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Chiropractic News

March 2008

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Medicine’s new direction

Osteoarthritis, rheumatoid arthritis, osteoporosis, periodontal disease, coronary heart disease, metabolic syndrome, and type-2 diabetes — these common and very different diseases typically require separate and different medical protocols.
 
In August 2007, a collaborative group of medical scientists from Columbia University, University of Cambridge, Penn State Medical Center, Northwestern University School of Medicine, and the Laboratory for Endocrinology Research in Lyon, France, authored a research paper that caught the attention of the medical world.
 
Their conclusion: The skeleton is an endocrine organ and has an effect on insulin signaling and adiponectin expression in adipocytes (fat cells).1
 
This extraordinary discovery links obesity, insulin resistance/metabolic syndrome, diabetes, and heart disease to bone physiology and the bone-derived hormone osteocalcin that regulates energy metabolism and the insulin/glucose axis.
 
Osteocalcin “speaks” to adipocytes and insulin secreting beta-cells of the pancreas, and influences both insulin action and insulin-sensitizing and the anti-inflammatory protein adiponectin.
 
In essence, the report defined skeletal health and function as principle factors in the risk to diseases of metabolism and demonstrated a direct relationship between skeletal health and the prevention of diabetes and heart disease.

BEYOND ‘WEAR AND TEAR’
 
Skeletal health is dependent upon lifestyle, genetic, structural, and nutritional factors. The lack of weight-bearing activities reduces the activity of the bone rebuilding osteoblast, in turn reducing the release of osteocalcin. The reduction in osteocalcin adversely influences insulin signaling and increases the risk to many chronic diseases. These same factors play important roles in maintaining the functional health of the bone remodeling cells: osteoblasts and osteoclasts.
 
The complex interconnections among these various cell types help explain the recent recognition of the connection between osteoarthritis and rheumatoid arthritis. We now know osteoarthritis is not simply the result of “wear and tear” on the joint. Rather, it results from an inflammatory process that engages bone, synovium, connective tissue, and joint lubricant substances.
 
Inflammatory processes are found in the joint space with increased osteoclastogenesis and angiogenesis, the hallmarks of progressive osteoarthritis.2
 
Musculoskeletal integrity is critically important in reducing the risk to inflammation. The problem in osteoarthritis is not just wear and tear; it is how the musculoskeletal system responds to stress factors influencing the release of inflammatory mediators, such as interleukin-1, interleukin-6, or tumor necrosis factor alpha.
 
That these characteristics are also factors in the etiology of rheumatoid arthritis suggests a common therapeutic approach to the prevention and management of both conditions.

MODIFYING KINASE ACTIVITY
 
The inflammatory signaling process connecting the etiology of these seemingly disparate diseases is, to a great extent, regulated by the activity of a family of enzymes termed “kinases.” Produced in every cell, kinases regulate the translation of events that occur outside the cell to the genes of the cell, triggering various cellular events, such as the inflammatory response.
 
The activation of the inflammatory family of kinases may result in a variety of clinical effects, such as type-2 diabetes, arthritis, heart disease, metabolic syndrome, and even certain forms of cancer.3
Certain phytonutrients and other natural compounds have been found to modulate kinase function and serve as “brakes” that help prevent the inflammatory process from running out of control.4 Well-publicized examples of such compounds include hops-derived reduced iso-alpha acids and O-methylated catechins from tea leaves.5,6
 
These compounds may be used in supplementary form to “reset” inflammatory kinase signaling, thereby influencing any cell types that have enhanced inflammatory functions. Their role in regulating the signaling that induces the primary cause of the disease suggests these compounds have promise as a new class of therapeutics that treats the intersection of the cause of a family of chronic diseases with a shared mechanism of origin.7

CROSS TALK AND SYSTEMIC DISEASE
 
Altered mechanical signaling through the connective tissue and fascia has been found to increase the production of inflammatory mediators that may contribute to the potentiation of the underlying cause of diseases as far ranging as arthritis, type-2 diabetes, and bone loss of osteoporosis.8
 
This discovery suggests a mechanistic role for physical medicine, structural medicine, and acupuncture in the treatment of these conditions.9
 
Interesting, too, is the fact that in September 2007 the National Institutes of Health provided funding for the first international conference on fascia.10 This conference brought together bodywork practitioners with basic scientists to better understand the role of fascia in chronic disease and what can be done to improve its
function.
 
Out of the conference emerged the recognition that the extracellular matrix, with its component connective tissue, serves not only a structural role, but also a signaling role, translating outside information to various cells. The translation of these messages through the fascia affects kinase signaling and different inflammatory responses.
 
