For 5 years now I’ve been collecting data to help support my claim that RLS is caused by inflammation. The evidence is overwhelming, but still the willingness by anyone to make the required lifestyle changes to lessen their RLS is a rare occurrence. The pharmacological solution still rules.
There are countless stories of people that have become free of their RLS through various natural methods. These methods (as I indicate on my website) always have an anti-inflammatory component to them.
Unfortunately this body of evidence will always be considered “anecdotal” in the eyes of scientists. We’re simply children entertaining the grownups with our wild imagination.
Scientists build truths based solely upon the studies of their peers. That’s the ONLY data that they will consider.
This is why Dr. Weinstock’s study on the relationship between RLS and inflammation was such a groundbreaking event. Even though Dr. Weinstock will not be continuing with further studies of the relationship between RLS and inflammation (due to a lack of funding) others are expanding on his findings.
That includes a study (below) that I just ran across. It was originally published in the Nov. 2012 edition of the scientific journal “Brain, Behavior and Immunity.”
The study clearly demonstrates that there is a direct correlation between elevated C-reactive protein (an indicator of inflammation) and Restless Legs Syndrome.
Here is the study …
“Elevated C-reactive protein is associated with severe periodic leg movements of sleep in patients with restless legs syndrome.”
by Lynn Marie Trotti, Rye DB, De Staercke C, Hooper WC, Quyyumi A, Bliwise DL. Brain Behav Immun. 2012 Nov;26(8):1239-43. doi: 10.1016/j.bbi.2012.06.003. Epub 2012 Jun 26. Emory Program in Sleep, Department of Neurology, Emory University School of Medicine, Atlanta, GA
Restless legs syndrome (RLS) is a common sleep disorder in which urges to move the legs are felt during rest, are felt at night, and are improved by leg movement. RLS has been implicated in the development of cardiovascular disease. Periodic leg movements (PLMs) may be a mediator of this relationship. We evaluated systemic inflammation and PLMs in RLS patients to further assess cardiovascular risk.
137 RLS patients had PLM measurements taken while unmedicated for RLS. Banked plasma was assayed for high sensitivity C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha).
Mean (SD) PLM index was 19.3 (22.0). PLMs were unrelated to TNF-a and IL-6, but were modestly correlated with logCRP (r(129)=0.19, p=0.03). Those patients with at least 45PLMs/h had an odds ratio of 3.56 (95% CI 1.26-10.03, p=0.02, df=1) for having elevated CRP compared to those with fewer than 45PLMs/h. After adjustment for age, race, gender, diabetes, hypertension, hyperlipidemia, inflammatory disorders, CRP-lowering medications, and body mass index, the OR for those with ≥ 45PLMs/h was 8.60 (95% CI 1.23 to 60.17, p=0.03, df=10).
PLMs are associated with increased inflammation, such that those RLS patients with at least 45PLMs/h had more than triple the odds of elevated CRP than those with fewer PLMs. Further investigation into PLMs and inflammation is warranted.