Inspired from Dave Feldman (https://cholesterolcode.com/, https://www.youtube.com/watch?v=jZu52duIqno, https://www.youtube.com/watch?v=kDOHw0qhT0A) I was wondering if someone has tried to observe basic biomarkers and correlate them with RLS severity. For example, has anyone tried to correlate blood sugar, insulin, triglycerides, cholesterol with RLS severity? Do we know if RLS patients tend to have high uric acid? I was wondering about that because one of the talks above mentions coffee sensitivity for some people where drinking coffee has dramatic effect on their blood triglycerides, which immediately reminded me that some RLS sufferers will activate their symptoms with coffee.
Basically, has anyone used a portable device that can measure trigycerides and blood glucose and found some correlation with RLS severity? I guess I'll purchase one of these babies myself, the cheapest devices that can measure triglycerides start around $150. As Feldman notes, of course no one can derive any useful information from sample size one, but the beauty of sample size one is that if 1000 people do the same experiment, it becomes sample size 1000 very quickly.
I can't elaborate on my ideas because most of them are only a gut feeling that there might be a connection. Maybe this: There has been a lot of research recently on consequences of insulin resistence, mechanics of silent inflammation and the role of carbohydrates (which we eat a lot more than 50 years ago) and polyunsaturated fats (the vegetable oils that are now omnipresent in kitchens). Could RLS be caused along the same mechanisms? Alzheimer is "diabetes of the brain", maybe RLS is something similar? Consider the connections:
- We know that diabetics have a fairly high RLS prevalence (https://www.ncbi.nlm.nih.gov/pubmed/30213520), and almost most of us (all people not a low carb diet) have some degree of insulin resistence (IR), that is, most of us are in early stages of diabetes. (Do make sure you are familiar with insulin resistence and the metabolic syndrome, basically we need more and more insulin to process the same amount of carbs over the decades, and diabetes type 2 is just the breaking point where the pancreas breaks down. But that process goes on for everybody on a high-carb diet, and it depends on individual factors whether the pancreas reaches that breaking point or not in the lifetime of the patient).
- Diabetes and IR are driven by carb consumption. Many RLS sufferers report that they get relief from staying away from carbs, especially refined sugar.
- Fructose drives uric acid (not the purine, there are tribes like some Inuit and Masai that used to eat nothing but meat, and they have no gout or diabetes). Uric acid inhibits some reactions in the body which in turn increases inflammation. Inflammation in the brain is assumed to be the main reason for neurologic diseases like Alzheimer, Parkinson, Multiple Sclerosis and others.
- Inflammation is driven by reactive oxygen species (ROS), which do affect the iron metabolism even though many details are fairly unclear (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1221947/pdf/11415455.pdf). But we do know that inflammation raises ferritin values, and it is possible that iron stores are depleted by ROS (after all, iron does react with those ROS like H2O2). Thus, we may have a pathway inflammation/oxydative stress -> low iron stores, but I'm very unsure about this.
As an addendum to the other thread, there is another possibility: Maybe we got it wrong just as we did in Alzheimer research? Maybe BID is a protective mechanism of the brain, as the amyloid plaques in Alzheimer (which appear to protect the brain from further damage, instead of causing the damage as we thought)? Maybe our brain is fighting inflammation and the depletion of the iron stores is just a side effect of that? In that case, iron IVs would solve the visible problem (RLS) but may cause damage because it exacarbates the original problem, possibly a silent inflammation?