WHAT IF YOUR PATIENT'S PAIN
COMES FROM CARDIOVASCULAR DISEASE?

By Guy R. Schenker, D.C.

Imagine being challenged by the following interesting and very difficult chiropractic case:

Old Delmar Bender was a retired farmer.  At 63 years of age he was not retired because he wanted to be, but because he was disabled.  Eight years ago he had fallen from a roof.  That fall subsequently resulted in two lumbar spine operations, which had left him not only with back pain, but with legs that were continuously numb and which became extremely fatigued upon prolonged standing.  Coincidentally, he had become diabetic shortly after his fall.  His sugar had been completely out of control for the last 6 years.  He took Micronase daily, but with minimal benefit.

Though Delmar had had to give up farming, he nevertheless did everything in his power to maintain his strength.  He rode an exercise bike daily to maintain leg function and to help control his sugar.  He also did a good job of avoiding sweets in his diet.

Now, Delmar is in your office in hopes that your chiropractic adjustments can help his leg numbness, weakness, and fatigue.  How do you handle a case like this?  Like most chiropractors you begin with an x-ray analysis plus a thorough orthopedic and neurological exam.  You then institute a program of chiropractic adjustments as indicated by your particular technique, perhaps supported by various ancillary procedures that are within your scope of practice.

Suppose in Delmar's case the results of the orthopedic and neurological exams were equivocal at best.  The patient's symptoms localized very poorly upon orthopedic testing, and there was no apparent dermatomal or sclerotomal distribution of pain.  You probably tell the patient (and yourself) something to the effect that while you can make no guarantees of a cure for his condition, you have achieved some success in similar cases in the past and you will give it your best shot.

After administering chiropractic care for two weeks there is neither objective nor subjective improvement in the patient's condition.  Do you give up?  Do you keep plugging away hoping things will take a turn for the better?

Recently we were faced with precisely this clinical challenge.  After a couple weeks working on Delmar's lumbar spine chiropractically his low back pain of many years duration had disappeared virtually entirely. Nevertheless, there was no improvement whatsoever in the numbness or weakness in his legs.  We began to suspect that the leg symptoms were not at all related to the back injury and the disc surgeries that he had had, but were instead the result of peripheral vascular disease.

Delmar's leg symptoms were no longer a case for chiropractic, but were still very definitely a case for a chiropractor.  Within each chiropractor's scope of practice is the use of clinical nutrition.  The purpose of this article is to show that as primary care physicians we chiropractors are routinely confronted with symptoms and conditions for which the chiropractic adjustment is not the entire answer, but for which clinical nutrition proves invaluable.

The further purpose of this article is to demonstrate that cardiovascular disease (CVD) in particular is responsive to therapeutic intervention by a knowledgeable clinical nutritionist.  The efficacy of clinical nutrition in such a severe pathology is particularly noteworthy since the medical profession has failed abominably as regards CVD, both in terms of treatment and prevention.

Nearly half of all Americans die of heart attacks.  Yet it was not always so.  Despite the supposedly heroic efforts of the medical establishment, CVD has progressed from almost a non-entity a hundred years ago to the leading cause of death in America today.  (1)

     That the medical profession has completely missed the boat on treating and preventing CVD is further illustrated by the scientifically unsound treatment protocol that is routinely prescribed.  For example, a recent study published in the New England Journal of Medicine demonstrated that Digoxin, the most universal treatment for heart disease, is totally impotent.  Its performance is no different than a placebo in preventing heart attacks.  (2)

Calcium channel blockers are one of the most prescribed medications for treating hypertension, angina, and cardiac arrhythmias.  Studies have shown that calcium blockers, while being very effective at lowering blood pressure, actually increase a patient's chance of having a stroke.  The pharmaceutical industry was still reeling from this finding when further studies proved that calcium blockers also increase the incidence of heart attacks. (3,4)

Literally millions of people are taking aspirin, presumably for protection against CVD.  Yet, like the calcium blockers, aspirin actually exacerbates CVD.  A study done at the University of Sidney and reported in the Medical Tribune in 1992 shows that patients with some degree of blockage of arteries to the brain are three times more likely to have a stroke if they are taking aspirin, and that that increased risk is from as little as half a tablet a day.  Other research done at the University of California and reported in the British Medical Journal shows that elderly men and women who take aspirin every day almost double their chances of developing ischemic heart disease.  The study also shows that there is an increased death rate in aspirin users from hemorrhagic stroke, not to mention the morbidity associated with intestinal bleeding and an increased incidence of both kidney and colon cancer.

