I lost the statin argument not having any medical standing. I'm helping care for a family member with alzheimers and their neurologist took her off one of the statins and months later we got a message from a lab tech demanding to know why she was taken off the statin.
I brought as much research and studies as the primary care giver/guardian would tolerate in a twenty minute reading session. They seemed unconvinced and ready to be spoonfed whatever pharmacaptured crap a lab tech or bought doc will tell them. It's frustrating but I really do not have any medical standing and can only differ to a system that I no longer trust.
Long story short I stopped my statin a few weeks ago.
Now what should I do? How much magnesium should I take a day? Right now I’m taking 375 mg of mixed OTC magnesium. I have always wondered if I should take more.
Any other recommendations that I could be missing?
"The prevalence of moderate to severe brain atherosclerosis was 54% among 1905-1914 births, 37% for 1915-1919, 30% for 1920-1924, and 22% for 1925-1930, while moderate/severe arteriolosclerosis ranged from 44% for those born from 1905-1914 to 28% from 1925-1930 (χ2 test: P<0.001 across birth year categories). However, there were no differences in age-standardized prevalence of gross chronic infarcts over time, and microinfarcts were more prevalent with later year of birth."
There are SO many variables here, and in these time frames, that I think it irresponsible journalism to lay it at the feet of one (statins) on the basis of sheer speculation. There is not even a speck of data cited for statin use in these populations, or comparators to non-dementia populations.
Also, why more micro-infarcts? Particularly in an era with MORE aggressive treatment of hypertension?
There is still much to understand about tau protein, amyloid, and dementias.
Dementia less bad, or statin use an unidentified confounding variable?
The brain is made of significant amounts of cholesterol and statins, I seem to recall, are associated with dementia for this reason.
https://jnm.snmjournals.org/content/62/supplement_1/102
Jennifer, your research and how you described cholesterol as a calcium cap with electrical destructive power coincides with my research of how calcium efflux is increased with emf: https://romanshapoval.substack.com/p/how-flu-is-an-electrical-illness
Don't statins also lower testosterone, and by that factor human growth hormone, which would also not help neurodegeneration?
I lost the statin argument not having any medical standing. I'm helping care for a family member with alzheimers and their neurologist took her off one of the statins and months later we got a message from a lab tech demanding to know why she was taken off the statin.
I brought as much research and studies as the primary care giver/guardian would tolerate in a twenty minute reading session. They seemed unconvinced and ready to be spoonfed whatever pharmacaptured crap a lab tech or bought doc will tell them. It's frustrating but I really do not have any medical standing and can only differ to a system that I no longer trust.
Long story short I stopped my statin a few weeks ago.
Now what should I do? How much magnesium should I take a day? Right now I’m taking 375 mg of mixed OTC magnesium. I have always wondered if I should take more.
Any other recommendations that I could be missing?
Would the use of a water soluble stain instead of a fat soluble statin help reduce the dementia in the brain?
"The prevalence of moderate to severe brain atherosclerosis was 54% among 1905-1914 births, 37% for 1915-1919, 30% for 1920-1924, and 22% for 1925-1930, while moderate/severe arteriolosclerosis ranged from 44% for those born from 1905-1914 to 28% from 1925-1930 (χ2 test: P<0.001 across birth year categories). However, there were no differences in age-standardized prevalence of gross chronic infarcts over time, and microinfarcts were more prevalent with later year of birth."
There are SO many variables here, and in these time frames, that I think it irresponsible journalism to lay it at the feet of one (statins) on the basis of sheer speculation. There is not even a speck of data cited for statin use in these populations, or comparators to non-dementia populations.
Also, why more micro-infarcts? Particularly in an era with MORE aggressive treatment of hypertension?
There is still much to understand about tau protein, amyloid, and dementias.