ICAK Clinical Applications Update V1, No.1

AK CLINICAL APLLICATIONS UPDATE

TheInternationalCollegeofAppliedKinesiology® USA(ICAK-USA)hasplayedacrucialrolein establishingthefoundationforclinicaland academicarenaforinvestigating,substantiating, andpropagatingA.K.findingsandconcepts pertinenttotherelationshipsbetweenstructural, chemical,andmentalfactorsinhealthanddisease.

Dr.JohnBandy

Dr.RichardBelli

Dr.DavidLeaf

Dr.EvanMladenoff

AK CLINICAL APLLICATIONS UPDATE

ICAK-USA Members:

Welcome to the first issue of our new HTML publication, AK Clinical Applications Update! This is unlike our current e-newsletters With AK Clinical Applications Update, we have asked the membership to get involved by sharing their knowledge, research and demonstrations.

We are seeking doctor members and accepting submissions of their current findings (ie Research), technique articles or a video demonstrating a technique that has helped diagnose and treat your patients

Our objective is to have 4 submissions per issue that would be distributed to the full membership and archived on the website as a resource. We are now accepting submissions! Please send your article, research summary or video, to icak@dci-kansascity com for review

Please reach out to Angela Capra, 913-387-5608 or email: acapra@dcikansascity com if you have questions or need additional information

Warm regards,

Richard Belli, DC, DIBAK

ICAK-USA Chairman

EVALUATION OF AUTONOMIC DYSFUNCTION UTILIZING ACETYLCHOLINE CHALLENGES

By: Evan Mladenoff BSC, DC, DIBAK, FASA

Otto Loewi 1921 German Nobel Prize winning Physiologist stimulated the Vagus Nerve that caused reduction in heart rate by triggering the release of Acetylcholine The first neurotransmitter ever discovered. . . .

Acetylcholine (ACh) is THE neurotransmitter in the first order neuron of the somatic nervous system and the autonomic nervous system and is necessary for most nerve functions In the first diagram note the following:

a) In the somatic nervous system ACh is responsible for skeletal muscle contraction. This occurs via the muscarinic receptors.

b) In the sympathetic nervous system, ACh is the first order neuron neurotransmitter that synapses with unmyelinated postganglionic axons to produce norepinephrine

c) In the sympathetic nervous system, ACh is the first order neuron neurotransmitter that synapses with the adrenal medulla to initiate epinephrine and norepinephrine production for release into the circulatory system

d) In the parasympathetic nervous system, ACh is the first order neuron neurotransmitter that synapses with unmyelinated postganglionic axons to continue ACh transmission that affects/controls smooth muscle (in the gut), glands and cardiac muscle

Acetylcholine has many roles:

When it binds to muscarinic receptors, it:

Regulates heart contractions and blood pressure and decreases heart rate

Moves food through your intestine by contracting intestinal muscles and increasing stomach and intestine secretions

Causes glands to secrete substances such as tears, saliva, milk, sweat and digestive juices

Controls the release of urine

Contracts muscles that control near vision Causes an erection

When it binds to nicotinic receptors, it:

Allows skeletal muscle to contract.

Causes the release of adrenaline and norepinephrine from your adrenal glands

Activates your sympathetic system with the release of norepinephrine

EVALUATION OF AUTONOMIC DYSFUNCTION UTILIZING ACETYLCHOLINE CHALLENGES

Both types of receptors are involved in memory, including long-term and working memory, memory formation, consolidation and retrieval Within your brain, acetylcholine is also involved in motivation, arousal, attention, learning and promoting rapid eye movement (REM) sleep

The rate-limiting steps in ACh synthesis are the availability of choline and acetyl-CoA. During increased neuronal activity the availability of acetyl-CoA from the mitochondria is upregulated as is the uptake of choline into the nerve ending from the synaptic cleft. Ca2+ appears to be involved in both of these regulatory mechanisms. As will be described later, the inactivation of ACh is converted by metabolism to choline and acetic acid.

Consequently much of the choline used for ACh synthesis comes from the recycling of choline from metabolized ACh Another source is the breakdown of the phospholipid, phosphatidylcholine One of the strategies to increase ACh neurotransmission is the administration of choline in the diet However, this has not been effective, probably because the administration of choline does not increase the availability of choline in the CNS

Causes of Diminished Acetylcholine include:

Oxidative stress

• Insulin resistance

• Mitochondrial dysfunction

• High cortisol

• Cofactors

• Brain injury

• Reproductive hormones

The clinical question is how can a physician determine if these neurophysiological functions are working properly? This is the profound reality of Diagnostic Muscle Testing With few exceptions, all activities of the CNS, receiving, processing, and integrating information, ultimately finds expression in contraction of a muscle (Color Atlas of Physiology, A Despopoulos, S Silberange, Year Book Medical Publishers, Georg Thieme Verlag)

Numerous members of the USA chapter of ICAK (Drs. Wally Schmitt, Michael Allen, Richard Belli) have documented that ‘all muscle testing ultimately tests the central integrative state of the ventral horn’.