So, if the medical approach to CVD disease has proved effective only as crisis therapy, what can the chiropractic profession offer as an alternative? As we will show below, in contrast to Digoxin, calcium blockers, and aspirin, the chiropractic nutritionist has a virtual arsenal of nutritional big guns that are shown in the scientific literature to be able to stop and even reverse CVD.  Let us consider a few of these nutrients.

CHONDROITIN-4-SULFATE (CS).  It has been known for more than 25 years that CS has a powerful impact on reversing CVD.  As early as 1969, two studies were cited in JAMA demonstrating the tremendous clinical effects of CS.  In both studies, the number of coronary incidents (myocardial infarction, coronary insufficiency, myocardial ischemia, and congestive heart failure) in CVD patients treated with CS was about 1/6 the number reported for the control patients who received no CS.  (5)

CS helps maintain arterial elasticity.  CS retards the arteriosclerotic and aging processes within the arterial wall.  CS also possesses lipid-clearing activity.  It lowers cholesterol; it lowers triglycerides; and it normalizes the ratio between HDL, LDL, and VDL.  CS supplementation has also been shown to significantly reduce angina pectoris in CVD patients.  In addition to clearing lipids, (both intra and intercellular) and maintaining arterial elasticity, CS has been found to protect against thrombus formation.  (6)

In addition to the striking reduction in mortality and morbidity in patients with ischemic coronary heart disease, the Institute for Arteriosclerosis Research at Loma Lind University School of Medicine reports experimental studies showing that CS can prevent, as well as accelerate regression and healing of, coronary and aortic atherosclerosis.

BROMELAIN.  Bromelain is a proteolytic enzyme that has the capacity to break down arterial deposits.  The use of bromelain as an oral chelating agent was pioneered by the famous German Doctor Hans Nieper.  To obtain chelation benefits from Bromelain as a sole therapeutic agent requires tremendous doses of this enzyme.  However, when used in conjunction with CS, bromelain is found to potentiate the chelating effect of CS at a much lower dosage.  (7)

MAGNESIUM ASPARTATE.  We could go on for many pages highlighting the amazing protective effects of magnesium on the cardiovascular system.  In order to give you just the essential information as concisely as possible we will list just the highlights as follows:  (8,9,10)

1.       Magnesium deficiency has been clearly identified as an independent risk factor for ischemic heart disease.

2.       Repletion of magnesium can correct hypokalemia. This is particularly

significant in those patients taking medications such as diuretics that deplete potassium.

3.       Magnesium supplementation reduces both ventricular and supra-ventricular arrythmias.

4.       Magnesium is a calcium antagonist.  It thus reverses the sympathetic (excess catecholamine) component of CVD and provides the same effect naturally that the dangerous calcium blockers are designed to provide pharmacologically.

5.       Magnesium is a vaso-dilator for the coronary arteries and the peripheral systemic arteries.  Magnesium reduces the secretion of catecholamines, potent vaso-constrictors.

6.       Magnesium inhibits platelet aggregation; it decreases platelet deposition and micro thrombi formation.

7.       Magnesium reduces the synthesis and release of thromboxane A2, a cyclooxygenase bi-product, as well as 12-HTE, a lipoxygenase product.

8.       Magnesium increases prostacyclin synthesis.

9.       Magnesium increases high-density lipo-proteins levels.

10.  Magnesium clears excess lipids, both cholesterol and triglycerides.

11.  Magnesium is essential for proper myocardial contraction.

To put all these amazing benefits of magnesium to work for your patients' cardiovascular systems most effectively, combine that magnesium with aspartic acid.  The efficacy of magnesium in aspartate form once again draws upon the phenomenal work of Hans Nieper.  He found that aspartic acid was an extremely effective carrier of magnesium.  When combined as aspartate, the magnesium is carried most effectively directly to the intracellular sites of biological activity.  (11)

L-CARNITINE.  This nutrient is another multi-paged story that we will reduce to a concise list of high points: (12,13,14)

1.     Carnitine improves fat metabolism in the heart (and other organs and tissues)

2. Carnitine reduces triglycerides and cholesterol; it significantly

increases high-density lipo-proteins.

