Here is my Lipid panel from 12 weeks ago and then recently on 12/30. The blood is analyzed in-house so I had results the next day. The only difference in my lifestyle was the berberine which I did not even take religiously and a can of sardines here and there. I did filll my prescription for Crestor (a statin) and stared at the bottle religiously every morning, but did not take it.
The studies with Berberine claimed this would happen. The studies also claim it will help build up our pathetic D2 receptors and beat down the excitatory D1 receptors. Gives one pause.
Standard Range
10/6/2110/6/2112/30/2112/30/21
CALCULATED LDL
<=129 mg/dL
181 H 140 H
CHOL/HDL
<=4.4
4.6 H 3.3
CHOLESTEROL
<=199 mg/dL
265 H 229 H
Fasting Status
0 - 999 Hours
1212
HDL
>=50 mg/dL
57 69
CALCULATED NON HDL
mg/dL
208 160
TRIGLYCERIDE
<=149 mg/dL
136 101
It’s hard to read, but total cholesterol went from 265 to 229. The bad LDL went from 180 to 140. The good HDL from 57 to 69 and triglycerides went from 136 to 101.
Maybe if I took the berberine everyday like I was supposed to, per the studies, I would be at 200 where the docs want me.
Sometimes I was dissolving with quercetin sometimes not. No difference whatsoever to RLS 😕, but I am a terrible test subject in terms of RLS. My RLS is mild, barely there and/or fleeting. generally. On top of that I take iron every night anyways, usually around 11pm or earlier if I feel a scintilla of restlessness so I negated any opportunity to see if the berberine improved my RLS.
So I really failed miserably to conduct a proper test of berberine’s effect on my RLS. I should have knocked off the iron. I should have taken the berberine religiously and always dissolved it.
I should also clarify that my RLS is barely there as long as I don’t eat anything late or eat a really big dinner. A really big dinner of any make up will lead to an hour or two of what I consider “severe” RLS. Whenever RLS makes it impossible to fall asleep I consider that severe. But an hour or two of severe RLS after my 7pm dinner is way before my bedtime. However, those 12am snack crackers always due me in and I end up having to take extra iron. Some people never learn do they. If the iron didn’t work so well for me I guarantee there would be no late night snacks for me. The point too is that you would think that the berberine would have allowed me to have a big evening meal or that midnight snack without worsening my RLS symptoms. That’s why I feel the berberine has yet to have an affect for me.
Plus and foremost, I didn’t do research and come up with berberine for me or for anyone with “baseline” RLS. I came up with berberine while looking for substances to help people going through augmentation and/or withdrawal from the DAs. I was looking for a substance that would return their receptors back to baseline quicker than time alone. My trialing of it was to see if there were any horrible, unacceptable side effects to this homemade “more bioavailable” berberine.
Anyways, I believe the only way to help people with augmentation and hasten their receptors return to baseline is with a substance that does the direct opposite of the dopamine agonists. Berberine, according to studies on rats, does just the opposite and for that reason should not be taken at any time other than the morning because it can make your symptoms worse before it returns your receptors to baseline. Instead of an agonist, berberine is a dopamine “antagonist” not all that different from SSRIs or melatonin or Benedryl. As a matter of fact if I didn’t happen on berberine I would have trialed benedryl. The substance has to have a very short half life otherwise it’s useless. Benedryl has a good safety profile and a short half life. If it didn’t have a short half life it would inflict too much additional night time suffering in the process of repairing the receptors. SSRIs have too long of a half life and are such a strong dopamine antagonist that even though they may up-regulate those DA down-regulated D2/D3 receptors quicker than time alone…it ain’t worth it.
Nice work. I need to schedule my next blood test. I have been trying inositol in my coffee. Vitamin B8, really it is a sugar. It is less sweet than sugar and mixes well with coffee and tea. I will let you know how I do.
Thanks. I can't keep up. Noting the correlation/ causation link between inflammation and RLS is today's insight. Inflamm->hepcidin increase ->serum iron decrease -> BID -> RLS.
80% of your blood lipids are produced by your liver from glycogen through a process called 'de novo lipogenesis' which are in turn produced from blood sugar when your liver and muscle stores are full, therefore the way to treat high lipids should be to lower your carbohydrate intake. High levels of blood sugar causes chronic inflammation which is the most frequent cause of rls. Taking statins to artificially lower cholesterol has minimal effect in stopping cardiovasclar disease.
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