Sherrington called the lower motor neurons of the spinal cord the “final common pathway” that controls behavior. These motor neurons, also called the somatic motor neurons, directly command muscle contraction. They are the output of the motor system. Inputs to lower motor neurons include the sensory afferents entering the dorsal horn (providing information about muscle length), the upper motor neurons in the motor cortex, and the interneurons within the spinal cord that participate in spinal motor programs.

EVALUATION OF AUTONOMIC DYSFUNCTION UTILIZING ACETYLCHOLINE CHALLENGES

Let me rephrase this: sensory input information enters from muscle length; upper motor neurons from the brain send information down the descending tracts and neurons in between the brain and the muscle, all participate in spinal motor programs Regardless of the source of the input, the output is the lower motor neurons, the final common path

This is profound when the corollary version is stated meaning that diagnostic muscle function can be used to evaluate spinal motor neurons, interneurons, upper motor neurons AND any input into these pathways

Examination Protocols

1. TL GB1 – located at the lateral aspect of the orbit on the bone. If inhibition occurs proceed to nutrient testing with AcetylCoA Factors, iStressedOut

2. TL EAV Vagus CMP – located at the base of the 2nd and 3rd carpal bones in the intercarpal space. . If inhibition occurs proceed to nutrient testing with AcetylCoA Factors, iStressedOUT.

3. TL Vagus at bifurcation of SCM then test

a Supraspinatus

b Subscapularis

c Muscle-Organ relationship related to the vagus nerve

If inhibition occurs proceed to nutrient testing with AcetylCoA Factors, iStressedout

4 OculoCardiac Reflex Protocol

EVALUATION OF AUTONOMIC DYSFUNCTION UTILIZING ACETYLCHOLINE CHALLENGES

5 Nicotinic Receptors Test

Can the patient sustain a gamma 2 motor neuron maximal contraction for 12-15 seconds?

Usually the patient can only hold the contraction for 4-5 seconds Confirm with TL to ipsilateral GB1 then repeat sustained contraction for improvement. If there is inhibition and facilitation with GB1 proceed to nutrient testing with AcetylCoA Factors, iStressedout.

6. Muscarinic Receptors

Test – shine a light in the nasal eye field and test ipsilateral subscapularis and gracilis TL to ipsilateral GB1 then repeat test protocol If there is inhibition and facilitation with GB1, proceed to nutrient testing with AcetylCoA Factors, istressedOut

7 Kreb’s Cycle Evaluation - a long time useful procedure to determine function of this chemical pathway(s) is easily administered

a Start with a normally facilitated muscle

b Have the patient re-breathe their own air (use a paper bag to have them exhale and inhale out of usually 5-6 times)

c Re-test indicator muscle for inhibition

d If inhibition occurs then evaluate for nutrients such as

i AcetylCoA Factors

ii CoQ10

iii Acetyl-L-Carnitine

e Repeat re-breathing challenge with specific nutrient to determine best approach to improving AcetylCoA production

Scan this QR Code with your phone to view a video demonstration of these protocols

VAGUS NERVE STIMULATION IN AK TESTING

By: David Leaf, D.C.

There has been a tremendous increase in books and published papers on the significance of the vagus nerve For example, earlier this year, a paper examined the effects of oriental practices like chanting or humming

The article went on to show that one of the positive benefits of these actions was to stimulate the vagus nerve

At the ICAK meetings for a few years, Dr George Gonzalez demonstrated testing for the cranial nerves While testing an intact normal muscle, stimulation was done to the cranial nerves or their function was challenged to see if it caused inhibition of the tested muscle

His test for the vagus nerve was to stimulate the pharynx with the tongue and have the person make noise during the stimulation Recent research shows that humming stimulates the vagus nerve This is the method used in chanting, humming, or singing that stimulates the vagus nerve

Suppose you are confronted with a patient with visceral problems, especially one with multiple organ malfunctions. First, test the related muscles for inhibition. Then ask the patient to hum, stimulating the vagus nerve, and test for facilitation of the inhibited muscles.

