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Dynamic Chiropractic – December 2, 2010, Vol. 28, Issue 25

A Blood Drive for Chiropractic

By Anthony Rosner, PhD, LLD [Hon.], LLC

The indomitable and eminently quotable Teddy Roosevelt once declared, "A man who is good enough to shed his blood for the country is good enough to be given a square deal afterwards." Without too much wordsmithing, I could easily substitute "clinician" for "country" and "diagnosis" for "deal" and wind up with: "A man who is good enough to shed his blood for the clinician is good enough to be given a square diagnosis afterwards" or "A physician who is good enough to draw blood from the patient is good enough to give a square deal afterwards."

This is my plea for enabling clinicians - particularly doctors of chiropractic - to perform more intensive and intelligent bloodwork in their diagnostic examinations. Almost two decades ago, when I first considered getting into chiropractic research, already having had extensive experience directing clinical chemistry programs at a Harvard teaching hospital and then at an affiliate of the Mayo Clinic, I was deeply impressed by the curricula in laboratory diagnosis offered by such chiropractic institutions as National and Northwestern. My feeling was that with this exposure, the chiropractic profession was being given the tools to arrive at early and significant diagnoses in their patient examinations - particularly since I had seen poor preparation in this area for hospital staff and actually had designed my own course in clinical chemistry to try to rectify this situation. The reality, unfortunately, is that state regulations involving blood drawing often act as one of several disincentives for chiropractors to put such a powerful diagnostic tool into everyday practice.

blood work - Copyright – Stock Photo / Register Mark The fact remains, however, that if the term subluxation is to be viewed from a progressive, 21st century perspective (as I have suggested in this space previously),5 it is pertinent to consider a variety of early warning signs throughout the body beyond fixations within the spine. These would include abnormal levels of an assortment of analytes within the blood serum that may very well occur subclinically, but that would still qualify as early indications for prompt intervention. The table below is but the smallest sampling of clinical problems that are disclosed with what have become routine determinations in blood serum alone, often automated.

Other analytes that may impress some as being a bit removed from the beaten track, but which are still easily assayed, include aldosterone and homocysteine. Elevated levels of aldosterone may be of significance in that they are associated not only with elevated blood pressure,6 but also vascular inflammation leading to congestive heart failure.7 The situation with homocysteine is far more complex, since elevated levels have been linked to vascular disease,8 cervical artery dissection,9 stroke,10 bone resorption,11 leukoariosis (white matter disease),12 brain natruietic peptide (associated with chronic heart failure),13-14 and hearing loss.15 Finally, interleukin-6 acts as a pro-inflammatory cytokine which is secreted by T-cells and macrophages to stimulate immune responses to trauma. It runs into trouble in that it functions as a key intermediate in the formation and rupture of atherosclerotic deposits along the arterial wall,16-17 eventually leading to cardiovascular events such as myocardial infarctions.

It turns out that there is more than just a casual connection of blood chemistry to chiropractic. Besides just making good sense to inform the patient, knowing about the levels of such analytes as these has resulted in several lines of research that speak loudly to the potential value of spinal manipulation beyond the musculoskeletal system:

  • Spinal manipulation appears, at least in the short term, to decrease levels of interleukin-618-19 and C-reactive protein,19 in addition to the inflammatory intermediate tumor necrosis factor,18-20 the latter being linked to the initiation of pain in the L5 vertebral region.21
  • Spinal manipulation with cavitations may also be associated with the suppression of the pro-inflammatory cytokine interleukin-2 under certain conditions.22
  • Spinal manipulation with cavitations has been linked to increased levels of the anti-inflammatory cytokine interleukin-10 in asymptomatic subjects.23
  • A pilot clinical trial has suggested that spinal manipulation is capable of reducing levels of serum aldosterone.24
  • Anti-oxidative activity (which would suppress inflammation and aging) through the stimulation of catalase activity has been shown to be a consequence of spinal manipulation.25
  • In just a single case study, the administration of spinal manipulation has led to the reduction of glycosylated hemoglobin. This is suggested to be an indication that the effects of diabetes in this particular patient may have been reversed.