3. Carnitine improves heart muscle exercise tolerance.

4.     Carnitine prevents cardiac arrythmias, including the occurrence of ventricular fibrillation in the early phases of ischemia.

5.     Carnitine prevents angina.

6.     Carnitine is a vaso-dilator of coronary blood vessels (and lowers blood pressure).

7.     Carnitine is essential for the transport of long chained fatty acids into the mitochondria: Thus Carnitine depletion causes intracellular lipid accumulation.

8.     Carnitine (because of its role in supplying fatty acids to the heart muscle) is valuable in the prevention of chronic heart failure.

COENZYME Q-10 (CoQ).  CoQ is an essential component of the mitochondrial electron transport chain, which is the fundamental unit for energy production in our cells.  In addition to being essential for generating energy, CoQ is an important antioxidant.  The heart, with its high energy requirements, is especially rich in CoQ.  (15,16)

1.     CoQ deficiency is a significant part of myocardial failure.

2.  CoQ improves cardiac response to exercise.

3.  End stage heart failure patients who supplement with CoQ have a 

40% survival rate compared to a 10% survival rate without CoQ.

4.      CoQ lowers blood pressure.

5.     CoQ reduces angina.

6.  CoQ prevents arrythmias.

DISPERSING AGENTS.  Potassium, when combined with a trivalent anion such as citrate or phosphate, functions as a dispersing agent.  As such, it helps maintain the electronegative colloidal properties of the body fluids.  It thus helps prevent precipitation of sludge in the arterial system and reduces the load on the heart.  It also facilitates the elimination of excess sodium salts by the kidneys.  (17)

TAURINE.  Taurine is an amino acid-like substance containing a sulfhydril functional group.  (18,19)

1.       Taurine reverses the adverse effects on CVD of excess catecholamines.

2.       Taurine also reverses the damage done by excess insulin levels in

3.       patients with insulin insensitivity carbohydrate intolerance.  There are studies estimating that perhaps in excess of 60% of all CVD is associated to some degree with poor carbohydrate tolerance along with the associated excess insulin levels.  (20)

4.       Taurine parallels magnesium in its beneficial effects on the heart and vascular system.

5.       Taurine antagonizes the central action of excess angiotensin II.  It thus lowers the blood pressure while at the same time reducing excess sympathetic activity.

6.       Along with decreasing blood pressure, Taurine protects the heart against excess calcium binding, but without the life-threatening side effects of calcium channel blockers.

7.       Taurine prevents cardiac arrythmias.

8.       Taurine reduces excess vaso-constriction.

9.       Taurine decreases the incidence of strokes.

10.  Taurine lowers cholesterol.

11.  Taurine possesses anti-thrombotic properties.

12.  Taurine prevents angina.

HISTIDINE.  Histidine is the most effective naturally occurring singlet oxygen scavenger.  That makes it probably the most important antioxidant found in our diet.  This antioxidant activity of Histidine has a specific protective effect on the arterial intima of your CVD patients.  Histidine is a vaso-dilator and thus decreases blood pressure.  Studies have also shown that Histidine decreases angina pain.

METHIONINE.  Methionine is a sulfur-containing amino acid.  Its active sulfur group assists in detoxification processes in the liver.  Most particularly, as regards CVD patients, Methionine is lipotrophic.  It helps the liver process and eliminate cholesterol and triglycerides.  (21)

With such an amazing array of high-powered ammunition to fight cardiovascular disease, the chiropractic nutritionist can provide patient service unmatched by any other health care provider.  How, then, does one make use of these powerful protective nutrients?  Little benefit is to be gained from taking a shotgun approach by prescribing all the above listed nutrients (plus the many others important to CVD patients).  To effectively rehabilitate a patient's cardiovascular-renal system requires that the clinician analyze the specific needs of that individual.