If the muscle is facilitated, test for the need for choline to produce acetylcholine Then test for involvement of the other nerves that exit the skull by the occipital bone

If other cranial nerve involvements of those that exit at the occipital bone are found, test for the need to do the jugular decompression technique. When Goodheart first talked about this problem, he found observable changes in the pharynx

Over contraction of the suboccipital muscles can adversely affect these cranial nerves Therefore, further investigation should be made as to why these muscles are over-contracted

If the vagus nerve is involved with the visceral problems first encountered, do not fail to consider testing for other nutritional and reflex techniques to normalize the function of the original muscle inhibition patterns

CERVICAL DISC SYNDROME

A PRECISE DIAGNOSTIC AND THERAPEUTIC PROCEDURE FOR CORRECTION OF CERVICAL DISC LESIONS

By: John Bandy D.C.

ABSTRACT: Certain characteristics and signs are exhibited by cervical disc syndrome Disc lesions generally do not therapy localize However, they do challenge Quite often disc lesions will cause neurological insult When this occurs, the myomere will be affected causing a muscle or muscles to demonstrate measurable changes in particular patterns

INTRODUCTION

In cervical disc syndrome, muscle change or weakness is different in character from the typical weakness found in Applied Kinesiology That is, these muscles are not "turned off" as is a muscle when a neuro- lymphatic, neurovascular, or a vertebral subluxation is involved, but rather show weakness indicating that they are not receiving full nerve supply This is much like a rheostat phenomenon In that the muscle strength is diminished in proportion to the degree of nerve root or cord pressure applied by the herniated disc This peculiarity can be used to diagnose not only the level of the disc lesion, but also the best position for its correction

There is disagreement among authors as to the myomere-muscle relationships This author has examined more than five hundred patients exhibiting this peculiar weakness and agrees with Rene Calliet, M D as to which muscles are supplied by the cervical myomeres He listed as his findings the following myomere-to-muscle relationships:

Deltoid, C6 nerve root, C5 disc: Triceps, C7 nerve root, C6 disc: Finger Abductors, C8 nerve root, C7 disc

He also lists areas of palpatory pain and tenderness that correlate to each specific lesion These areas are depicted in Figure 1 In addition, a positive Dejerine's sign may be present along with neck rigidity and diminished range of motion (ROM) towards the involved side Calliet also states that palpatory pain is often elicited over the exit of the cervical nerve root involved

Paresthesia and/or numbness may also occur in the later stages of a cervical disc syndrome (CDS), and these locations are given in Figure 1

The procedural outline that follows has been found to be most accurate in the determination of cervical disc lesions First, test the muscles listed on each upper extremity to determine any weakness After determining that there is a muscle weakness (i e the right deltoid), there are two diagnostic procedures

CERVICAL DISC SYNDROME

A PRECISE DIAGNOSTIC AND THERAPEUTIC PROCEDURE FOR CORRECTION OF CERVICAL DISC LESIONS

The procedural outline that follows has been found to be most accurate in the determination of cervical disc lesions. First, test the muscles listed on each upper extremity to determine any weakness. After determining that there is a muscle weakness (i.e. the right deltoid), there are two diagnostic procedures. First, find the direction of correction by directly challenging the vertebrae above and below the disc (C5) associated with the weak muscle (deltoid). The direction of challenge that strengthens the weakened muscle is the direction of the corrective thrust. Secondly, you must now determine the proper head position of the patient for your thrust by the following method:

1 Again determine that you have a muscle weakness

2. Next, ask the patient to place their neck into full extension. Many times this in itself will strengthen the muscle. Frequently, however, this alone is not sufficient and you must add rotation to one side or .the other to negate the weakness.

3. When the proper head position is found, muscle weakness will be abolished, and this is the proper head and neck position for your corrective thrust. Sometimes one corrective thrust is not sufficient to make a total correction. Here, the author has found that an additional line of correction is necessary and can be determined by repeating the same procedure until all muscle weakness is abolished.

It may be Important in certain situations to place the patient in a sitting position to again check for a cervical disc syndrome Occasionally a posturally dependent cervical disc problem will not show any positive checks while the patient is recumbent Also, on rare occasions when a patient states that relief from their pain did not last, and yet you do not find any return of cervical disc signs, the patient will show positive signs when placed in a sitting or standing position

Quite often, not all signs or patient symptoms may be at the stage where typical diagnostic procedures would pick up a cervical disc herniation. With the above Applied Kinesiological approach, many disc lesions are discovered long before usual methods of determination would be diagnostic.

