Angiogenesis a bypass

[Max_123]

My father has blocked arteries, but it appears there is adequate blood flow around a completely blocked left-side large vessel.of the heart.  I'm concerned and interested because this may happen to me so I have done some reading on the subject.  I read angiogenesis is the process and posts on this forum indicate the process is collateral vessel?  Thank you in advance.:)

[RogerInTexas]

Ed, it's frightening that your GPs never addressed your BP, although the readings you cite are perfectly acceptable to many physicians, depending on your age.  Like blood sugar readings and cholesterol levels, mainstream medicine has been prodded by the lobbyists and drug makers to continually lower the "acceptable" levels, rather than address the underlying causes of the readings.  Many enlightened physicians now focus on pulse pressure (systolic minus diastolic reading) rather than the raw numbers themselves, and ideally it should be around 40.  Since yours is, I wouldn't be terribly worried.  And it's hard to say why you haven't more plaque in your arteries, but as you note, the first step in atherosclerosis is endothelial damage, and you seem to have avoided that  --  probably because of your diet.  I'm sure you're aware that the body manufactures cholesterol daily, and the amount manufactured is several times more than you consume  --  another reason that the lipid hypothesis is absurd.  One's cholesterol level, in the absence of a severe diet, is thus a function of one's body and of the liver's ability to regulate it.  And another factor is insulin level, and how much starchy and sweet food you consume.  Good luck when you meet with your GP.

Jon, I hope it's clear that anything I write is simply my opinion, unless I cite a source.  But there are sources for everything I've come to believe; otherwise I'd still be a medical sheep, following the mainstream line like I did for about 40 years, leading up to my heart surgery.

Regarding the Italian study and the CORONA study, which you dismiss as having been done on people subsequent to heart problems:  It's the mainstream statin position that all people who've experienced heart problems SHOULD be on statins, period.  So dismissing those results seems imprudent if you believe statins work.  Wouldn't you be taking them if you'd experienced heart failure?

I agree with your comments on Vytorin, but again, while the statin component of Vytorin may lower serum cholesterol, if cholesterol per se isn't the problem, so what?  My point is that drugs are approved at the behest of the makers, without having been adequately tested in many cases.  I mentioned Januvia earlier; it was brought to market in two years, and couldn't have been thoroughly tested, although the testing continued after it was approved.  And there are many other examples.  Here's the latest on Vytorin:

"The makers of the popular cholesterol drugs, Vytorin and Zetia, have agreed to pay $41.5 million in a Vytorin class action lawsuit.  Merck and Schering-Plough were accused of withholding unfavorable study results about the pharmaceutical blockbusters, Vytorin and Zetia, which showed that the drugs were not as effective at unclogging arteries as other less expensive alternatives. The study - completed almost two years prior to the release date - is one of several recent studies that has questioned the effectiveness of the drugs."

Three studies also showed that Vytorin may cause cancer, and numerous studies showed that adding the ezetimibe (Zetia) to Zocor had no beneficial effect.

The third quote you dispute is of course my opinion, but it's incontestible that there are many scientists and physicians, and an increasing number of medical journals, that are coming to realize that cholesterol itself is not the cause of heart disease; that diet has everything to do with health, cardiac and otherwise; that statins do nothing that can't otherwise be done without their risk and expense; and that saturated fat is not an evil to be banished.  The culprit in today's diet is the absurdly high level of sweets and high-starch foods, most loaded with unhealthy fats, which is principally responsible for diabetes and obesity, both of which can lead to coronary artery disease and related problems.

Ed, it's ironic that you cite stress among your issues.  Your countryman, Dr. Malcolm Kendrick, in his book "The Great Cholesterol Con," blames stress (and inflammation) instead of cholesterol for causing the endothelial damage that results in arterial problems.  And here's a URL to a site that addresses cholesterol much better than any I've seen:  www.cholesterol-and-health.com.  As Chris Masterjohn states on the first page, science should be a search for truth, not a war, and he presents a fascinating and enlightening variety of facts and opinions about cholesterol.  He's also posted reviews of all the current books on the topic.

Jon, thanks for the kind words at the end of your posts.  Discussions like this one make all parties involved do investigating and research, and can only be beneficial to all.  And I certainly appreciate and respect your tone, too.

