidepressants.
The patient with
depressive bipolar disorder will need
amino acids and mood stabilizing drugs
for the rest of his or her life.
Depression for
Health Care Professionals:
EXOGENOUS AND LIMITED
ENDOGENOUS DEPRESSION
The difference
between these two types of depressions
is with limited endogenous, you cannot
identify a social stress that has
precipitated the depression. In general,
if managed properly, both are short in
duration. Proper management of both
hinges on two things:
Ø
Use of amino acids to
gain control of symptoms.
Ø
Use of psychotherapy to
help the patient cope more effectively
with the situation.
Depression for
Health Care Professionals:
CHRONIC ENDOGENOUS
DEPRESSION
PERMANENT DAMAGE!
Chronic endogenous
depression is the most common form of
depression seen in clinics. Under the
treatment guidelines on page two, all of
these patients can obtain full relief of
symptoms. In these patients, previous
attempts to remove prescription drugs
(without amino acid therapy) or the
decision to no longer use amino acid
therapy fails repeatedly and depression
symptoms return or worsen.
As to why they need
long-term treatment, we look to the
disease of Parkinsonism as a model for
explanation. Parkinsonism is caused by
permanent damage to the dopamine
neurons, which make up the neuron
bundles of the substantia nigra. These
dopamine neuron bundles regulate fine
motor control and when they can’t
conduct electrical impulses required for
proper motor control, the classic
Parkinson pill rolling tremors start.
Like the rest of the
neurotransmitters, dopamine does not
cross the blood brain barrier. You don’t
need to look to basic science for
confirmation of this fact; the
confirmation is sitting in the practice
of medicine. In the emergency room, when
a Parkinson’s patient arrives in shock,
a dopamine drip is started. The shock
responds to the treatment, but the
Parkinson symptoms do not improve
because dopamine does not cross the
blood brain barrier.
In order to get
Parkinson’s symptoms under control, it
is necessary to give L-dopa. L-dopa is a
dopamine precursor that is able to cross
the blood brain barrier and is
synthesized without regulation into
dopamine.
By using levodopa, you
can literally create dopamine levels in
the system as high as you want since
there is no regulation of the synthesis
of dopamine from L-dopa.
I firmly believe that
chronic endogenous depression, like
Parkinsonism, is the result of damage to
the neuron bundles that regulate and
prevent depression. When enough neurons
bundles are damaged, the result is
chronic depression.
Depression for
Health Care Professionals:
LOW VERSUS NOT HIGH
ENOUGH
The common wisdom is
that low levels of neurotransmitters
cause disease. But, after testing
thousands of patients, it is apparent
that there are no significant
differences between the starting labs of
healthy patients and patients with
depression. It would appear that like
Parkinson’s patients, patients with
depression need increased
neurotransmitter levels to stimulate the
remaining viable neurons. This increased
stimulation results in an increase in
electrical outflow, which if improved
enough will cause depression symptoms to
be relieved. This is not a matter of low
levels of neurotransmitters causing
disease; the problem is that
neurotransmitter levels are not high
enough to compensate for neuron damage
in the bundles, which results in
depression. |
