Why Tapping Works:
Speculations from the Observable Brain
WHY
TAPPING WORKS: Speculations
from the Observable Brain
Ronald A. Ruden,
M.D., Ph.D.
ABSTRACT
A new therapy for
phobias, PTSD, addictive behaviors and other psychological issues was first
described by Dr. Roger Callahan and involves thought activation of the problem
followed by tapping on certain acupoints in a specific sequence. For most
cases, the problems were reportedly cured in a matter of minutes. We speculate
on a neuroanatomical and neurophysiological mechanism for this technique.
We propose that
tapping and other sensory stimulation increase serotonin in both the prefrontal
cortex and the amygdala. The success of this technique requires that glutamate
be first increased in the circuit by activating affect. We suggest the
name ‘Affect Activation/Sensory Stimulation’ to encompass this general
approach. AA/SS represents a paradigm shift for the treatment of these
problems.
INTRODUCTION
In 1986, Dr. Roger
Callahan discovered that tapping under the eye of an individual with a water
phobia immediately and permanently cured this problem (Callahan,
2001). Tapping on specific traditional Chinese medicine acupoints
in a specific sequence literally appears to throw a switch. After a
successful treatment, disturbing thoughts decrease and the phobic response
disappears, for good!
A large study that
involved over 29,000 patients was conducted using these tapping procedures. The
remarkable results (Andrade & Feinstein, 2003) covered a wide range of
problems, such as specific phobias, panic disorders, post-traumatic stress
disorders, acute stress disorders, and anxiety-depressive disorders. This
method was successful in 76% of the subjects.
A neurobiological
model must explain several characteristics of this therapy:
* Why must the
distress be activated before it can be treated?
* Why is the
treatment specific to one phobia at a time?
* Why does the same
protocol work for many different problems?
* Why does the
distress appear to diminish during tapping (Wolpe 1958)?
* What is the
transduction event that converts tapping into a biological event in the brain?
* How and why does
this treatment produce a rapid and permanent change in an individual’s response
to the distressful thought?
THE AMYGDALA AND
EMOTION
Neuroimaging (Phan,
Wager, Taylor & Liberzon, 2004), lesional (Cousens & Otto, 1998),
(LeDoux, Ciccheti, Xagoraris & Romanski,1990), (Blanchard & Blanchard,
1972) and neuroanatomic (Sah, Farber, Lopez De Armentia & Powers, 2003)
studies point to the amygdala as the final common pathway for expression of
emotions. The amygdala is well suited for this job, receiving input from the
hippocampus, the prefrontal cortex, the thalamus, midbrain nuclei, and other
cortical and subcortical areas (Maren, 2001). The amygdala is made of several
nuclei; the basolateral (BL), the lateral (LA) and the basomedial (BM) make up
the basolateral complex, the BLA (Maren, 2001). The lateral nucleus receives
the information from other areas. The associations between a conditioned
stimulus and response are believed to be stored in the BLA, and when
appropriate, a signal is sent to the Central (Ce) nucleus of the amygdala.
Activation of the Ce is necessary to produce the behavioral, autonomic and
endocrine components of an emotional response by activating other areas of the
brain, including projecting neurons to the nucleus accumbens, locus coeruleus,
paraventricular nucleus, the hypothalamus, and the prefrontal cortex.
ENCODING FEAR
Of all the emotional
states we experience, fear is the most primitive and powerful. If we
understand how a fear response is disrupted, we may be able to understand how
tapping works. Phobias are characterized by a persistent, irrational and
excessive fear of objects or situations like bugs, colors, numbers, light,
dark, bridges, tunnels, elevators and planes. Since no imminent danger is
associated with these objects or situations, they can be considered
conditioning stimuli (CS). A special genetic and environmentally
modulated neurobiological landscape is necessary to encode a phobia
(Gapenstand, Annas, Ekbolm, Oreland & Fredrikson, 2001). Treatment that
disrupts the encoded phobic response may therefore extinguish it forever.
Phobias are learned
and as such are fundamentally different than responses to innate fears. A fear
response is generated by sensing an innate fear, also called Unconditioned Fear
Stimuli (UFS). Such stimuli reflect the fear of being killed and are hard wired
in the brain, including fear of the unknown (novel situations), heights
(falling), closed spaces (being trapped), open spaces (no place to hide),
creepy crawly things (land based predators) and something coming out of our
visual fields (air based predators). These survival stimuli do not reach
consciousness because details are unimportant: only the emotion of fear is
experienced, mandating avoidance. Accordingly, the thalamus, which is the first
sensory connection in the brain, has direct projections to the amygdala (Doron
& LeDoux, 1999).