CERVICAL DISC SYNDROME A PRECISE DIAGNOSTIC AND THERAPEUTIC PROCEDURE FOR CORRECTION OF CERVICAL DISC LESIONS

The Cervical Disc Syndrome and The Lower Extremities

Cervical disc syndromes can and do at times impair nerve supply to the lower extremities The nerve roots L4 (rectus femoris), L5 (anterior tibialis) and S1 (gastrocnemius) have all been found at one time or another to be involved in CDS cases In these cases, the author has found that the clue to this is with a patient presenting with multiple muscle weaknesses of the lower extremities, which are negated when the patient places the head and neck in the correct hyperextended position After proper correction of the CDS, the doctor will find that these multiple lower extremity muscle weaknesses will be abolished

Research conducted by Torkildsen, lended credence to the above etiology He supports the view that changes in the cervical intervertebral canal giving rise to brachialgia may simultaneously be the cause of pains in the leg resembling sciatica He terms this situation as brachialgic sciatica, and this differs in nature from pure lumbar disc lesions Torkildsen discusses some differential diagnostic points relating to pyramidal tract signs These include:

1 2 3 4

Increased deep tendon reflexes on the involved (painful) side; An extensor response to the plantar reflex;

Two or more involved dermatomes on the involved (painful) leg side

The bilateral Achilles reflexes remain equal

These clues are concomitant to the peripheral nerve lesions of the arm

Since it can take six to twelve months for annular fibers to heal, care must be used in avoiding activities, which would again force nuclear material through the injured area Therefore, strict avoidance of activities employing neck flexion is to be carried out This would include watching T V supine with the head propped up, reading in such a manner, or sewing in the lap while looking down Computer monitor position is extremely important The author recommends that the center of the screen be at eye level Lap top computers can be a real problem

References

Calliet, Rene, M D , Neck and Arm Pain, F A Davis Company, Philadelphia, 1973, pp 70-72

Ibid

Torkildsen, Acta Psychiatric Neurology Scan, 1956, 31:333-44

AN AK APPROACH TO KREBS CYCLE DYSFUNCTION AND BEYOND

By: Richard Belli, DC, DACNB, FABNN

We need ATP not just for physical exercise, but for every biochemical reaction that takes place in the body At the heart of the cell is a merry-go-round of energy and matter known as the Krebs cycle It is also sometimes called the “citric acid cycle” or the “tricarboxylic acid cycle” But for this discourse we will stick with the common name of Krebs cycle

Each step in the Krebs cycle is an ostensibly trivial rearranging of carbon, hydrogen, oxygen atoms with a byproduct of carbon dioxide The textbooks tell us that the Krebs cycle generates energy by stripping out hydrogen atoms from the carbon skeletons of food and feeding them to the ravenous beast that is oxygen This is the process of cellular respiration The energy released at each step is ingeniously captured and used in the cell, while the inert carcass of water and carbon dioxide are discharged to the outside world

You will read that the Krebs cycle is about the oxidation of food stuffs, and especially glucose to synthesize ATP, but, in addition to the primary source of ATP, the Krebs cycle is considered the engine of biosynthesis For example, most amino acids are directly or indirectly from molecules in the Krebs cycle So are the long-chain lipid molecules needed to make cell membranes Even the letters of DNA termed nucleotides are made from sugars and amino acids also derived from the Krebs cycle

The Krebs cycle is also important for production of neurotransmitters, including the excitatory neurotransmitter Glutamate and the inhibitory neurotransmitter GABA. Glutamate is directly produced by the Krebs cycle, then converted to GABA via a decarboxylation reaction and a cofactor Peridoxal-5-Phosphate, the phosphorylated form of B6. The balance of Glutamate and GABA production is imperative for normal cerebral cortex function. This imbalance can lead to disorders of mood, anxiety and in extreme cases seizures.

Considering the previous discussion, it is very easy to appreciate the myriad of symptoms and maladies that may occur with dysfunction of the Krebs cycle. Including everything from fatigue, pain, digestive disorders, anxiety, and heart issues.

Krebs cycle dysfunction is so impotent that it is hard to believe a patient can move towards optimal health until it is corrected. Therefore, two questions immediately come to mind, what causes Krebs cycle dysfunction and how do we treat it.

The Krebs cycle is susceptible to many assaults, which include a simple lack of vitamin and mineral cofactors, toxins, virus, as well as inflammatory hormones, immune cytokines, alcohol, heavy metals, and other commonly abused substances.

