Should high cholesterol be actually the culprit for heart disease ?

Actually, you're wrong here as well. My degree includes Biochemistry, it's just not the field I chose to work in.

You should probablys top nvesting emotional currency in being right, and start offering some apologies.

 

Not to me (or not just to me).

And that doesn't count as an apology.

 

I don't go around bragging about what I know. I presented cogent arguments that, it seems, have persuaded nearly every other reader in this discussion that I have at least some knowledge on the topic of discussion.

That alone should have been an alarm bell for you.

Incidentally...

According to Berkley HeartLab:

How do I know if a Berkeley HeartLab test is appropriate for me?
If you have had two or more of the following, a Berkeley HeartLab test should be considered:

Heart disease or a heart attack (This counts as two)
Diabetes (This counts as two)
Family history of either heart disease or a heart attack before the age of 55
Total cholesterol > 200 mg/dL
LDL cholesterol (the bad cholesterol) > 130 mg/dL, or
LDL cholesterol > 100 mg/dL if you have had a heart attack
Triglycerides > 150 mg/dL
HDL cholesterol (the good cholesterol) < 40 mg/dL
Systolic blood pressure (the top number) > 140 mmHg
Diastolic blood pressure (the bottom number) > 90 mmHg
Obesity
Cigarette smoker
Physical inactivity​

​

Now, this is the advice from the people who developed and commercialized the test, as to when having the test is appropriate.

According to another MD's website, this is what it tests for:

Routine lipid panel, including total cholesterol, LDL, HDL, TG
LDL particle size
HDL particle size
Apo B - LDL particle number
Lp(a) – high levels can cause blood to clot too easily, inherited, can alter with medications
Homocysteine
Lp-PLA2 – measures imminent stroke risk
Highly Sensitive CRP – measures inflammation
Fibrinogen – another measure of inflammation
NT-proBNP – a measure of cardiac stress
Insulin – measure of early insulin resistance and risk for diabetes
Genetic Tests:

• Apo E Genotype - identifies how people respond to dietary fat
• Kif6 Genotype – identifies if certain medications would be helpful
• LPA Genotype - identifies if taking aspirin would reduce risk heart disease
• 9p21 Genotype - identifies people with a risk of early onset heart attack, abdominal aortic aneurysm and heart disease risk​

According to the same MD, with insurance it can cost up to USD 209, but without insurance it can cost up to USD 790.

 

That's not a claim that was ever made, it's a straw man hypothesis - this is why I have stated, repeatedly, that you don't know what you're talking about.

I've outlined the mechanism to you in a previous post in fairly straightforward language.

To recap:
- Small lipo-proteins get stuck between arterial cell walls, causing plaques/fatty streaks when macrophages attempt to consume them.
- Lipoproteins contain cholesterol with them.
- Lipoproteins can be fractionated.
Therefore measuring the amount of cholesterol in your blood is still the most cost effective predictor for heart disease that we have.

 

What's your point, I haven't made a claim one way or the other in this regard. You, however, are making a claim which is just parroting what you've been told by someone else. Tell me, does Jonny Bowden ever actually present a mechanism by which the plaques grow?

Which is why cholesterol is tested for. Blood is polar, cholesterol is non-polar. You do not have cholesterol in your blood unless it is encapsulated within lipoproteins.

I've you've got USD 300 to spend on a blood test (assuming you have insurance) then I'm sure you can find the $20 it would take to buy a dictionary.

Alternatively, you can follow this url: Link

Again, you show you don't know what you're talking about.

The standard cholesterol blood test tells you total cholesterol, HDL, LDL, and triglycerides.

 

My understanding, such as it is, is that it's not that it penetrates the cell wall, but that it becomes 'lodged' between cells in the arterial wall. Most kids over the age of ten have fatty streaks in their arteries which are the first visible step in plaque formation. My recollection such as it is, is that once it's stuck there, it becomes oxidized and then is consumed by macrophages, which eventually become sponge cells.

My understanding is that diet is at best contentious. I know that Jonny Bowden, for example, promotes diet over the use of statins, but he promotes a diet low in oxidants, and high in antioxidants (from what I can tell). That may or may not be unreasonable, when you think about the 'accepted' mechanism of plaque formation - it requires the oxidation of the lipoproteins as its first step.

To some extent, it seems, that public opinion and media reporting may have taken the focus on dietary fat further than the science eg: http://www.sciencemag.org/content/291/5513/2536 (PPV).

Jonny Bowden cites the Lyon study as proof of his hypothesis, although I question his interpretation of the results. It does appear to support his assertion that diet does not influence HDL and LDL levels, however, I note that the study was done in 1999 and while they made the "standard" blood cholesterol measurements (triglycerides, LDL, and HDL) they do not appear to have tried to characterize the pattern of LDL particle size distribution. So while the diet does not appear to have changed the amount of LDL in the blood stream, it may still have shifted the distribution from Pattern B to Pattern A and had a protective effect in that regard. There's no evidence presented by the Lyon study one way or the other in that regard.

I did note, howeever, while researching this post and other posts today, that according to Berkeley Heartlab as of 2008 ADA, ACC and AACC have all recommended that "apoB and/or other alternative laboratory measurements of lipoprotein particle number be incorporated into existing consensus guidelines for advanced cardiometabolic risk management."

ApoB is a protein that occurs only in low density lipoproteins, and each LDL has only one ApoB unit. This introduces a 1:1 stoichiometry between the number of LDL's in your blood and the amount of ApoB in your blood, which, in turn gives you information about the size distribution. If you have normal levels of cholesterol, but lots of ApoB in your blood, then you have a lot of LDL in your blood, which means that each LDL is holding less cholesterol and is therefore smaller, meaning you're at higher risk.

I'd like to see the Lyon study repeated, but with attention paid to something like ApoB in addition to the other factors considered.

 

Which is exactly what I have been saying right from the beginning, and you have been saying is wrong.

The difference between anything I have said and the what Jonny Bowden has said, is that Jonny Bowden requires pre-existing damage to the vessel walls, where what I have said does not. What I have said, which, to the best oif my understanding is a reflection of the mainstream thinking is this:

LDL gets stuck.
If not already so, LDL gets Oxidized.
Macrophages consume LDL's, become foam cells, and die, forming the plaque.

Cholesterol is tested for because LDL's contain cholesterol and lipoproteins (regardless of their density) are the only, repeat ONLY source of cholesterol in the blood. Cholesterol is used instead of other tests, because other tests are significantly more expensive without providing any extra benefit for most people. For some people, however, if they have sufficient risk factors - high blood cholesterol being one of those risk factors, should get the more specific tests done.

Regardless of what the Media says, and the public understands, that is what the science says.