What these preliminary data tell us is that there are systemic indicators of metabolic imbalances that are measurable through the assay of blood serum components which cannot be ignored. Several lines of evidence also point to the conclusion that spinal manipulation may lead, at least in the short term, to the suppression of inflammatory intermediates, many of which lead to coronary heart disease26 and the vascular effects which so often and often so erroneously have often been said to be the consequence of cervical manipulation.27-28

Serum blood determinations have much to do with the future of both the practice and research of chiropractic, and as such should be strongly encouraged. The conceptual limitation of spinal manipulation to vertebral fixations without this broader view is, in my opinion, an impediment to the potentials of chiropractic as an integrated approach to health care.

Enzymes [elevations]:    
Acid phosphatase
Alanine aminotransferase
Alkaline phosphatase
Aspartate aminotransferase

Creatine kinase
Glutamate dehydrogenase
N-glutamyl transferase
Lactate dehydrogenase
  Carcinoma of prostate
Hepatic parenchymal disease
Muscle disease
Bone and hepatobiliary diseases
Pancreatic diseases
Myocardial infarction, hepatic parenchymal
Diseases, muscle disease
Myocardial infarction, muscle diseases
Hepatic parenchymal disease
Hepatobiliary disease, alcoholism
Hepatic parenchymal disease
Pancreatic diseases
IgG elevation
IgA elevation
IgM elevation
Monoclonal Ig's (paraproteins)
Alpha-antitrypsin defi ciency

C-reactive protein (CRP)3 elevation
Interleukin-6 elevation4
  Autoimmune response
Skin, gut, respiratory, renal infections
Primary viral infections, blood serum infection
Congenital defi ciency, neonatal respiratory
distress syndrome
Myocardial infarction
Myocardial infarction risk factor
Atherosclerosis intermediate, CRP precursor
Carbohydrates [elevations]:    
Glycosylated hemoglobin
  Diabetes mellitus
Diabetes mellitus
Sodium defi ciency

Sodium elevation

Potassium defi ciency

Potassium excess
Chloride defi ciency

Chloride excess
Total carbon dioxide defi ciency
Total carbon dioxide elevation
  Excessive sweating, prolonged vomiting,
severe polyruria, metabolic acidosis
Hyperaldosteronism, hyperadrenocorticism
(Cushing's syndrome)
Alkalosis, primary or secondary aldosteronism,
postoperative therapy with potassium-poor
Acute or end-stage renal failure
Salt-losing nephritis, certain metabolic
acidoses, prolonged vomiting
Dehydration, renal tubular acidosis, acute renal
Renal failure, respiratory alkalosis
Metabolic alkalosis, respiratory acidosis


