The Neurological Rationale for a Comprehensive Clinical Protocol Using Applied Kinesiology Techniques

Walter Schmitt, D.C, D.I.B.A.K


A procedural protocol for the application of applied kinesiology techniques is presented. It is based on neurological and biochemical principles and thirty years of clinical observations of comparative applications of techniques. Short summaries of each section are included prior to the section to enable a brief review of the information.


5. Test Aspirin, Acetaminophen, Ibuprofen Mix - If Strengthens:

  1. Check Essential Fatty Acids (BCSO, FSO, EPA, etc.)
  2. Check EFA Cofactors (B-6, Mg, Zn, Niacin)

6. Test Antihistamine Mix – If Strengthens:

  1. Challenge Orally for Offender(s) (Allergen)
  2. IRT Chapman’s Reflexes with Offender(s)

7. Sniff Tests – Aldehydes, Bleach, Ammonia

8. Test Nutrients Based on Patient History:

  1. Vitamin E (Low Back Muscles), Vitamin C (Shoulder Muscles)
  2. Iron, Folic Acid, Vitamin B-12
  3. Cholesterol Lowering Nutrients (If Indicated)
  4. Chondroitin Sulfate – If Strengthens:

    i. Check Sulfur (Cysteine) & Associated Nutrients
    ii. Check Blood Sugar Handling (Insulin, Magnesium)

Summary: Identifying and correcting these biochemical imbalances with nutritional supplementation and/or diet are essential for cellular, neuromuscular, and neurological support to encourage proper healing.

Some nutritionally treatable biochemical conditions are so important that they should be addressed very early on in the treatment process, regardless of the presenting symptoms. Each of the systemic nutritional factors in the protocol will have global impact at the cellular level. Each of these factors will also have global impact on muscle testing responses (assuming that injuries are corrected first.) In addition, most of these factors will have a direct impact on nerve function – either by directly supporting neurological metabolism and/or impacting neurotransmitter activity (synthesis or breakdown.)

Biochemically speaking, there are three factors affecting all nutrients that are applicable to both macronutrients or micronutrients. These are: 1) adequate dietary intake; 2) adequate delivery to cells; and 3) adequate metabolism of the nutrient in the cells.

It is difficult to prioritize within the systemic nutritional factors group. Each may be the most important biochemical issue in a given patient. There is, of course, a patient history driven priority. The history gives the best clues as to which nutritional factors to address first. In difficult cases, just work through the list.

It should be noted here, however, that assessment of the oxidative phosphorylation pathways for the synthesis for ATP [citric acid cycle (CAC) and respiratory chain or electron transport chain (ETC)], that could be arguably at the top of the list, are delayed in the protocol until later. The main reasons for this are as follows. Allergies (and chemical hypersensitivities) produce cytokines that are inhibitory to the CAC. Certain interleukins and tumor necrosis factoralpha will cause the intracellular production of nitric oxide that inhibits the CAC aconitase enzyme thereby truncating the CAC at this step. The patient will test positive for carbon dioxide and CAC nutrients, but the need for supplementation of these nutrients at this juncture will be reduced or negated by the elimination of the cytokine blockade of CAC enzymes. ***

The ETC is dependent on coenzyme Q10 (CoQ10), iron, and copper. Iron and copper will be addressed in this section when looking at the oxygen carrying capacity of the blood. In fact, it could be appropriate to check for CoQ10 at this juncture, especially in heart patients, or others with classical CoQ10 indications (gingivitis, myalgia, history of cholesterol lowering statin drugs.) But little is lost by checking it in conjunction with the CAC slightly later in the protocol.

5. Test Aspirin, Acetaminophen, Ibuprofen Mix - If Strengthens:

  1. Check Essential Fatty Acids (BCSO, FSO, EPA, etc.)
  2. Check EFA Cofactors (B-6, Mg, Zn, Niacin)

    Prostanoids, which are derived from essential fatty acids (EFA) include prostaglandins (PGs), leukotrienes (LTs), and thromboxanes (TXs). Prostanoids influence inflammation, immune function, platelet aggregation, cholesterol synthesis, and modulate the responses of intracellular chemistry to membrane receptor driven functions. This includes neurotransmitter (NT) activity. In addition, EFA imbalances are reflected in a variety of muscle imbalances that must be normalized for proper joint support and afferentation that is necessary for healing.

    Further, prostanoids produced in the presence of improper EFA balance are highly inflammatory. These inflammatory substances (prostaglandin-2 family and leukotriene-B4 family) depolarize NOCs and cause an increase of potentially pain-causing sensory activity. We must control the prostanoids and negate their peripheral inflammatory effects in order to normalize afferentation from NOCs.

