Should high cholesterol be actually the culprit for heart disease ?

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

  1. Trippy ALEA IACTA EST Staff Member

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    River: Are you actually capable of giving a coherrent response? The reason I ask is that the last two responses you have given me do not actually appear to address the points that I was making...
     
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  3. river Valued Senior Member

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    Because your point is irrelevant

    And you have missed my point
     
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  5. Trippy ALEA IACTA EST Staff Member

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    And you're a fraud, or an idiot, or quite possibly both.

    In your OP you stated that cholesterol should be discarded as an indicator for heart disease. You cited sugar, oxidative stress, and inflammatory markers as being more important indicators.

    I pointed out that the link between inflammatory markers and heart disease had been known about for some time.

    Any time anyone mentions the word cholesterol you leap upon them uttering the mantra that not all cholesterol is bad, that some forms are good, and that every cell in the body produces cholesterol.

    I pointed out that every cell in the body produces carbon dioxide, you failed to understand my point, so I elaborated by pointing out that there ae any number of trace elements and micronutrients that the body requires that are otherwise toxic when there is too much, it's in the wrong place, or it's in the wrong form. Your response was to repeat your mantra that not all cholesterol is harmful. This response has no bearing on my point, I didn't comment on cholesterol directly, I commented on you assertion/implication that produced in body, therefore good. Semen is produced in the body, is non toxic, but, is capable of causing a life threatening reaction, the point being that just because something is produced in the body doesn't mean that it's not capable of inducing a toxic reaction or disease if there's too much of it or it's in the wrong form, o the wrong location.

    Incidentaly, if you go to a Dr and ask them to test your blood cholesterol they don't test for total cholesterol, they look at (for example) the ratio of HDL to LDL, and if you present with hypertension, as well as looking at your blood cholesterol, they will look at your diet and lifestyle as well, which suggests that your criticism is out of date or completely irrelevant.
     
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  7. river Valued Senior Member

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    Where did I say , discard ...point that out

    I have said over and over and over again to you , it is the LDL-B and HDL-3 , which are sub-cholesterol problematic molecules



    What were the markers , that you didn't elaborate on ?

    This is true

    Your point about carbon dioxide is a tangent on the OP , hence makes it irrelevant to the OP

    From the book

    HOW CHOLESTEROL IS MEASURED

    OLD SCHOOL

    A standard blood test will tell you your total cholesterol level and your HDL and LDL levels


    NEW SCHOOL

    Measure cholesterol with the newer particle tests , which tell you how much of your LDL is type A and how much of your LDL is type B ( see chapter 9 for more information ) . Measure the number of the actual particles , and the amount of the potentially dangerous Lp(a) . That is the only information that matters .

    RELATIONSHIP TO HEART DISEASE

    OLD SCHOOL

    High levels of cholesterol are an important risk factor for heart disease because cholesterol builds up in the arteries , inhibiting blood flow from the heart


    NEW SCHOOL

    Cholesterol is a relatively minor player in heart disease and a poor predictor of heart attacks. More than half of all the people who are hospitalized with heart attacks have perfectly normal cholesterol levels.

    End quote from the book
     
  8. river Valued Senior Member

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    Further from same book

    DIETRY ADVICE


    OLD SCHOOL

    Eat less than 300mg of cholesterol a day and eat less than 10 percent of calories as saturated fat


    NEW SCHOOL

    According to the Framingham Heart Study , people who consumed the most cholesterol in their diets did not have any higher blood cholesterol levels than those who consumed the least amount . The effect of dietary cholesterol on blood ( serum ) cholesterol is very variable and individual , and for most people - though not all - the effect of dietary cholesterol on serum cholesterol is insignificant .

    In any case , because cholesterol is not an important risk factor for heart disease as once believed , it doesn't matter much . Saturated fats raise cholesterol, but it raises the overall HDL cholesterol and the GOOD part of LDL cholesterol ( LDL-A ) far more than it raises the bad part of the LDL cholesterol ( LDL-B ) . There is no evidence that supports the DIRECT relationship between saturated fat and heart disease .