[ed34]

I think I need to have a serious discussion with my GP about medication and my cholesterol to get her view point and explanation on a few matters. My personal experience has been,
1. High blood pressure since a child yet no GP did anything about it.
2. Atherosclerosis problems started when I began a very stressful period in life (age 44).
3. My cholesterol has always been high. 8.9 mmol/L which is 343.63 mg/dl.
4. Lots of arteries have been scanned and the only ones which apparently seem affected
    are the coronary arteries, well, the LAD and RCA. Circumflex is clear.

So, with such a high cholesterol level, and cholesterol being the cause of Atherosclerosis, I have to ask some questions.....

1. With my cholesterol being so high for all my life, why aren't my arteries in much more
    of a mess. I have seen people with normal cholesterol with worse coronary arteries.
2. It is fact that cholesterol is not the first phase in atherosclerosis, the lining of the
    artery being damaged is the first phase. So with this in mind, if my blood pressure
    is controlled with medication, why would I need to lower my cholesterol?

In my opinion my blood pressure is still high. When I went to have my recent stress echo, my BP was 148/112. They commented on how it was far too high and would be retaken a few minutes later. After 30 minutes the test was repeated. It then read 140/99
and I was told "oh that's much better, that's lovely now". 99 is good? I don't think so.
I believe I am at much more risk of more disease from this than I am from cholesterol.

If nobody can tell me why my arteries are in good shape apart from the heart when I had such high cholesterol, then I have to conclude that I don't need statins because the cause was obviously from something else.

I will see what my GP says and let you know.

[erijon]

Your comment;
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"Results from this large, randomized study corroborate those of the earlier CORONA study (JW Nov 29 2007): Rosuvastatin did not lead to longer survival in patients with heart failure. Although these findings raised no safety concerns about rosuvastatin, the authors recommend against routine use of statins in this population. However, ω-3 polyunsaturated fatty acids appear to confer a small but significant survival advantage and might merit routine use along with other established therapies for heart failure."
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I have read this argument before, it's posted on all the anti-statin sites. You really can't use this conclusion as this study was aimed at people who are already in heart failure so it really can not be used in a discussion concerning the general population. It's just apples and oranges.

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And of course Vytorin has been a huge disappointment, and is considered a treatment of last resort by most physicians.

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Also not completely true. As you most likely know, Vytorin is simply simvastatin and Zetia. This combination has not been more effective than simvastatin alone, but also has not seen any additional harm. Most doctors (including mine) have switched to simple simvastatin plus a fenofibrate as it is more effective than Vytorin. This is not to say that Vytorin does not lower cholesterol, just that the addition of Zetia does not provide any further benefit so to say it is a disappointment is true to an extent, but it still is effective in lowering serum cholesterol. It is the addition of a non-statin that is the disappointment in clinical findings so it really is not related to the statin used.

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In crime, the wise detective asks "Cui bono," i.e., who benefits?  And while pushing statins on an ignorant patient population isn't a crime, it has the potential to do immense harm.  It's clear to me why physicians with ties to pharma, the pharmaceuticals themselves, and an uncritical body of mainstream medicine has accepted the lipid hypothesis.  But why do so many scientists and physicians oppose statin use?  It can only be because they've seen enough evidence to sound the alarm.  They have no conceivable way of benefiting from the discontinuance of statins.  

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Again, show me the data to back up this statement. I welcome an opposing point of view, I am here to learn as well but I prefer fact over conjecture. Every drug has side effects and the potential to do harm. Again, what about the masses that take statins without side effects and get a true benefit? I have read both sides of the argument so I am aware of the position you are taking. There is still much to be sorted out, I think we both agree on that.

I can certainly see your passion for this, you are definitely well informed.

thanks!

Jon

[RogerInTexas]

Nor have I heard of a raising of the acceptable level of serum cholesterol, Ed.  It wouldn't concern me if it happened, because I'm convinced beyond question that the total cholesterol number is meaningless.  

Professor Harlan Krumholz of Yale University did a study in 1994 on this topic.  He concluded that "people with high cholesterol levels live longest."  He also determined that the elderly die twice as often from heart disease if they have low cholesterol rather than high cholesterol.  A similar result was reported by Dr. Gregg Fonarow of UCLA following a 1,000-patient study.  Needless to say these finding were ignored or ridiculed by the establishment.  

And here's an interesting summary of a four-year study done in Italy in 2007, funded by the manufacturer of rosuvastatin (Crestor):

"Results from this large, randomized study corroborate those of the earlier CORONA study (JW Nov 29 2007): Rosuvastatin did not lead to longer survival in patients with heart failure. Although these findings raised no safety concerns about rosuvastatin, the authors recommend against routine use of statins in this population. However, ω-3 polyunsaturated fatty acids appear to confer a small but significant survival advantage and might merit routine use along with other established therapies for heart failure."

