Cholesterol—specifically, the importance of “cholesterol” (actually, lipoproteins) numbers—is a hotly contested topic. There are so-called cholesterol wars about it. The mainstream position has been slowly evolving from “cholesterol is the devil” to “LDL is the devil” to “You need to look at HDL and trigs as well, but LDL is bad anyway” to “It’s complicated” :-/
Doctors, unfortunately, tend to have a hard boundary in mind and if your cholesterol is above it, they feel the need to drive it below that boundary. I am not a fan of this approach.
Statins are a whole big separate issue. My impression is that statins have been shown to be quite effective for cardiac patients, that is, people who already had a cardiovascular event and are at high risk for another one. The use of statins for primary prevention, that is for people without any history of CVD is another thing. Pharma companies, obviously, really really want statins to be used for primary prevention.
The problem is that the effectiveness of statins for primary prevention is iffy. Essentially claims for it rest on a single trial called Jupiter. Before it, the Cochrane Collaboration stated that the use of statins for primary prevention was not shown to be useful. After that trial Cochrane changed the review and said that “Reductions in all-cause mortality, major vascular events and revascularisations were found with no excess of adverse events among people without evidence of CVD treated with statins.” You can read the entire review (pay attention to absolute risk reduction numbers).
ETA: What, Cochrane reviews are behind a paywall now? I thought they were free-access. In any case, here is a link to a freely-available version.
If you feel you need to do something about your LDL without statins, try changing your diet. In particular, saturated fats push up LDL (but they also push up the “good” HDL).
You did the 23andMe thing, right? What’s your APOC3 status?
Actually, check APOE first as it has pronounced effects. It’s usually considered to be an Alzheimer’s risk factor, but besides that it affects your cholesterol levels and specifically how they react to the saturated fat in your diet. See e.g. this paper or a high-level overview.
Cholesterol—specifically, the importance of “cholesterol” (actually, lipoproteins) numbers—is a hotly contested topic. There are so-called cholesterol wars about it. The mainstream position has been slowly evolving from “cholesterol is the devil” to “LDL is the devil” to “You need to look at HDL and trigs as well, but LDL is bad anyway” to “It’s complicated” :-/
Doctors, unfortunately, tend to have a hard boundary in mind and if your cholesterol is above it, they feel the need to drive it below that boundary. I am not a fan of this approach.
Statins are a whole big separate issue. My impression is that statins have been shown to be quite effective for cardiac patients, that is, people who already had a cardiovascular event and are at high risk for another one. The use of statins for primary prevention, that is for people without any history of CVD is another thing. Pharma companies, obviously, really really want statins to be used for primary prevention.
The problem is that the effectiveness of statins for primary prevention is iffy. Essentially claims for it rest on a single trial called Jupiter. Before it, the Cochrane Collaboration stated that the use of statins for primary prevention was not shown to be useful. After that trial Cochrane changed the review and said that “Reductions in all-cause mortality, major vascular events and revascularisations were found with no excess of adverse events among people without evidence of CVD treated with statins.” You can read the entire review (pay attention to absolute risk reduction numbers).
ETA: What, Cochrane reviews are behind a paywall now? I thought they were free-access. In any case, here is a link to a freely-available version.
If you feel you need to do something about your LDL without statins, try changing your diet. In particular, saturated fats push up LDL (but they also push up the “good” HDL).
You did the 23andMe thing, right? What’s your APOC3 status?
I’m not sure which SNP or position for the APOC3 gene you are referring to.
Actually, check APOE first as it has pronounced effects. It’s usually considered to be an Alzheimer’s risk factor, but besides that it affects your cholesterol levels and specifically how they react to the saturated fat in your diet. See e.g. this paper or a high-level overview.
APOC3 is this.
I’m E3/E3 for APOE which I guess means I have less to worry about.