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  2. Antman EM, ST-Elevation myocardial infarction: Management. In: LibbyP, Bonow RO, Mann DL, Zipes DP [Eds]. Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th Editiion. Philadelphia, PA: Saunders, 2007. Chapter 51.
  3. Verma S, Devaraj S, Jialal I. C-reactive protein promotes atherothrombosis. Circulation, 2006; 113: 2135-2150.
  4. Danesh J, Whincup P, Walker M, Lennon L, Thomson A, Appleby P, et al. Low grade inflammation and coronary heart disease: Prospective study and updated meta-analyses. British Medical Journal, 2000; 321: 199-204.
  5. Rosner A. "Revisiting the S-Word: A Fresh Look at the Subluxation." Dynamic Chiropractic, April 9, 2010; 28(8).
  6. Whaley-Connell A, Johnson MS, Sowers JR. Aldosterone: Role in the cardiometabolic syndrome and resistant hypertension. Progress in Cardiovascular Diseases, 2010; 52(5): 401-409.
  7. Weber KT. Aldosterone in congestive heart failure. New England Journal of Medicine, 2001; 345(23): 1689-1697.
  8. Graham IM, Daley LE, Refsum HM, et al. Plasma homocysteine as a risk factor for vascular disease: The European Concerted Action Project. Journal of the American Medical Association, 1997; 277: 1775-1781.
  9. Gallai V, Caso V, Paciaroni M, Cardaioli G, Arning E, Bottiglieri T, Pernetti L. Mild hyperhomocyst(e)inemia: a possible risk factor for cervical artery dissection. Stroke, 2001; 32: 714-718.
  10. Tanne D, Halm M, Goldbourt U, Boyko V, Doolman R, Adler Y, Brunner D, Behar S, Sela B-A. Prospective study of serum homocysteine and risk of ischemic stroke among patients with preexisting coronary heart disease. Stroke, 2003; 34: 632-636.
  11. Hermann M, Widmann T, Colaianni G, Colucci S, Zallone A, Herrmann W. Increased osteoclast activity in the presence of increased homocysteine concentrations. Clinical Chemistry, 2005; 51(12): 2348-2353.
  12. Censori B, Partziguian T, Manara O, Poloni M. Plasma homocysteine and severe white matter disease. Neurological Science, 2007; 28(5): 259-263.
  13. Hermann M, Hermann M, Joseph J, Tyagi SC. Homocysteine, brain natriuretic peptide and chronic heart failure: a critical review. Clinical Chemistry and Laboratory Medicine, 2007: 45(12): 1633-1644.
  14. Tucker KL, Qiao N, Scott T, Rosenberg I, Spiro A III. High homocysteine and low B vitamins predict cognitive decline in aging men: the Veterans Affairs Normative Aging Study. American Journal of Clinical Nutrition, 2005; 82: 627-635.
  15. Gopinath B, Mitchell P, et al. Serum homocysteine and folate concentrations are associated with prevalent age-related hearing loss. Journal of Nutrition, June 23, 2010 [Epub ahead of print].
  16. Packard RS, Libby P. Inflammation in atherosclerosis: from vascular biology to biomarker discovery and risk prediction. Clinical Chemistry, 2008; 54(1): 24-38.
  17. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation, 2002; 105: 1135-1143.
  18. Teodorczyk-Injeyan JA, Injeyan HS, Ruegg R. Spinal manipulative therapy reduces inflammatory cytokines but not substance P production in normal subjects. Journal of Manipulative and Physiological Therapeutics, 2006; 29(1): 14-21.
  19. Roy RA, Boucher JP, Comtois AS. Inflammatory response following a short-term course of chiropractic treatment in subjects with and without chronic low back pain. Journal of Chiropractic Medicine, 2010; 9: 107-114.
  20. Ormos G, Mehnishi JN, Bakacs T. Reduction in high blood tumor necrosis factor alpha levels after manipulative therapy in 2 cervicogenic headache patients. Journal of Manipulative and Physiological Therapeutics, 2009; 32(7): 586-591.
  21. Xu J-T, Xin W-J, Zang Y, Wu C-Y, Liu X-G. The role of tumor necrosis factor-alpha in the neuropathic pain induced by lumbar 5 ventral root transection in rat. Pain, 2006; 123: 306-321.
  22. Teodorczyk-Injeyan JA, McGregor M, Ruegg R, Injeyan HS. Interleukin-2-regulated in vitro antibody production following a single spinal manipulative treatment in normal subjects. Chiropractic & Osteopathy, 2010; 18: 26 doi: 10.1186/1746-1340-18-26. D
  23. Teodorczyk-Injeyan JA, Injeyan HS, Ruegg R. Spinal manipulative therapy [SMT] augments production of anti-inflammatory cytokine IL-10 in normal subjects. Proceedings of 9th Biennial Congress of the World Federation of Chiropractic, pp. 143-144.
  24. Wagnon RJ, Sandefur RM, Ratliff CR. Serum aldosterone changes after specific chiropractic manipulation. American Journal of Chiropractic Medicine, 1988; 1(2): 66-70.
  25. Kolberg C, Horst A, Kolberg A, Bello-Klein A, Partata WA. Effects of high-velocity, low-amplitude manipulation on catalase activity in men with neck pain. Journal of Manipulative and Physiological Therapeutics, 2010; 33(4): 300-307.
  26. Danesh J, Whincup P, Walker M, Lennon L, Thomson A, Appleby P, et al. Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses. British Medical Journal, 2000; 321: 199-204.
  27. Rosner A. CVA risks in perspective. Manuelle Medizin, 2003; 3: 1-9
  28. Rosner A. Spontaneous cervical artery dissections: another perspective. Journal of Manipulative and Physiological Therapeutics, 2004; 27(2): 124-132.

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