This once again demonstrates the “cross talk” that occurs among different tissues that sets up the potential for many different diseases.
 
In another example, it is increasingly accepted that obesity, in and of itself, does not cause diabetes and heart disease. Rather, obesity is an effect of a process associated with the infiltration of various tissues, such as the fat tissue, with pro-inflammatory immune cells.11 This inflammatory process triggers the pathology of obesity and relates to the cause of type-2 diabetes and heart disease.
 
For obese patients, a treatment plan that seeks to nutritionally modulate kinases associated with the inflammatory process while improving body composition may be a more effective approach than weight loss alone.

CLINICAL APPLICATIONS
 
These extraordinary recent advances in the understanding of the etiology of chronic diseases that previously seemed so different from one another have now created the understanding that they all share common mechanisms of etiology. Rather than treating the disease effect, the new medicine is to treat the cause.
Additionally, environmental factors, such as chronic infection, xenobiotic or heavy-metal toxicity, or intestinal dysbiosis and food allergy can increase the inflammatory response. These are modifiable if the practitioner asks the patient the correct questions, including questions about family history, personal health history, diet, environment, lifestyle, and exercise patterns.
 
Consequently, a patient with a history of chronic inflammatory disorders would be a candidate for a personalized intervention program that incorporates regular musculoskeletal therapy and a healthy diet, plus nutritional intervention that might include a low-allergy-potential diet; supplementary intake of anti-inflammatory phytonutrients that modulate kinase function; fish oils containing omega-3 EPA/DHA; and botanicals, such as Curcumin, Boswellia serata, and ginger.
 
Supplementation with probiotics, such as specific strains of Lactobaccilli and Bifidobacterium, might also be administered to improve gastrointestinal immune function and reduce inflammation.
 
These are exciting times related to the advancement in the understanding of the mechanisms of origin of chronic disease. These advancements are timely because, if a new model for the prevention and management of chronic disease is not soon found, the rising tide of age-related chronic disease will economically drown the aging baby boomers in healthcare expenditures.
 
The news from the latest research indicates a new paradigm in healthcare is evolving, and with it, a validation of the importance of a functional medicine approach to chronic disease that integrates lifestyle, environment, physical and structural medicine, diet, and nutrient therapies, with the focus on managing the intersection of the root cause of the diseases.

Jeffrey Bland, PhD, FACN, is the chief science officer of Metagenics Inc. and president of MetaProteomics in Gig Harbor, Wash. In 1991, he founded the Institute for Functional Medicine. He can be reached at 800-692-9400 or through the Web site, www.metagenics.com.

References
 
1 Lee NK, Sowa H, Hinoi E, et al. Endocrine regulation of energy metabolism by the skeleton. Cell. 2007;130(3):456-469.
 
2 Bonnet CS, Walsh DA. Osteoarthritis, angiogenesis and inflammation. Rheumatology. 2005;44:7-16.
 
3 Bain J, McLauchlan H, Elliott M, Cohen P. The specificities of protein kinase inhibitors: an update. Biochem J. 2003;371(Pt 1):199-204.
 
4 Suzuki T, Miyata N. Epigenetic control using natural products and synthetic molecules. Curr Med Chem. 2006:13(8):935-958.
 
5 Minich DM, Bland JS, Katke J, et al. Clinical safety and efficacy of NG440: a novel combination of rho iso-alpha acids from hops, rosemary, and oleanolic acid for inflammatory conditions. Can J Physiol Pharmacol. 2007;85(9):872-883.
 
6 Maeda-Yamamoto M, Inagaki N, Kitaura J, et al. O-methylated catechins from tea leaves inhibit multiple protein kinases in mast cells. J Immunol. 2004;172(7):4486-4492.
 
7 Lila MA. From beans to berries and beyond: teamwork between plant chemicals for protection of optimal human health. Ann N Y Acad Sci. 2007;1114:372-380.
 
8 Langevin HM, Churchill DL, Cipolla MJ. Mechanical signaling through connective tissue: a mechanism for the therapeutic effect of acupuncture. FASEB J. 2001;15(12):2275-2282.
 
9 Langevin HM, Yandow JA. Relationship of acupuncture points and meridians to connective tissue planes. Anat Rec. 2002;269(6):
257-265.
 
10 Grimm D. Cell biology meets rolfing. Science. 2007;318:
1234-1235.
 
11 Segenès C, Miranville A, Lolmède K, Curat CA, Bouloumiè A. The role of endothelial cells in inflamed adipose tissue. J Intern Med. 2007;262:415-421.




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