Updated: Oct 16
JOINT DEGENERATION-INSULIN RESISTANCE COMORBIDITY CLINICAL TRIAL IN CANINE SUBJECTS USING SPECIEIS SPECIFIC FORMULATION DESIGN
Clinical Research Division Biologic Nutrigenomic Health Research Corp.
688-2397 King George Hwy, BC V4A 7E9 www.biologicpharmamedical.com
Research/Trial Director: Prof Franco Cavaleri BSc NB
Original post: September 9, 2010
Canine metabolism differs slightly from that of the human but the few metabolic differences can play a monumental role in the treatment of inflammatory cascades. In particular the eicosanoid desaturase activity leading to inflammatory prostaglandins has been intensely investigated in previous studies at Biologic Health Research Corp and reported on by the organization to clinicians and manufacturers of nutrient-based medicines in order to optimize COX efficiency and inhibition in animals with related inflammatory diseases.
These differences justify mild alterations of natural joint protocols studied for human use in order to maximize results and safety for canines. In addition, mild pH, enzymatic and structural differences between human and canine gastro-intestine change the pharmacokinetic potential of these nutrient-based medicines and preventive strategies warranting a repeat of the human trial with these considerations incorporated into the study design.
Irrefutable evidence duplicated and validated at Biologic Health Research in previous investigative trials show that glucosamine does, in fact, have an effect on the hexosamine biosynthetic pathway in glucose-induced insulin resistance. Since joint disease is more common in the aged population, the factors that advance insulin resistance such as age, obesity, lack of physical activity, and even glucosamine supplementation can all compound the problem for these adults and seniors. These additive metabolic influences can reach a point in the patients’ treatment that is insurmountable.
Prolific use of glucosamine warrants further evaluation of safety and justification of concomitant nutraceutical ingredients that circumvent these proven metabolic interferences. In addition, because canines age at a faster rate than humans, the insulin resistance factor can play a more significant role in this equation and must be investigated with species-specific accommodations.
The objective of the clinical trial at Biologic Health Research is to demonstrate that concomitant treatment of joint disease with glucosamine, chondrocyte activators as well as treatment of insulin resistance improves interruption of the disease cycle and improves the course of treatment of what is believed by our investigators to be a true ‘syndrome’ by scientific definition. If these two metabolic pathways (insulin activity & chondrocyte proteoglycan synthesis and the related inflammation) are found to be linked and influenced by glucosamine as suggested in the previous discussion, then the concurrent treatment of both the metabolic and structural syndromes is justifiable for the: i) Prevention of further joint damage ii) Improvement of connective tissue restoration iii) Reduction in the risk or rate of insulin resistance progression to clinical stages of type II diabetes iv) Improvement of lifestyle for reduced risk of obesity and insulin resistance. v) Improvement of glucosamine efficacy at lower doses. vi) Better understanding of glucosamine’s role and secondary effects vii) Clearer understanding of systemic implications of insulin resistance This study premise is being duplicated in human trials and through the multi-species application we may be able to find a more clinically meaningful interpretation of the study results.
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