Nancy wrote: There is also wisdom in using common sense.
Beta-sitosterol is found in plant-based foods, such as fruits, vegetables, soybeans, breads, peanuts, and peanut products. Beta-sitosterol is also present in bourbon and oils, such as olive, flaxseed, and tuna. Plant oils contain the highest concentration of phytosterols. Nuts and seeds contain moderate amounts of phytosterols, while fruits and vegetables generally contain the lowest phytosterol concentrations. For example, roasted peanuts contain 61-114 milligrams per 100 grams, 78-83% of which is in the form of beta-sitosterol. Peanut butter contains 144-157 milligrams per 100 grams. These values indicate that peanut products are a good source of phytosterols, specifically, beta-sitosterol. Avocados have also been identified as a good source of beta-sitosterol.[Emphasis mine]
The amount of total sterols in extra virgin olive oil found by different groups varies between 113-265 mg/100g oil (5;6). Two factors influencing this amount are the cultivar and the degree of ripeness of the olives (5). By far the major sterol in olive oil is ß-sitosterol, constituting up to 90-95% of total sterols (5;6)[Emphasis mine]
Juliegee wrote:Zetia (Ezetimibe) can effectively lower LDL-C, but doesn't seem to have any effect on actual CVD events. Even when combined with a statin, the benefit appears to be negligible leading me to have doubts about this approach. Mechanistically, it makes sense for hyperabsorbers, but the data just isn't there...
Stavia wrote:Juliegee wrote:Zetia (Ezetimibe) can effectively lower LDL-C, but doesn't seem to have any effect on actual CVD events. Even when combined with a statin, the benefit appears to be negligible leading me to have doubts about this approach. Mechanistically, it makes sense for hyperabsorbers, but the data just isn't there...
Agreed Julie. I only use them or prescribe them under shared care situations with cardiologists in two circumstance. The first situation is combination with a statin in those with familial hyperlipidaemias at very high risk, where the baseline numbers are extremely high and statins are unable to get the numbers down enough. We're talking totals of 9mml/l or more even (350). There are no trials in these persons and the population data cannot be accurately extrapolated to them.
The second is alone in those at high-risk due to previous events who are completely intolerant of statins due to liver effects or rhabdomyolysis. But in this latter situation I am very aware that there is no evidence that further events are prevented.
Things may be different in the US and it may be used more liberally. This is the British-based medical approach to ezetimibe.
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