A phobia is generated
by an innate (unconditioned) fear stimulus leading to a fear response in the
presence of another object or situation. For example, traveling over a
bridge (CS), you look down and see the height (UFS). The height causes fear,
leading to a phobia of bridges.
NEUROPHYSIOLOGY
Animal studies of
conditioned fear suggest that glutamate agonists enhance learning and glutamate
antagonists inhibit the learning of the fear response in mice (Myers &
Davis, 2002). Glutamate, an excitatory amino acid, is involved in activating
genes that are necessary for memory storage and retrieval (Reidel, Platt &
Micheau, 2003). These genes alter the wiring and firing of neurons. This
implies that glutamate is released locally where learning takes place. GABA, an
inhibitory amino acid, inhibits glutamate and, as such, GABA agonists inhibit
fear conditioning and GABA antagonists accelerate it (Myers & Davis,
2002).
EXTINCTION TRAINING
Chemical approaches
have extinguished fear conditioning in animals using infusions of anisomycin, a
protein synthesis inhibitor (Nader, Schafe & LeDoux, 2000) and the GABA
agonist muscimol (Muller, Corodimas, Feidel & Ledoux, 1997). The
conclusions were that a fear response could only be disrupted shortly after
being activated, that protein synthesis was involved, and that a GABA agonist
could temporarily disrupt the fear response. In another experiment,
depletion of serotonergic neurons prevented extinction of the fear. These
results imply that serotonin plays a role in extinction (Fiberger, Lepiane
& Phillips, 1978).
Research has
documented a group of inhibitory neurons intercalated between the BLA and the
central nucleus (Ce) of the amygdala as the potential mechanism for this fear
extinction. (Pare, Royer, Smith & Lang, 2003).
WHY TAPPING WORKS
We believe that
“affect activation” is the critical aspect for success of the tapping
method and propose that during affect activation, glutamate is locally released
in areas corresponding to the neural circuit that initially encoded the conditioned
fear. Without local release of glutamate, no amount of tapping will be
effective. Tapping or other sensory stimulation (massage, eye movement, etc.)
then causes a global, non-specific release of serotonin via ascending pathways.
During sensory
stimulation, we speculate that serotonin decreases the inhibitory signal from
the prefrontal cortex to the intercalated neurons and allows for GABA release,
thus inhibiting the outflow from the central nucleus (Ce) of the amygdala, and
the patient experiences a decrease in distress.
Simultaneously,
serotonin causes GABA release via serotonergic receptors in the BLA. We
speculate that this combination, GABA and serotonin, inhibits glutamate from
activating protein synthesis, preventing the re-storing of the fear response
and thus de-linking the CS to UFS pathway.
To better understand
de-linking, imagine the brain like a beach filled with holes (CSs). As a
specific thought activates a fear response, a certain hole in the BLA fills
with glutamate, then links with a UFS and sends a signal to the Ce.
During tapping, when a serotonin wave flows in, GABA is released, and the
glutamate filled hole and only the glutamate filled hole solidifies, inhibiting
protein synthesis and disrupting the link to the UFS. Since the hole is
now gone, the ability to re-activate the CS to UFS link by glutamate release is
lost. Distress is decreased by directly blocking the Ce outflow.
How tapping raises serotonin and GABA remains uncertain, but a simple
mechanical process involving sensory receptors has been proposed (Andrade and
Feinstein 2003).
CONCLUSIONS AND
OTHER THOUGHTS
This model suggests
that activation of affect followed by sensory stimulation provides a
neurobiological basis for tapping therapy. This model outlines an explanation
for permanence, specificity, and ability to generalize to other types of
affective problems via amygdala de-linking.
Among the major
controversies present in the field of Energy Psychology, of which TFT is representative, is the location and sequence
of tapping. While the neurobiological model does not require a specific
sequence of tapping, sensory receptor density (location where you tap) may
affect the rate and intensity of serotonin release. Any stimulation that
affects the serotonin system can be used. Thus, tapping, humming, mind-full
meditation, cognitive tasks, and eye movements may be useful. The goal
for this therapy then becomes how best to activate the affect and find the
appropriate sensory stimulation for the individual. Herein lies the skill of
the therapist.
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