In other words, the death rate from cardiovascular disease was higher among those taking rosuvastatin than among those who weren't taking it.  And of course Vytorin has been a huge disappointment, and is considered a treatment of last resort by most physicians.

In crime, the wise detective asks "Cui bono," i.e., who benefits?  And while pushing statins on an ignorant patient population isn't a crime, it has the potential to do immense harm.  It's clear to me why physicians with ties to pharma, the pharmaceuticals themselves, and an uncritical body of mainstream medicine has accepted the lipid hypothesis.  But why do so many scientists and physicians oppose statin use?  It can only be because they've seen enough evidence to sound the alarm.  They have no conceivable way of benefiting from the discontinuance of statins.  

This whole arena mystifies me.  In the mid-19th century a few alert physicians and scientists began correlating obesity with diet composition, not just calories, and determined that those obese invidiuals consuming a high-refined-carbohydrate diet, (wheat and sugar products, potatos, rice, pasta, beer) regardless of quantity, gained weight and/or became diabetic.  This was accepted until the 1950s and 60s, when heart disease supposedly became epidemic, and the culprit was (wrongly) perceived to be a high-fat diet.  Thus was born the low-fat diet and the infamous food pyramid, which lowered the "acceptable" levels of protein foods and increase the levels of carbohydrates.  In actuality the two driving forces for a high-carb, low-fat diet were both erroneous:  There was no epidemic of heart disease, just much better reporting and people living longer because of the virtual elimination of other causes of death, and there was no basis for the incorrect assumption that people were eating more fats.  But Ancil Keys and his adherents, along with Paul Dudley White, triggered the stampede to a low-fat diet.  It persists to this day.

But heart disease declined only modestly and obesity and diabetes continued to increase despite the so-called "heart-healthy" approach to eating.  And they continue to grow to this day, with about one-third of the country obese and no significant reduction in cardiac-related deaths despite the vastly increased use of statins.

But in spite the rigid posture of the powers-that-be in this area (FDA, NIH, AHA, AMA, med schools, medical journals, pharmaceuticals), truth will out.  There are already thousands of physicians and clinicians who recognize the problem and are doing something about it.  Ronald Krauss and his research over the past 15 or so years identified the various sub-particles of lipoproteins, and determined that particle size, not quantity in the bloodstream, is key to the effects of LDL, VLDL and IDL.  The denser the particles the greater the danger.  

In most labs, lacking a ultracentrifuge, LDL isn't measured; it's calculated from total cholesterol, HDL and triglycerides, using the Friedewald formula.  In some labs LDL direct testing is done, but it isn't any better, since it also lumps in IDL, VLDL and lp(a).   In my situation, with very low triglycerides, the accuracy of the Friedewald result is unclear.  Also, what's listed as LDL  is actually LDL, IDL and lp(a).  And even if the calculation is near correct, the most important factor  --  viscosity  --  isn't measured except in advanced blood testing, which is not widely available.  Shameful.

We've gone far afield from the original question, but everything we've discussed is relevant to the blocked arteries of Max's father.  If he were my father I'd suggest a very-low-carb, high-protein diet, 4 or 5 grams of niacin per day, aerobic exercise to better develop the collaterals, advanced blood testing and lots of research.  And a cardiologist who isn't blindly committed to statins.

It's working for me.

[ed34]

When I went to cardiac rehab in 2007 the recommended level for LDL was 3 mmol/L or less. In 2009 it had raised to 4 mmol/L. Questions immediately entering my mind were....

1) What is the minimum that the body requires to survive healthily
2) If the miminum is unknown, then who can decide a limit for CHD patients
3) why the sudden increase in allowance. Is it because 3 is too low for health reasons
    or is it so fewer patients need to take statins.

Having familial hypercholesterolemia, I have no choice but to take statins and they certainly have lowered my LDL cholesterol to around 2.8 mmol/L . Nobody has contacted me regarding the new limits and so will make an appointment with my GP to see if I can reduce my 40mg of daily Atorvastatin to 30mg or even 20mg.

[erijon]

Why would that have anything to due with side effect claims? Also, I'm not aware of anything here concering raising recommended cholesterol levels here, are they making changes in the UK?