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.

References

Andrade, J. & Feinstein, D. (2003). Preliminary report of the first large scale study of energy psychology. www.emofree.com/research/andradepaper.htm.  

Blanchard, D.C. & Blanchard, R.J. (1972). Innate and conditioned reactions to threat in rats with amygdaloid lesions. J. Comp. Physiol. Rev. 81:281-90.   

Callahan, R. (2001). Tapping the Healer Within. Contemporary Books, Chicago Ill.   

Cousens, G. &  Otto, T. (1998). Both pre- and post-training excitotoxic lesions of the BLA abolish the expression of olfactory and contextual fear conditioning. Behav. Neurosci. 10:1062-1069.   

Doron, N.N. & LeDoux, J.E. (1999). Organization of projections to the lateral amygdala from auditory and visual areas of the thalamus in the rat. J Comp Neuro. 412(3):383-409.  

Fibiger, H.C.; Lepiane, F.G. & Phillips, A.G. (1978). Disruption of memory produced by stimulation of the dorsal raphe nucleus. Mediation by serotonin. Brain Res. 155:380-386. 

Gapenstrand, H.; Annas, P.; Ekbolm, J.; Oreland, L. & Fredrikson, M. (2001). Human fear conditioning is related to dopaminergic and serotonergic biological markers. Behav. Neurosci. 115:358-64.   

LeDoux, J.E.; Cicchetti, P.; Xagoraris, A. & Romanski, L.M. (1990). The lateral amygdaloid nucleus: sensory interface of the amygdala in fear conditioning. J. Neurosci. 10:1062-69.   

Maren, S. (2001). Neurobiology of Pavlovian fear conditioning. Ann. Rev. Neurosci. 24:897-931.   

Muller, J.; Corodimas, K.P.; Feidel, Z. & LeDoux, J.E. (1997). Functional inactivation of the lateral and basal nuclei of the amygdala by muscimol infusion prevents fear conditioning to an explicit conditioned stimulus and contextual stimulus. Behav. Neurosci. 111:683-691.   

Myers, K.M. & Davis, M. (2002). Behavioral and neural analysis of extinction. Neuron 36:567-584.   

Nader, K.;, Schae, G.E. & LeDoux, J.E. (2004). Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature 406:722-726.   

Pare, D.; Royer, S.; Smith, Y & Lang, E.J. (2003). Contextual inhibitory gating of impulse traffic in the intra-amygdaloid network. Ann. N.Y. Acad. Sci. 985:78-91.   

Phan, K.L.; Wager, T.D.; Taylor, S.F. & Liberzon, I. (2004). Functional neuroimaging of human emotions. CNS Spectrum 9(4)258-66.   

Reidel, G.; Platt, B. & Micheau, J. (2003). Glutamate receptor function in learning and memory. Behav. Brain Res. 140:1-47.    

Wolpe, J. (1958). Psychotherapy by reciprocal inhibition. Stanford University Press, Stanford, CA.

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