CVD has an anabolic component, and it has a catabolic component; it can involve vaso-constriction; it can involve insufficient oxidation and it can involve excess free radical oxidation; it can involve excess catecholamines, excess cortisol, and/or excess insulin; it can involve a respiratory acidosis or a potassium depletion alkalosis.  (22,23)

What you need is the means to systematically analyze each individual patient's metabolic imbalances.  Having identified through objective clinical testing the specific metabolic imbalances associated with a particular patient's CVD, you may then prescribe precisely the nutrition regimen that will most favorably impact that particular case. (24)

Such an analysis was performed on our old friend Delmar.  Delmar was found to have a strong anabolic component and a strong catecholamine component to his vascular disease, along with the carbohydrate intolerance and renal dysfunction associated with his diabetes.  Within three weeks of beginning his individualized nutrition regimen based on specific nutrition testing protocol, Delmar's blood pressure had decreased from 164/104 to 130/80. 

    From that point on, the patient began to experience gradual improvement in his leg function.  He had a little less numbness and a little more strength after each week.  He also reported an over-all increase in energy level.  The way he described it was, "I seem to have a lot more ambition."

Within three months of beginning his specific nutrition program Delmar showed a urinary glucose reading of only 250.  He had never before been even close to dropping below 2000.  Delmar was so excited he began to test himself regularly at home, and within a month his urinary glucose was totally clear.  He then went five weeks without a single trace of glucose in his urine.  In the many months subsequent to that his highest glucose reading was 500, and that was only after "cheating" on his diet at the county fair.

There are several important clinical tests which must be performed to thoroughly evaluate each patient's status with respect to the potential for CVD.  One of the most important of these is the measurement of the urine surface tension.  The surface tension measures the degree to which the body fluids have lost their colloidal properties.  It also tells much about the potential for anabolic vs. catabolic damage to the cardiovascular system.  (25)

Another important consideration in evaluating a patient for CVD is, obviously, the blood pressure.  But more important than the actual level of blood pressure are considerations such as the ratio of the systolic blood pressure to the diastolic blood pressure.  Another even more important consideration is the response of the blood pressure to orthostatic challenge.  A decompensated heart or an inelastic vasculature will show telltale signs in response to these tests.  (26)

     The patient's pulse must also be thoroughly examined. The pulse must be tested in the supine position and then its clinostatic response evaluated upon standing.  Finally, a resting pulse in the standing position must be compared to the recumbent pulse.  A test procedure involving one recumbent pulse, one recumbent blood pressure, then three standing pulses and one standing blood pressure has proved to yield a tremendous amount of clinical information about the cardiovascular-renal system.  Such testing has the advantage of being performed in just a few minutes time and right in the clinician's office.

Another case history is warranted here: Elsie was a 71 year old, moderately obese woman who had been a chiropractic patient in our office for several years, during which we fairly well controlled some pretty extreme back, hip, and leg pain.  Recently she mentioned her concern over her heart.  She had had a heart attack seven years ago and was being medicated with Tenormin (a beta-blocker) and Isordil (a vaso-dilator).  A recent visit to her cardiologist had revealed her heart was substantially enlarged.  She knew of our nutrition work from friends who had benefited, and asked what we could do to help her heart.  Our testing for nutrition-related metabolic imbalances revealed exactly what causes underlay her CVD.

Her blood pressure and pulse combinations were: 

168                        166

  94                          96

  60     72     72        76

There are two points to note about these blood pressures and pulses.  First, these high blood pressures existed despite the blood pressure medication she was taking.  Second, the first three of her pulses are actually artificially low readings because she had such an extreme arrhythmia that she skipped several beats during each counting of her pulse.

The patient was put on the regimen indicated by her objective clinical test pattern.  In only three weeks time her blood pressure and pulse readings were as follows:

144                                  146

  80                                    82

  76          80          84        80

Not only were her blood pressures restored essentially to normal, but there was not a single skipped beat in any of her four pulses.  In other words, specific nutrition had done in three weeks what Tenormin and Isordil had failed to do in seven years.

    One very important point you must realize is that Delmar and Elsie received entirely different recommendations, both as regards supplementation and diet.  In other words, neither was given an allopathic treatment protocol for cardiovascular disease.  Quite the contrary, each was given a specific nutrition plan based on the specific test pattern demonstrated on the 43 tests that make up the analysis.

Carefully consider what you have just read.  Think about the change in Delmar's and Elsie's blood pressures and pulses.  Think about the power returning to Delmar's legs.  Think about his severe diabetic condition being brought under control.  Consider Elsie's life threatening arrhythmia disappearing within three weeks.