    End of quote
     
  9. river Valued Senior Member

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    For those that may be interested in the book

    ISBN# 978-1-59233-521-3

    Our health is important

    I bought this book , not because I have a condition , but as part of my preventative health step , among many that I have taken
     
  10. exchemist Valued Senior Member

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    River, I've read the correspondence and I don't think you have (yet) made a coherent case for why you think conventional medicine is wrong about this. I don't claim to be any sort of expert on it, but it seems to me any scientifically educated person who's talked to their doctor after a health check-up has known, for decades now, that the "cholesterol" of layman's parlance is lazy journalists' shorthand for LDL + HDL + Triglycerides, which is what gets measured. Furthermore he or she will be fully aware that it is the Low Density Lipoproteins that are believed to be implicated in atherosclerosis, not in fact the molecule "cholesterol" itself at all. So there's no shock-horror value in that "discovery", and no conflict whatsoever with the importance of the cholesterol molecule in human biochemistry.

    The conventional view of this condition (atherosclerosis) seems to be summarised here:http://en.wikipedia.org/wiki/Atheroma

    Perhaps you could summarise for us the respects in which this picture is said to be wrong, according to authors you cite. Then we would have a basis for a scientific discussion, at least.
     
  11. Trippy ALEA IACTA EST Staff Member

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    Thankyou. I had somthing similar to say, but I ran out of time to make my point, probably wasn't going to have time to try again until tonight.
     
  12. Trippy ALEA IACTA EST Staff Member

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    Let's start with the OP title then move on from there eh?

    You don't even know what you're talking about. They are not "sub cholesterol molecules".
    Low density lipoproteins (and high density lipo proteins) are (to put it in laymans terms) are essentially like bubbles. They're bubbles that are made up of varying amounts of different kinds of protein units. I call them bubbles because the proteins involve have lipophillic (fat loving) and hydrophillic (water loving) portions. They are used by the body to distribute cholesterol and tryglicerides through the body using the water based blood stream. They arrange themselves as a sphere (hence bubbles) with a lipophillic interior and a hydrophillic exterior. If I recall correctly, LDL is used by the human body to distribute cholesterol from the liver, and HDL is used by the body to scavenge cholesterol and return it to the liver.

    Within the two types of (relevant) Lipoproteins there are a range of particle sizes. This is where LDL-A and LDL-B (and in some cases LDL-C) come from. It means Low density lipoprotein, pattern A; and Low density lipoprotein, pattern B. It's a reflection of the distribution of particle sizes within a sample. Smaller particles are higher risk, because they're more likely to get stuck in the space between cells in arterial walls, which is the first step in the plaque forming mechanism. LDL Pattern B is the range of smaller sizes. LDL-C is a designation used (as near as I can tell) by some authors to indicate an "intermediate" distribution.

    Cholesterol is measured not because it is a strong indicator, but because it is (or was - things may have recently changed) the most cost effective measure we have. LDL and HDL can be seperated, and by measuring the amount of cholesterol, we know how much lipoprotein of that type is in the sample.

    They're a set of biochemical markers that show up in blood tests that indicate inflammation. One example that, if I recall correctly, is directly relevant to the discussion is C-Reactive protein.

    You're monkeying things without understanding them.

    This comment, by you:
    Makes the point illustrated by the analogy entirely relevant to the OP.
     
  13. exchemist Valued Senior Member

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    6,298
    By the way, you might be amused by this quote from the Wiki article on one of the protagonists of this stuff, one Dr Stephen Sinatra:

    "Dr. Sinatra advocates a controversial alternative health practice called "grounding" or "earthing." According to the theory of grounding, the earth's surface is negatively charged and contact with the earth transfers allows electrons to neutralize free radicals in the human body. Advocates say this can be accomplished by lying or walking barefoot on grass, sand or earth, or by lying on a special pad connected to the earth by grounding wires or a rod, or plugged into a wall outlet with a "modern earth ground system."

    Sounds like utter ballocks to me. To put it more charitably, this guy certainly believes in doing his science "My Way".........
     