AN AK APPROACH TO KREBS CYCLE DYSFUNCTION AND BEYOND

Before we can fix the Krebs cycle, we need to have a clinical predictor of dysfunction Referring to our early discussion you will remember that a byproduct of ATP production is carbon dioxide Carbon dioxide is not a waste product as many would think It is used for many important reactions is the body including respiration, kidney function, as well as hydrochloric acid and pancreatic acid production to mention a few. Therefore, if the mitochondria are not producing enough carbon dioxide, metabolic dysfunctions will likely occur.

We can easily identify Krebs cycle dysfunction with manual muscle testing and increasing carbon dioxide (Co2) Simply identify an inhibited or weak muscle and have the patient rebreathe their own air to increase Co2 titers Rebreathing is simply done using a brown paper lunch bag The patient covers both the nose and mouth with the bag and rebreathes 6-8 breaths If rebreathing facilitates the inhibited muscle one can assume that there is a decrease in Co2 titers as a result Krebs cycle dysfunction.

If it has been determined that there is Krebs cycle dysfunction the actual cause must now be determined Th where a little clinical investigation comes into play First, y will want to test the patient for the vitamin and mineral cofactors that make the Krebs cycle spin These include B B2, B3, B5, Lipoic Acid, Manganese, and Magnesium as indicated to the right

Additionally, Coenzyme Q10 is necessary for the final step in ATP production called the electron transport chain Coenzyme Q10 is depleted by medications, including statins Also phosphorylated B6 or P-5-P is necessary for Q10 synthesis in the liver One or more of the above may strengthen the inhibited muscle which indicates a need for supplementation

Once ATP cofactors have been examined and necessity determined, it will be wise to address the other Krebs cycle inhibitors that were previously mentioned Including free radical damage from insufficient antioxidants and insufficient subcellular melatonin from lack of exposure to near infrared sun rays

AN AK APPROACH TO KREBS CYCLE DYSFUNCTION AND BEYOND

Taking it beyond the Krebs cycle we can see that it is necessary to look at the effects of ATP production and other byproducts such as Glutamate, GABA, and Adenosine

Adenosine is essential for proper function of every cell in the body It is important to know that ATP acts as an excitatory co-transmitter with norepinephrine and Adenosine as an inhibitory neurotransmitter ATP gets metabolized to Adenosine with a hydrolysis reaction and Magnesium as a cofactor

When awake Adenosine rises by the hour resulting in the desire to sleep or sleep pressure If Krebs cycle dysfunction is corrected and the patient becomes more irritable or doesn’t feel like sleeping Magnesium supplementation may be necessary to move from ADP to Adenosine as indicated below And finally, Adenosine has an anti-nociceptive effect and well as dilates coronary arteries

If Krebs cycle dysfunction is corrected and the patient is much calmer and anxiety has decreased, you can assume that more GABA is being formed. If there is increased anxiety and agitation as well as poor sleep, Glutamate may not be converting to GABA. If this is the case B6 and P-5-P should be considered as indicated below.

AN AK APPROACH TO KREBS CYCLE DYSFUNCTION AND BEYOND

In summary, you will locate an inhibited or weak muscle. Next have the patient rebreathe their own air with a brown paper lunch bag. If the inhibited muscle strengthens it implies that there is Krebs cycle dysfunction. In addition, you will want to check other muscles to get the big picture. This is indicated in the flow chart below. If rebreathing facilitates the inhibited muscle and does not inhibit a normal muscle, it is most likely just Krebs cycle dysfunction. If rebreathing facilitates the inhibited muscle and inhibits the supraspinatus, it is most likely Krebs cycle dysfunction and glutamate conversion to GABA. If rebreathing facilitates an inhibited muscle and inhibits a normal muscle this implies that there is Krebs cycle dysfunction and inhibits a normal muscle ATP is not being converted to Adenosine.

Rebreathing Facilitates a conditionally inhibited muscle and:

1 Does not inhibit a normally facilitated indicator or supraspinatus

Krebs cycle and electron transport chain

Typically treat the small intestine Chapmans Reflex

2 Inhibits supraspinatus

Krebs cycle and glutamate conversion to GABA

Typically treat the brain Chapmans Reflex

3. Inhibits normally facilitated indicator

Krebs cycle and ATP conversion to adenosine

Typically treat the heart Chapmans Reflex

Taking into consideration the evidence provided, it is easy to conclude that mitochondria health and Krebs cycle function should be at the top of the list in systemic nutritional and physiological factors considered when treating a patient Even if no other nutrition is considered, mitochondria and Krebs cycle should be to assure optimal treatment outcome and patient health