Are such gratifying clinical results within your capabilities?  Certainly so, as there are hundreds of Doctors employing such an analytical system of clinical nutrition.  Is the treatment of cardiovascular disease within your scope of practice?  Not per se.  But the philosophy underlying the proper use of clinical nutrition is very much in parallel with chiropractic philosophy.

Chiropractic takes a patient-specific approach to health care.  In other words, chiropractic is not so much a matter of treating conditions or symptoms as it is restoring normal neuro-musculo-skeletal function such that the body heals and maintains itself.  Such is the proper approach to clinical nutrition.  With an analytical system of clinical nutrition you can take a patient-specific approach to restoring metabolic balance rather than treating diseases or conditions. (27)

What this article has demonstrated is that once metabolic balance is restored, many conditions, even including the severe pathology associated with cardiovascular disease, can respond most satisfactorily.

REFERENCES

1)       Willix, R.D., "Maximum Health," Agora, Inc., Baltimore, MD., 1993.

2)       New England Journal of Medicine, October, 1996.

3)       New England Journal of Medicine, June 1994.

4)       Lancet, January, 1996.

5)       Morrison, Lester, JAMA July, 1969.

6)       Bradford, R.W., Allen H. W., "The Biochemistry of Chondroitin Sulfate," Bradford Research Institute, BRI Report #1.

7)       Felton, G., Fibrinolytic and antithrombic action of bromelain in heart patients, Med Hypoth 6: 1980.

8)       Burch, G.E., & Giles T.D., 1977. "The Importance of Magnesium Deficiency in Cardiovascular Disease." Amer. Heart J., 94:649-657.

9)       Altura, B., et al, 1981. "Hypomagnesemia and Vaso-Constriction:  Possible Relationship to Etiology of Sudden Death Ischemic Heart Disease and Hypertensive Vascular Diseases."  Artery 9(3) 212-231.

10)  Whang, R., et al 1982, "Hypomagnesemia and Hypokalemia in 1,000

Treated Ambulatory Hypertensive Patients." J. Amer. College Nutr.,

1:317-322.

11)  Nieper, H.:  Mineral Transporters, PPNF Journal, Vol. 9, 4, 1985.

12)  Fritz, I. et al, "Specificity of Carnitine Actions of Fatty Acid Oxidation 

by Heart Muscle."  Am. J. Physiol. 202:117-121, 1962.

13)  Maebashi, N. et al, "Lipid-lowering Effect Of Carnitine in Patients

with Type IV Hyperlipoproteinaemia."  Lancet 2:805-807, 1978.

14)  Thomsen, et al: "Improved Stress Tolerance of the Ischemic Human

Myocardium After Carnitine Administration."  J. Amer. Cardiology

39:289, 1977.

15)  Van Gaal, et al, 1984.  "Biomedical and Clinical Aspects of Co-

Enzyme Q," Volume 4  p.369. Biomedical Medical Press, New York.

16)  Folkers, K. et al, Biochemical Rational and Myocardial Tissue Data

on Cardiomyopothy Therapy with Co-Enzyme Q 10. Proc. Natl. Acad.

Sci., 1985 82, 901-904.

17)  Riddick, Thomas M. "Control of Colloid Stability Through Zeta 

Potential," Livingston Press, Wynnewood, Pennsylvania, 1968.

18)  Kagaku, et al:  "Effective Taurine on Cholesterol Metabolism," Chem.

Absts. 103, 1985.

19)  Azuma, J.:  " Taurine for Treatment of Congestive Heart Failure," Int.

J. Cardi. 2:303-304, 1982.

20)  Circulation, May 1996.

21)  Rivici, Emmanuel:  "Research in Physiopathology As A Basis Of

Guided Chemotherapy," New York, 1961.

22)  Davenport, Horace:  "Acid-Base Chemistry For Medical Students and

Physicans,"  University of Chicago Press, Chicago, 1958.

23)  Rivici, op. cit.

24)  Schenker, Guy R. "An Analytical System of Clinical Nutrition,"

Pennsylvania, 1995.

25)  Rivici, op. cit.

26)  Low, Phillip A. "Clinical Autonomic Disorders," Little, Brown and

Company, Boston, 1993.

27)  Schenker, op. cit.