ABSTRACT
An
amino acid, vitamin and mineral formulation was designed to restore
GABAergic, opioidergic, and serotonergic deficits observed in persons
suffering acute and protracted withdrawal symptoms associated with
reduced use of benzodiazepines. In addition amino acids, vitamins
and minerals were added which have been shown to further reduce
anxiety provoked responses of striated and cardiac musculature.
Seventeen adult male and eighteen adult female subjects who had
been prescribed benzodiazepines for periods of time ranging from
one to fifteen years, and who were all experiencing withdrawal symptoms
as a result of attempting to reduce and stop the drugs, volunteered
for the study. Twenty seven of the participants were following an
individual tapering regimen. This approach is strongly supported
by the author of this study.
Each respondent understood they would not know whether they were
receiving placebo or experimental product. Each was given a 30 day
supply of either placebo or experimental. At the end of 30 days
the products were switched and those having received placebo received
experimental and visa versa. Symptoms were described and noted for
each participant prior to beginning the study and during the study.
Symptoms varied from extreme to moderate withdrawal depending on
the benzodiazepine being used. Those persons attempting to taper
Klonopin, Xanax or Ativan had a more difficult time due to rapid
cycling of highs and lows of Norepinepherine activity. Those persons
on long acting benzodiazepines such as Valium were more successful
in the tapering process and experienced lower levels of anxiety
and associated symptoms. Regardless of the drug being used, however,
all respondents but two expressed that they were better able to
function and were more clear headed when using the supplement as
part of their tapering. The time period for this study was relatively
short and further results will be documented over the coming months.
At this time the product is scheduled to be tested in Europe as
well as the United States.
INTRODUCTION
Since 1964 the use of benzodiazepines in this country
has exploded to epidemic proportions. Librium, the first discovered,
became known as “mothers little helper” and prescriptions
for these “tranquilizers” were soon in the millions
per year. People began to expect a pill to solve their problems
of worry and anxiety and we soon stopped “solving” our
problems and took drugs to change the way we felt. No one knew or
expected that the use of these pharmaceuticals would one day create
a monster of a problem linked to their use.
As patients took these drugs for longer periods of time and then
attempted to stop they were confronted with terrible psychological
and physiological withdrawal symptoms which incapacitated them.
People in withdrawal have lost jobs, families, their very lives
as the extreme anxiety, sleeplessness, confusion, heart problems
and other extreme withdrawal factors prevented them from interacting
in society in any meaningful manner.
Even patients who attempted to very slowly taper their dosages and
gradually withdraw from this dependency experienced some degree
of discomfort and the difficulty remained for months and years after
use. While these people were no longer “dependent” on
the benzodiazepine they continued to suffer protracted withdrawal
and a significant degree of disability.
Over the years even more potent benzodiazepines have been developed
with the result that even more debilitating withdrawal is now evident.
Recently, persons who were familiar with NeuroGenesis products and
successes with nutritional supplements ask that we look at the “benzo”
problem and determine if we could help those suffering with this
dependency with a nutritional supplement.
Upon reviewing testimonies of people withdrawing from benzodiazepines
and talking with numbers of people in this predicament it soon became
clear that each person’s experience of withdrawal is unique.
Although there are many features in common, every individual has
his/her own personal pattern of withdrawal symptoms. These differ
in type, quality, severity, time-course, duration, and many other
features. Such variety is not surprising since the course of withdrawal
depends on many factors: the dose, type, potency, duration of action
and length of use of a particular benzodiazepine, the reason it
was prescribed, the personality and individual vulnerability of
the patient, his or her lifestyle, personal stressors and past experiences,
the rate of withdrawal, and the degree of support available during
and after withdrawal, to name but a few.
SUBJECTS
AND METHOD
Eighteen
adult female and seventeen adult male subjects from all areas of
the United States made it known they would be willing to participate
in a study related to benzodiazepine withdrawal. All but three of
the subjects were currently taking benzodiazepines and the others
had been off the drugs for periods of time up to 12 months. Of those
on the drugs all but two were following some kind of a tapering
regimen for gradual withdrawal. Ten of the subjects were taking
Klonopin, eight were taking Xanax, two were taking Ativan and twelve
were taking Valium.
