Note, that you may not be getting particularly high levels of phytosterols from the sources you mentioned. The presence of phytosterols in vegetables, fruits and nuts also differs depending on the strain. In general, for many phytosterols, you will find much higher levels in vegetable oils, such as canola. And people absorb them at different rates. To know your particular levels, you need to measure them.
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Ray1
#22
I am not losing sleep over it, nor giving up my oatmeal with walnuts. Dr. Dayspring referenced this study: Genetic variability in the absorption of dietary sterols affects the risk of coronary artery disease - PubMed
He cautioned that some people should avoid phytosterol supplements due to their genetics.
Similarly, Dr. Dayspring advocates the correct use of statin drugs. We should all be following his X feed as he is a steady stream of good information.
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Beth
#23
My former cardiologist advised me to use butter with sterols to lower my cholesterol.
I said, ābut I donāt use butterā. He advised I start. 
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Reminds me of a doctorās visit many years ago. In reference to some complaint I had, the doctor mentioned remedies - it was the usual list, diet, sleep, exercise, oh and stopping smoking. Since my diet, sleep and exercise were already optimal, there was nothing I could do, so I was mildly irritated at how useless the advice was, however I did note the advice to stop smoking. But as I never smoked, I proposed that I start smoking just so that I could stop, and fulfill that last piece of advice, that way I could say Iāve followed all the sage advice of my physician. He was not amused.
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Oats lower your apoB via beta-glucan, not via phytosterols. The amount of phytosterols in foods is benign for everyone except people with ABCG5 or ABCG8 loss-of-function mutations, which are normally evident because you have crazy-high LDL-C. You can also do a campesterol blood test to be sure. Nuts lowered CVD mortality in PREDIMED.
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Thatās the way these things ought to work!
Iām pretty sure phytosterols use the same transporter for absorption that is blocked by ezetimibe, so if youāre taking ezetimibe it should be a non-issue.
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59vw
#28
I saw his X comment on rosuvastatin as well and was a bit surprised. Iād like to see the data/paper showing rosuvastatin significantly inhibits cholesterol synthesis in the brain. He didnāt site a study so I have no way of assessing the validity of his comment. It may be true that some rosuvastatin crosses the BBB but I would think it would be a very small percentage and significantly different amount than the lipophilic statins.
I agree itās interesting, but I think itās important to remember thatās itās an academic issue, and the better question is whether it matters much. As Dayspring himself has pointed out many, many times, there are so many benefits of statins (including pleiotropic effects), and there is no evidence that low ApoB/LDL-C is harmful. As he points out, thereās no evidence that statin use in children is detrimental to their brain health, even though their brain is growing rapidly.
Basically, there would have to be a finding of something absolutely terrible (like a huge increase in dementia or similar) to convince me that a statin would be overall harmful than beneficial.
We have roughly 30 years of data since statins were introduced. The biggest one, atorvastatin, came out in 1996. Obviously, it was prescribed to many people in their 40ās, 50ās, and 60ās. So these people are in their 70ās and 90ās. And the question is: where are the bodies? Did we see a spike in dementia in these people compared to non-users? No, we did not. Color me skeptical that statins, whether lipophilic or hydrophilic cause dementia. I think itās possible that for a very specific subgroup - thatās obviously not very large, otherwise weād see it in the stats - there may be some deleterious effects of statins increasing dementia rates⦠as there may be a small specific subgroup where statins cut down on dementia rates. But the big overall trend seems to be null. FWIW, I did a deep dive on statins and PD, and reached the conclusion that PD being a very heterogenous disease, contains subgroups of patients that do poorly on certain doses of statins, and there are conversely, some subgrous of PD patients who do well on statins depending on what stage of the disease process of PD the statins are introduced. There is no one blanket conclusion that āstatins are good/bad for PD patientsā - itās all very context dependet. I rather suspect itās not too different with dementia.
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Ray1
#31
Many cases of dementia are caused in part by impaired circulation. I intend to keep taking my daily rosuvistatin and baby aspirin until a better alternative comes along. Pcsk9 inhibitors may be both safer and more effective than statins, but at high cost.
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59vw
#32
Agree statins are great drugs and the data shows they are safe and effective for controlling cardiovascular disease. Iāve been on a statin myself for over 30 years.
The water does get a little muddy when you focus on apoE4 carriers with increased dementia risk and add to that the observation that a significant difference between apoE4 carriers and carriers of other apoE alleles is a deficiency in cholesterol transport in the brain.
I may have missed it but I donāt believe a dementia study looking at the effect of statins on prevalence has been done in apoE4 sub groups. Thatās why I like the idea of using a hydrophilic statin to control intravascular cholesterol levels while hopefully leaving brain cholesterol synthesis untouched.
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