  14. river Valued Senior Member

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    Look trippy

    If you have a problem with what either of these authors are putting forth then communicate with them directly

    I've given their sites

    Discuss with them

    And then report back , objectively , to us the results of this discussion with either of them

    I'll wait and see what happens

    By the way , what name will you use to communicate with them because I will ask them , to verify that you have actually done so
     
  15. river Valued Senior Member

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    There is also Uffe Ravnskov( Danish scholar ) , M.D., PH.D. , to quote from the book , again

    " His exemplary scholarship is supported by hundreds of referenced citations and studies from prestigious peer- reviewed medical journals and can be found in his book , THE CHOLESTEROL MYTHS, or on his website

    www.ravnskov.nu/cholesterol.htm
     
  16. billvon Valued Senior Member

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    Just one of the many culprits. High cholesterol (specifically high concentrations of LDL and low concentrations of HDL) are just one way to die of heart disease. Lack of exercise, smoking, fluid overload, electrocution etc are other good ways to off yourself via heart failure.
     
  17. river Valued Senior Member

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    The point is though that , coronary disease is not largely due to fat in the diet , refer to the site above in my last post
     
  18. Trippy ALEA IACTA EST Staff Member

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    The point is, you have repeatedly failed to understand anything in this discussion. I should just close this thread and be done with it, if you're going to resort to posts like:
    The thing that makes you look really stupid, however, is that I am 99% confident that they would agree with everything I said here: http://www.sciforums.com/showthread...eart-disease&p=3057347&viewfull=1#post3057347

    Especially in light of some of the excerpts you have quoted. All of which combined tells me you don't have the foggiest clue when it comes to the stuff you're parroting.
     
  19. exchemist Valued Senior Member

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    Actually, the Wiki entry on this Danish bloke Ravnskof is quite interesting. He seems to be a maverick but by no means a peddler of pseudoscience, as Sinatra seems to be. He seems to be a supporter of the infection/scarring hypothesis and basically seems to be questioning whether the high level of lipids found in atherosclerotic plaque has any connection with diet.

    Of course the problem he faces is the statistical correlation between diet and risk of heart attack. To be taken seriously, he and people like him need to come up with an observable mechanism for plaque formation that can predict heart attack risk more accurately than diet can.
     
  20. Trippy ALEA IACTA EST Staff Member

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    One of the important points that people forget when it comes to the formation of atherosclerotic plaques is that as well as having the fatty component, they have an immune component. It requires both to form them. You can no more form an atheroclerotic plaque without lipoprotein particles than you can form one without macrophage involvement. All this thumping on about "50% of people who have heart attacks have normal blood cholesterol" misses the point that they still have blood cholesterol, but, rather than the blood cholesterol being the antagonist leading to the plaque formation it's the immune system.

    The thing, I think, that I find funniest, which led me to the comments to which you are replying was that if we compare this:
    To this:
    River, it seems, thinks that THE BOOK is right when it suggests that LDL Pattern B is the high risk pattern without offering an explanation why, but, when I suggest that LDL pattern B is the high risk pattern and offer a causal mechanism I am, apparently, wrong and disagreeing with the book.
     
  21. billvon Valued Senior Member

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    12,725
    Like I said, fat is just one reason for heart disease. However, fat in the diet (specifically high concentrations of LDL and low concentrations of HDL) will almost always lead to heart disease.
     
  22. Read-Only Valued Senior Member

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    It's no surprize when we consider that river doesn't have a background in ANYTHING scientific - physics, medical, etc. He quickly falls for every single conspiracy theory or anti-establishment bit of fluff he comes across. <shrug>
     
  23. exchemist Valued Senior Member

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    Yes, I see what you mean. But I'm now intrigued, as my own sketchy knowledge of this subject is nearly exhausted. From what you say about "blood cholesterol [mainly type B LDL, I suppose?] being the antagonist", I take this to mean that according to the conventional model, this class of lipoproteins penetrates the cell wall, exciting an immune response, which then initiates the plaque formation process. Is that right?
    If so, then I suppose the next question is, what evidence is there that diet affects the degree of invasion of the artery wall by LDL? Is this now well-documented, or does it still rely only on epidemiological correlations?
     

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