Each
person was interviewed by telephone and asked to describe the dose
they were taking, any other medications, any other supplements and
the symptoms they experienced on a daily basis. As expected the
symptoms varied greatly but all described a torment that prevented
the person from interacting in family and society successfully.
(Persons taking antidepressants at the same time as benzodiazepines
were excluded from the study). Each was then sent either placebo
or experimental product sufficient to last 30 days and asked to
take six capsules per day in divided doses. Each person was reinterviewed
at periods between two and four weeks of the study and asked to
again describe symptoms present at that time.
Not
surprising those on placebo expressed little relief from the previous
symptoms. Those on experimental product, however, indicated an awareness
that some of their symptoms had diminished, and this added hope
to their process. Interestingly, when the original experimental
group was sent placebo for their second 30 day period they all stated
they could tell the original discomfort was returning by the third
week. They all requested that the previous “product” be sent to
them when reinterviewed at the second and fourth week of the second
month.
Eighteen
of the original participants have remained in contact at the four
month mark and all are still taking “experimental product”. They
all report that the symptoms of withdrawal continue to wane as they
taper their use of the tranquilizer. Several have stopped the benzodiazepine
and are continuing on NeuRecover BZ and are expected to do so for
an unknown period of time.
One
factor that stood out as each reported their progress/lack thereof
was that those persons taking Valium were much more able to taper
their use and experienced improved functionality sooner than those
on the other benzodiazepines. Klonopin was the most difficult to
taper and assist with symptom reduction via nutritional supplementation.
All Klonopin users described extreme mood swings and difficulty
functioning when attempting to taper the drug. Xanax users reported
the same phenomenom and Ativan appeared to be almost as difficult.
As Ashton points out in her manual, it much more simple to taper
the long acting Valium and this was born out in our study.
RATIONALE FOR FORMULA
The Gamma Amino Butyric Acid (GABA) receptor is an extremely complex
receptor system. GABA accounts for almost 40% of all neurotransmitters
in the brain and this fact indicates it’s importance in maintaining
calm and logical thinking. Located on the GABA receptor are several
other sites that become occupied by other various neurotransmitter
chemicals. Principal among these auxiliary receptors are those that
receive benzodiazepines. When a benzo occupies a receptor site it
assists GABA in opening a channel into the neuron on which it is
located and chloride (from NaCl, salt, for instance) passes through
this channel into the neuron. This then reduces the firing rate
of that neuron and “calms” down activity. While it is obvious that
we were not born with a receptor for benzodiazepines, which were
not known until 1964, it is obvious that we have a normal and natural
neurotransmitter to act at these sites. These natural transmitters
act very quickly and are so quickly degraded that they have not
been positively identified and named at this time.
The issue that is most important and the issue that causes all the
problems of dependency is this: when the auxiliary receptors are
occupied for longer than normal periods of time by drugs such as
benzo’s the result is that the brain begins to reduce the supply
of GABA. The brain works to maintain balance, homeostasis, and will
not do what it doesn’t need to do. If auxiliary receptors are busy
doing most of the work it does not need to make GABA, and it does
not. The problem comes when the person attempts to stop the use
of the drug which is assisting GABA and now there is not enough
GABA to do the job on its own. Also, since “artificial” neurotransmitters
in the form of a benzo were being introduced the brain makes less
of its’ own auxiliary transmitter and the problem is compounded.
Dependency now exists for the benzodiazepine to open channels to
allow chloride to calm activity. If the channels are not opened
then adrenalin and noradrenalin run rampant and continually fuel
the fight or flight response. Heart rate increases, sleep decreases,
appetite decreases, all the states that are required for an alert
are constantly present. Normal everyday human activity is not possible
when the brain and body are engaged in the process of fighting or
fleeing. |