Statins are sometimes described as being either lipophilic (hydrophobic) or hydrophilic (lipophobic) as though that were a binary condition. While Pravastatin is extremely hydrophilic, fluvastatin is an example of a statin occupying an intermetiate position.
Lipophilic: Lovastatin and Simvastatin are the most lipophilic. Atorvastatin & Cerivastatin less so.
I have seen Fluvastatin placed in both categories.
The lipophilic statins tend to increase insulin resistance, which may be a significant issue in PCa, IMO.
"... lipophilic statins diffuse across cellular membranes and exert their metabolic effects in the liver and other tissues; hydrophilic statins require active transport across the cell membrane in order to exert their actions intracellularly. This action of hydrophilic agents is therefore predominantly hepatic and not peripheral" [1]
Lipophilic statins may be required if the intent is to stop cholesterol synthesis within PCa cells.
[1] (2012 - U.K.)
"Bone marrow stroma (BMS) was isolated with ethical approval from consenting patients undergoing surgery for non-malignant disease."
"PC-3 binding, invasion and colony formation within BMS was assessed by standardised in vitro co-culture assays in the presence of different statins."
"Statins act directly on PC-3 cells with atorvastatin, mevastatin, simvastatin (1 μℳ) and rosuvastatin (5 μℳ), but not pravastatin, significantly reducing invasion towards BMS by an average of 66.68% ... and significantly reducing both number ... and size ... of colonies formed within BMS."
"Lipophilic statins and rosuvastatin significantly reduced the number of colonies to a similar degree in clonogenic assays and BMS co-culture (Table 1), with simvastatin being the most potent (reduction of 75.44% and 49.44%, respectively)."
This new knowledge I gained about the main two classification Lipophilic ( hydrophobic ) and Hydrophilic ( lipophobic ) and various statins falling into these two groups is interestingly useful. I knew some of them only by the names previously.
I have been using a small dose of atorvastatin ( 10mg ) for the last 10 years to keep my LDL and Triglycerides under control although I don't have any cardio vascular issues. Coupled with good dietary habits and regular exercise, my control has been excellent even with my two years' ADT treatment for PCa.
The key points I have noted about STATINS from your explanation, in relation to PCa are :
- The lipophilic statins tend to increase insulin resistance which may be a significant issue in PCa.
- Statins act directly on PC-3 cells with Atorvastatin, Mevastatin, Simvastatin, and Rosuvastatin but not Pravastatin ( I could learn many statins - Thank you ). They significantly reduce invasion towards BMS by an average of 66.68%
In my interpretation of the facts given by you Simvastatin and Rosuvastatin are the most potent in supporting PCa treatments. Atorvastatin could be considered as intermediate.
In the last paragraph of your explanation the percentages given as 75.44 and 49.44 is a little bit unclear with the word "respectively" because you say Simvastatin is the most potent whereas Rosuvastatin has been mentioned first.
Could you kindly attach the 75.44% to the statin by name and also correct me if I have perceived anything wrongly from your useful post on STATINS.
I thought that PC-3 was a laboratory cell line, and so an assertion of the effect of drugs on a lab cell line is of only speculative interest to cancer patients unless they know that their cell line is similar to the PC-3 line as opposed to the LNCaP line or any of the others. No?
It's not really about the specific cell-line, but rather the differential effect of lipophilic & hydrophilic statin uptake. PC-3 cells were as good a test as anything else.
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Rosuvastatin Issue
