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dr kendann cbd cream

At our last visit, Dr. Stewart had some news that he was excited to share with us. He had identified four compounds that, in his research, proved to help turn chronic inflammation down—and even off—in individuals with faulty switches.

The beautiful thing is that this genetic testing requires no needles, no poking, no prodding. Simply request a 55 Gene Test Kit from a Genomix Nutrition Provider or good friend of mine and Nutrition Therapist, Christy Thiel.

But onward we go.

Vanilla Bean

The Inflammation: What It is and How Does it Affect Our Health Coffee With Doctor Stewart podcast episode goes into greater detail about these latest techniques for managing chronic inflammation, be sure to give it a listen.

“Let’s remove this food, experiment with that supplement, try this therapy and see what happens.’

If you were to see Dr. Stewart today, the first thing he’d want to do is take a good look at your genes—particularly your genetic abnormalities. He’d do this with a simple cheek swab. Soon enough you’d realize what a game changer knowing your genetic weaknesses can be.

Inflammation has affected his speech and movement, and has landed him in the hospital with asthma more times than I want to recount.

As a measure of spontaneous pain, limb posture was scored daily in the morning while animals were in their home cages by a scientist blinded to the animal’s treatment. A subjective pain-related behavioural scale was used (Sluka et al., 1993) with 0 – normal; 1 – curling of the toes, 2 – eversion of the paw; 3 – partial weight bearing; 4 – non-weight bearing and guarding and 5 – avoidance of any contact with the hindlimb.

Immunocytochemical localization of inflammatory biomarkers. (A) CGRP and (B) OX42 are shown in ipsilateral spinal cord dorsal horn for naïve, complete Freud’s adjuvant (CFA) arthritic and cannabidiol (CBD) treated CFA arthritic rats. (C) TNFα is shown in the ipsilateral dorsal root ganglia of naïve, CFA arthritic and CBD treated CFA arthritic rats. Bar = 100 μm.

2.3 Assessment of joint inflammation

Almost 50 million (22.2%) adult Americans over 18 were diagnosed with arthritis in 2007–2009, most prominently osteoarthritis and the autoimmune disease rheumatoid arthritis. A projected increase to 67 million is anticipated by 2030 (Centers for Disease Control and Prevention (CDC), 2010). The most effective treatment for rheumatoid arthritis is injectable fusion-proteins which sequester the most prominent proinflammatory cytokine tumour necrosis factor α (TNFα). These chimeric antibodies may halt progression of the disease, but side-effects include immune suppression (Crawford and Curtis, 2008; Furst, 2010; Hastings et al., 2010). Neurogenic drive also contributes to severity of arthritic inflammation (Sluka et al., 1994), and may contribute to its reoccurrence.

The pro-inflammatory/pro-pain spiral is further driven by similar mechanisms which induce the expression of pro-inflammatory biomarkers in the DRG of the afferent nerves and centrally in the spinal cord. Transdermal CBD application was successful in decreasing monoarthritis-associated increases of pro-inflammatory biomarkers in neuronal tissues. Here, adjuvant-induced monoarthritis led to significant increases of TNFα expression in DRG which was decreased to baseline levels by transdermal CBD application.

Peripheral inflammation and hypersensitivity are reversed by pharmacological inactivation of both central and peripheral neurons and central microglia (Sluka et al., 1993, 1994; Guo and Schluesener, 2006; Roberts et al., 2009). Although CBD is described as an attenuator of both mechanical and heat hypersensitivity induced by inflammatory and neuropathic pain models, the exact mechanism of action is as yet unknown (Mechoulam and Hanus, 2002; Kress and Kuner, 2009). Unlike THC and related cannabinoids, phytocannabinoid-CBD, an important bioactive component of Cannabis sativa without psychotropic effect, is an antagonist of orphan G protein-coupled receptor 55 (GPR55, a potential third metabotropic cannabinoid receptor) without binding to CB1 and CB2 receptors (Begg et al., 2005; Brown, 2007). CBD interacts with GPR55 resulting in inactivation of its pronociceptive signalling (Ryberg et al., 2007; Staton et al., 2008; Godlewski et al., 2009).