    Most EFA imbalances are due to excessive intake of bad fats – rancid fats, saturated fats or most importantly, trans fats. Patients with EFA imbalances are prone to inflammation and tend to by users of aspirin and non-steroidal anti-inflammatory drugs (NSAIDs.) The small intestine takes the primary abuse from both bad fats and NSAIDs. This results in interference with proper absorption of other nutrients as well as inhibition of the quadriceps and/or abdominals, essential muscles for postural support. Although the presence of excess bad fats may be found when investigating cholesterol metabolism just below or digestive function later on in the protocol, the importance of proper EFA metabolism, both for clinical symptoms and cellular function, needs to be addressed at this earlier point.

    Any problem will be made worse by EFA – prostanoid imbalance.

    6. Test Antihistamine Mix – If Strengthens:

    1. Challenge Orally for Offender(s) (Allergen)
    2. IRT Chapman’s Reflexes with Offender(s)

    7. Sniff Tests – Aldehydes

    Allergic reactions and chemical hypersensitivities result in mast cell release of histamine and other inflammatory agents. As mentioned above, cytokines from allergies (or other immune responses) will inhibit the CAC and consequently energy production. Histamine is a NT with potential global impact on cortical function as a part of the extrathalamic cortical modulatory systems (formerly called the reticular activating system.) Histamine neurons arise from the ventral posterior area of the hypothalamus (HPT) and project to nearly every region of the central nervous system as well as extensive projections to the cortex. 10 Clinically, we have observed that histamine reactions induce right brain – left brain activity in muscle testing responses. 11 These hemispheric imbalances must be addressed in order to obtain a clear picture of hemispheric dominance, so important in the chiropractic neurology approach.

    Histamine is one of the most (some say, “the most”) powerful stimulator of the adrenal glands. Histamine produced by allergic reactions will disrupt adrenal activity, causing (resulting in) a hyperadrenia response initially, and possibly causing or aggravating a hypoadrenia further along the General Adaptation Syndrome progression. Adrenal problems, or any endocrine dysfunction, are best evaluated after correcting allergic responses and normalizing histamine levels.

    Histamine is also one of the substances that depolarizes NOC resulting in an increase of potentially pain-inducing sensory activity. Therefore, we must neutralize the effects of histamine in order to normalize afferentation from NOC in the same manner that we must control the prostanoids for both their effects on both intracellular modulating and peripheral inflammation.

    Food allergies and chemical sensitivities stress the immune system (thymus and spleen) which is why we address them prior to immune function. Detoxification of excess histamine stresses the spleen and liver, uses methyl groups related to sulfur amino acid metabolism that is essential in joint repair (as discussed below), and can deplete reserves of vitamin C. Degradation of histamine uses up the nutrients B-6 and folic acid. Both are essential for neurotransmitter (NT) synthesis. B-6 is necessary for ammonia metabolism, in particular as a transaminase enzyme (transports ammonia groups) activator. Ammonia groups are necessary for synthesis 10 and degradation of amino acids as well as urea cycle function. Folic acid is important for many vital functions, not the least of which is cell replication. Its deficiency can also cause right brain – left brain imbalances and switching related to the hyoid. All of the B-6 and folic acid related functions can be compromised in the presence of histamine mediated allergic reactions.

    As with improper fat intake, food allergies create distress in the GI tract. Although any GI tract organ (or any body tissue for that matter) may be adversely affected by food or other histamine mediated allergies, the small intestine is the primary receiver of the abuse. As with bad fat intake, problems with nutrient absorption and weakness of the quadriceps and abdominals are once again implicated.

    Chemical hypersensitivities deplete antioxidants, particularly selenium. In the presence of Candida Albicans or in other mycoses, the acetaldehyde produced by the fungus depletes molybdenum, an essential trace mineral necessary for aldehyde oxidase, xanthine oxidase, and sulfite oxidase enzymes. Impaired xanthine oxidase function interferes with ammonia elimination via uric acid and the build up of ammonia will shift NT functions, most notably, driving glutamate to glutamine instead of GABA and aspartate to asparagine. Impaired sulfite oxidase function intereres with the conversion of sulfite into sulfate. Sulfate is essential for liver detoxification as well as cartilage synthesis.

    We check for and correct the need for Mo early on, helping many other functions further down the list. Also, in the presence of digestive fungal overgrowth, supplying Mo will help metabolize local acetaldehyde, a significant irritant of small intestine function. It is prudent to supply Mo in these patients prior to attempting to correct the digestive dysfunction.

