According to the Centers for Disease Control and Prevention (CDC), between 2013 and 2015, over 50 million adults have been told that they have osteoarthritis, rheumatoid arthritis, gout, lupus, or fibromyalgia. If you have been diagnosed with any of these, or have begun to feel more pain in your joints and less mobility overall, you are certainly not alone.
A well-known supplemental ingredient, chondroitin sulfate, can help. Chondroitin sulfate is a glycosaminoglycan (often shortened to GAG) which, in turn, makes up cartilage, connective tissue, bone, and skin. It helps extend the life and activity of chondrocytes (cartilage producing cells), reduces inflammation, and strengthens the load-bearing bones in the joints that sit just under the cartilage, called “subchondral” bone.
Often used in combination with glucosamine, chondroitin can help relieve pain by stopping joint damage. And even used alone, it has been shown to reduce the sensation of pain in the MRI brain scans of patients in a clinical study.
So while chondroitin might seem like old news, it doesn’t have to be. Used in conjunction with glucosamine, type II collagen (to help adjust the body’s immune response – especially helpful for people with rheumatoid arthritis), and boswellia to fight 5-LOX inflammation, chondroitin could be one of the best nutrients for restoring your joints.
Monfort J, Pujol J, Contreras-Rodríguez O, et al. Effects of chondroitin sulfate on brain response to painful stimulation in knee osteoarthritis patients. A randomized, double-blind, placebo-controlled functional magnetic resonance imaging study. Med Clin (Barc). 2017 Jun 21;148(12):539-547.
INTRODUCTION: Knee osteoarthritis is causing pain and functional disability. One of the inherent problems with efficacy assessment of pain medication was the lack of objective pain measurements, but functional magnetic resonance imaging (fMRI) has emerged as a useful means to objectify brain response to painful stimulation. We have investigated the effect of chondroitin sulfate (CS) on brain response to knee painful stimulation in patients with knee osteoarthritis using fMRI.
METHODS: Twenty-two patients received CS (800mg/day) and 27 patients placebo, and were assessed at baseline and after 4 months of treatment. Two fMRI tests were conducted in each session by applying painful pressure on the knee interline and on the patella surface. The outcome measurement was attenuation of the response evoked by knee painful stimulation in the brain.
RESULTS: fMRI of patella pain showed significantly greater activation reduction under CS compared with placebo in the region of the mesencephalic periaquecductal gray. The CS group, additionally showed pre/post-treatment activation reduction in the cortical representation of the leg. No effects of CS were detected using the interline pressure test.
CONCLUSIONS: fMRI was sensitive to objectify CS effects on brain response to painful pressure on patellofemoral cartilage, which is consistent with the known CS action on chondrocyte regeneration. The current work yields further support to the utility of fMRI to objectify treatment effects on osteoarthritis pain.