Should high cholesterol be actually the culprit for heart disease ?

Discussion in 'Chemistry' started by river, Mar 30, 2013.

  1. river

    Look guys I Don't know much about the bio-chemistry of cholesterol , I bought the book because I was intrigued by its going against the conventional wisdom

    I wanted to know WHY they did so

    Now if you want to gather more information about their position then I suggest you get in direct contact with them , as I mentioned before

    And I find that it is interesting that instead of doing so you attack me , knowing I don't know much about the subject , and I'm NOT going to recite the whole book

    I've given the websites in which you can contact these people , now do so if your serious about learning more about the position , or buy the book

    Since NONE of you are educated formally on the bio-chemistry either

    I have never suggested or even hinted that am some sort of expert on the this subject , I just put it out there to be considered rationally

    The sites given are by experts

    Explore them , if your serious


    By the way all the sites including the Personal sites by Both authors of the book were given freely and taken from the book

    I'm sure that they anticipated flack from the mainstream
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  3. gmilam Valued Senior Member

    To quote you...

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  5. billvon Valued Senior Member

    As a suggestion, if you do not want to talk about a topic, and consider yourself unqualified to do so, then not bringing the topic up for discussion would be a good strategy.
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  7. river

    I have talked about the subject

    Then who would bring up the topic ?

    Would you ?

    Its about learning new ideas , new ideas on old thinking

    A quote from the book ;

    " The mind is like a parachute- it only works if it is open " - Anthony J. D'Angelo

    This is important

    You can take or leave what the OP is suggesting but it does get one thinking about what we have been told , presently about cholesterol

    And the research backs it up
  8. billvon Valued Senior Member

    Yes, many people have been thinking about cholesterol and its role in heart disease for decades. And they have determined that a high level of cholesterol (specifically high concentrations of LDL and low concentrations of HDL) is a primary risk factor for heart disease. That's why statins work for people with cardiovascular disease, and that's why cholesterol is carefully monitored nowadays in patients at risk for cardiac disease.

    It is certainly not the only factor that leads to atherosclerosis - or to any disease of the heart or circulatory system - but it is one of the primary factors. Reducing your LDL levels through exercise and diet is a very good idea if you want your heart to work for decades to come.
  9. gmilam Valued Senior Member

    I remember being a kid at family gatherings in the 1960s and hearing most of the "old" people (people probably in their 50s) discussing "Hardening of the arteries". I assumed it was something that happened to everyone as they got older. Most of them were dead 10 to 15 years later.

    Coincidence, probably not.

    My mom has been managing her cholesterol for the last 25 years or so and she is now into her 80s.

    Coincidence, probably not.
  10. river

    Bill the reason that statins work is because it can reduce the inflammation of the heart , not because of the reduced cholesterol levels , at least that is what their thinking is of why statins work

    But Statins also reduce the production of the coenzyme Q10 which the heart needs , its important

    First it depends on what type of LDL cholesterol you are trying to reduce , B is the one you want to reduce

    Diet IS important and so is exercise , as you mentioned before

    But the specifics of your cholesterol can only be understood by the Berkely test

    Plus The liver will either take up the slack in cholesterol intake or reduce cholesterol manufacture if the diet has sufficient cholesterol in it , that has not been mentioned up to this point
  11. Trippy ALEA IACTA EST Staff Member

    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.
  12. river

    Apology given
  13. Trippy ALEA IACTA EST Staff Member

    Not to me (or not just to me).

    And that doesn't count as an apology.
  14. river

    To who else

    Thats all your going to get

    You could and should have mentioned from the top , you lead me along until I called you out
  15. Trippy ALEA IACTA EST Staff Member

    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.


    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
    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
    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.
  16. river

    Well I would have the test as a preventative measure
  17. river

    So now trippy do you have a problem that cholesterol is not the major culprit of heart disease ?
  18. Trippy ALEA IACTA EST Staff Member

    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.
  19. river

    Fine but the information I have is from people who do though

    As you do

    1) because they are oxidized

    2) yes they do

    3) not sure what you mean by fractionated

    4) yes of course but being more specific of the TYPE of cholesterol is better
  20. Trippy ALEA IACTA EST Staff Member

    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.
  21. Trippy ALEA IACTA EST Staff Member

    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: (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.
  22. river

    I'm not sure who does explain the , mechanism of plaque growth but here goes

    It starts with the oxidized LDL , otherwise harmless for the most part

    The oxidized LDL , infiltrates the endothelium ( the thin layer of cells that lines the inner surface of blood vessels ) inflammation begins

    The LDL-B penetrate the arterial walls , the smaller the B the more inflammatory they are

    Enter the immune system

    Which sends monocytes to the situation , which releases cytokines , which regulate the immune response , but of which many are highly inflammatory

    The lining of the blood vessels secrete , adhesion molecules , which grab on to the monocytes , to put out the fire as they put it

    The monocytes are now converted to macrophages , which are to consume damaged LDL

    The keep this action to their death , leaving behind what is called , lipid core of plaque , foam cells
  23. Trippy ALEA IACTA EST Staff Member

    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.

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