    Allergies and hypersensitivities can cause or aggravate any problem, any problem at all, regardless of whether or not the patient’s symptoms seem to be related to typical allergic reactions.

    7. Sniff Tests – Bleach, Ammonia

    The need for Mo will usually be associated with a positive aldehyde sniff test and ammonia sniff test. The bleach sniff test may also be positive. The ammonia sniff test opens the door to assessing amino acid metabolism. The bleach sniff test is an excellent screening test for free radical pathology and the need for additional antioxidants beyond those already tested.

    A positive ammonia sniff test causes alterations in amino acid synthesis and degradation and is usually accompanied by improper neurotransmitter synthesis of such important NTs as GABA, glycine, glutamate, and aspartate. Protein synthesis, essential for tissue repair and healing as well as intracellular (especially neuronal) metabolic function, depends on proper ammonia metabolism.

    A positive bleach sniff test suggests free radical pathology which is a state of over oxidation of the tissues. This test is placed here prudently to assure the protection of tissues from oxidative free radical activity prior to instituting therapies which are designed to increase oxygen supply to tissues (red blood cell synthesis nutrients) and oxidative metabolic pathways (CAC and ETC.)

    A positive bleach sniff test leads to consideration of both sulfur amino acid metabolism and antioxidant needs. Sulfur metabolism is discussed more thoroughly below under chondroitin sulfate and joint problems. In the absence of joint symptoms, a positive bleach sniff test will guide the clinician into this critical area of body chemistry mentioned below including homocysteinemia.

    Free radical pathology is often driven by allergies and poor EFA metabolism, two issues that have already been addressed. So the bleach sniff test may be already negative by this juncture. If not, assessment of free radical chemistry and the antioxidants required to negate it are necessary at this point. This may include vitamins E and C, but we include these two important nutrients in a separate step immediately below since their need may be present even in the absence of a positive bleach sniff test.

    Neurological problems, both named and unnamed, are associated with a positive bleach sniff test. This may be due to the effects of homocysteinemia (homocysteic acid) on neuron metabolic function and/or the damaging effects of free radical pathology.

    The long term devastating effects of homocysteinemia as a risk factor for neurological disease, heart disease, and cancer are well known. It is to the benefit of all homocysteinemia patients to have this problem identified as soon as possible in their lives so that counter measures may be put in place to negate the consequences. A positive bleach sniff test (and/or assessment of cartilage synthesis soon to follow) will guide the clinician to identify homocysteinemia in many patients who would otherwise continue to suffer the silent, degenerative effects of this condition leading to pathology. Screening for elevated homocysteine will also give us an early identification of important nutrient needs for other metabolic and NT activities including folic acid, vitamin B-12, magnesium, and vitamin B-6.

    Any inflammatory problem, painful or not, visible or microscopic (such as autoimmune and neurological diseases) will likely show a positive bleach sniff test. Tissue healing response (of any unhealthy tissue) is dependent on removing the free radical destruction of the tissues by providing appropriate antioxidants. Free radicals will also interfere with the citric acid cycle and energy production as mentioned previously which is another reason that we perform the bleach sniff test prior to CAC assessment.

    Correcting a positive ammonia sniff test and/or bleach sniff test will clear the way for proper neurochemical function that is essential for full neurological impact of subsequent structural therapies.

    8. Test Nutrients Based on Patient History:

        1. Vitamin E (Low Back Muscles); Vitamin C (Shoulder Muscles)

      Vitamin E and C are essential anti-oxidants. To supply them without first addressing the sources of oxidative (inflammatory) activity is to place the cart before the horse. So we place the testing of these nutrients after first addressing EFA imbalances and allergies / hypersensitivities. In the same hierarchy, we check for E and C (and the bleach sniff test) prior to testing for oxygen supplying nutrients to insure that increasing oxidation does not increase oxidative stress. The effects of normalizing antioxidants will also be seen by decreasing NOC activity in the presence of tissue inflammation.

      Dr. Goodheart learned in the late 1970s that these two antioxidants were associated with right brain (vitamin E) and left brain (vitamin C) activity. 12 Once again, hemispheric imbalances may be manifested by the requirement of these two nutrients. Therefore, attempting to determine hemispheric activity without considering these vitamins may create an incomplete or even false picture.

      Vitamin E is important for so many low back and pelvic muscles that to leave it out of the patient’s program is to perpetuate musculoskeletal problems. The same is true for vitamin C and shoulder problems. So early on in the care of these symptoms, we test for these important antioxidants. Supplementation will help the associated muscle(s) maintain correction as well as provide the obvious biochemical effects.

      8. Test Nutrients Based on Patient History:

          2. Iron, Folic Acid, Vitamin B-12

        Oxygen supply to the tissues is of course, essential. But we first want to make sure that we have reduced any sources of excess oxidation (EFA, allergies/hypersensitivities, antioxidant 12 depletion.) So we place the assessment of the oxygen carrying capacity of the blood here. But we also place the oxygen supplying nutrients ahead of CAC and ETC assessment since adequate oxygen is necessary for these oxidative phosphorylation pathways.

        Iron will first be depleted from reserves, then from muscles, and finally there will be a decrease in red blood cell (RBC) production. Aerobic muscle weaknesses and lack of muscle stamina, hence lack of treatment holding capacity, are present in iron deficiency.

        Folic acid and B-12 are now evaluated. (We may have already identified the need for these two nutrients if a patient demonstrates excessive histamine and/or homocysteinemia.) It must be recalled that these two nutrients are not only necessary for RBC production, but for WBC production as well. Therefore, we check for these nutrients prior to immune assessment below. As mentioned, folic acid deficiency can also cause right brain – left brain imbalances and switching related to the hyoid. Folic acid is essential in the synthesis of a number of NTs including the catecholamines (dopamine, norepinephrine, and epinephrine) and the indoleamines, serotonin and melatonin. Iron plays a role in the synthesis of indoleamines as well. It is interesting to note that iron is also necessary for the CAC, and metabolites from the CAC are necessary for several other important NTs including glutamate, GABA, and aspartate.

        8. Test Nutrients Based on Patient History:

            3. Cholesterol Lowering Nutrients (If Indicated)

          Cholesterol problems may not seem as important in the hierarchy, yet recent awareness of the clinical findings of elevated cholesterol makes it important to evaluate fairly early. When cholesterol is elevated, there is a secondary muscle weakness present that will be recurrent until the cholesterol is addressed. In some patients, screening for cholesterol farther down the protocol (along with other liver detoxification procedures) might be appropriate, but if elevated cholesterol is known, it should be addressed earlier to encourage a more effective patient neuromuscular response.

          Additionally, some of the nutrients (e.g., vitamin A, niacin, betaine) necessary for cholesterol metabolism will be important for other body functions, and if not checked here, they might not otherwise be checked until the associated muscle weakness recurs. Cholesterol metabolizing efforts are aided by proper EFA balance, already addressed.

          When treating elevated cholesterol, a very common finding is large intestine toxicity. In light of elevated cholesterol, we might jump ahead and evaluate digestive activity, or at least large intestine function at this time, and then return to this point in the protocol.

          8. Test Nutrients Based on Patient History:

              4. Chondroitin Sulfate – If Strengthens:

                  i. Check Sulfur (Cysteine) & Associated Nutrients

                  ii. Check Blood Sugar Handling (Insulin, Magnesium)

          If the patient displays cartilage or connective tissue disorders, assessment of nutrients for joint repair must be done at this juncture if any progress is to be made. A need for these nutrients will often result in muscle imbalances that may perpetuate joint instability and altered ranges of motion interfering with sensory activity arising from affected joints and slowing the healing process.

          Normalizing sulfur metabolism will lead the clinician into looking at sulfur amino acid metabolism and the methylation process that, when impaired, is usually related to elevated homocysteine and increased risk for heart disease, cancer, and neurological degenerative disorders such as Alzheimer’s disease and Parkinson’s disease.

          Homocysteine converts to homocysteic acid, a potent excitatory neurotoxin. In the presence of homocysteic acid, metabolically challenged neurons will be placed at increased risk of metabolic exhaustion from over stimulation; even normal excitatory activity may place some neuron pools at risk for cell death by apoptosis. All manipulative therapies have excitatory and inhibitory effects. If the homocysteine patient is experiencing excitatory neuronal stress, some therapies will likely over stimulate neuron pools with short-lived success at best, and irreversible neuron damage at worst. Correction of sulfur metabolism is critical in the clinical course of these patients. Overlooking it can be neurologically disastrous, especially in patients who receive the powerful neurological effects of AK therapies. This is the second step included early on in this protocol to identify and correct the disastrous effects of elevated homocysteine.

          When finding a need for addressing blood sugar handling problems as part of a joint problem, it is a good idea to address them and sulfur at the same time. So it may be appropriate to jump ahead in the protocol to the assessment of hyperinsulinism and then return to this point in the protocol.

          Sulfur is also necessary for liver detoxification, especially for detoxification of steroid hormones, NSAIDs, and many other drugs. Finding a need for sulfur at this point in the protocol will lay a good foundation for addressing liver and/or hormone problems further downstream.

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