Several years ago, an alternate method for measuring coronary risk was adopted by the National Cholesterol Education Program's adult treatment panel as an outgrowth of the famous Framingham Heart Study. The newer method, which was referred to as a point-based approach, attempted to make it easier to classify patients into risk groups in order to pursue the appropriate treatment.
However, a new study, which is published in the Journal of General Internal Medicine, compares the two approaches and finds the point-based system "misclassifies millions of Americans" and places them in higher risk groups for which different treatments are recommended. In other words, the implication is that a higher risk classification may prompt greater use of such treatments as cholesterol meds.
The findings: Among 39 million eligible adults, the study notes the original Framingham model categorized 71 percent of the subjects as having moderate risk (or less than 10 percent risk of a major coronary event in the next 10 years), 22 percent with moderately high risk (or a 10 percent to 20 percent chance) and 7 percent with high risk (or a greater than 20 percent chance).
But the study says risk estimates between the original and point-based models "often differed substantially." How so? The point-based system classified 15 percent of adults into different risk groups, with 10 percent "misclassified" into higher risk groups and 5 percent into lower risk groups. As a result, 2.1 million adults were placed in higher risk groups. And these differing classifications could alter treatment strategies for 25 percent to 46 percent of those affected, the study concludes (you can read the study here and the appendix here).
This raises an interesting issue: depending upon the classification, a person may or may not be placed on a statin. And which statin would depend upon LDL goals. For instance, Pfizer's Lipitor and AstraZeneca's Crestor are more potent, which means these pills are more likely to be used for people who need to lower their LDL. The study does not indicate the extent to which the point-based system is employed, but using this logic may lead one to conclude that favoring the point-based system would be in the interest of those drugmakers.
This brings us to an interesting point: one of the study authors is Jesse Polansky, a former Pfizer exec who filed a whistleblower lawsuit accusing the drugmaker of illegally scheming to boost Lipitor sales by misrepresenting federal cholesterol guidelines, among other things (back story with the lawsuit). As noted in the study, Polansky charges that Pfizer promoted the use of the point-based system by distributing a "point-based risk calculator" and funding a software program that uses the point-based model. But whether this study will find its way into his litigation remains to be seen. We imagine that Pfizer. which has previously denied the charges, is certain to object.
77 Comments
No matter which guidelines you choose to follow, one fact is abundandly clear from the original LRC-CPPT and other subsequent well-controlled coronary prevention rials. That is, for every one per cent lowering of LDL cholesterol there is a corresponding two per cent lowering of coronary risk. This makes it easier for me to treat the individual patient, if necessary with a statin in the context of all other patient-specific risk factors.
According to the article by pharmalot -"And which statin would depend upon LDL goals. For instance, Pfizer’s Lipitor and AstraZeneca’s Crestor are more potent, which means these pills are more likely to be used for people who need to lower their LD."
My only concern is that healthcare is so costly and medications contributed greatly to the everyday cost for a patient. Lipitor and Crestor will have an annual cost of approximately $1,800 per year without insurance. If the LDL is no higher than 180, simvastatin will lower LDL to below 130 and cost $360 annually. Even if a senior who has Plan D prescription coverage, brand drug cost would contribute to reach the $2,500 donut gap. Then the patient pays full price.
Balanced against what risk of life-altering and prolonged side effects? And please don't bother to spam me with that oft use smear "very rare", when the trials used the perfect patient, and out there in the real world, doctors will not report.
Pay attention to the work done by James Wright, at Therapeutic Initiative. Any physician today who is prescribing on the dubious benefit of lowering numbers is woefully uninformed and risks harming his patients. He won't ever admit it though.
How statins were developed (sic) and marketed:
http://chronicle.com/article/The-Secret-Lives-of-Big/124335/
These are the risk reduction indications from the Lipitor PI, unless of course people believe that this is just another FDA-Pharma conspiracy to deprive people of their health. Certainly some of you bloggers seem to believe this:
Reduce the risk of MI, stroke, revascularization procedures, and angina in patients without CHD, but with multiple risk factors (1.1). • Reduce the risk of MI and stroke in patients with type 2 diabetes without CHD, but with multiple risk factors (1.1). • Reduce the risk of non-fatal MI, fatal and non-fatal stroke, revascularization procedures, hospitalization for CHF, and angina in patients with CHD (1.1). • Reduce elevated total-C, LDL-C, apo B, and TG levels and increase HDL-C in adult patients with primary hyperlipidemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (1.2). • Reduce elevated TG in patients with hypertriglyceridemia and primary dysbetalipoproteinemia (1.2). • Reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia (HoFH) (1.2). • Reduce elevated total-C, LDL-C, and apo B levels in boys and postmenarchal girls, 10 to 17 years of age, with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy (1.2). Limitations of Use LIPITOR has not been studied in Fredrickson Types I and V
What study are you getting this information from?
As for your "conspiracy theory" smear: I think you're reading challenged. About six year's ago, someone who didn't have time to read the literature could claim not to know; now, anyone claiming it's a "conspiracy theory" that debunks statins use in all but a small percentage of people with established cardiovascular disease is simply broadcasting his/her ignorance all over the internet. Best stick to the pseud. But I know who you are.
We can't forget about all of the incredible evidence clearly demonstrating effective cardiovascular prevention generated with pravastatin and simvastatin 15-20 years ago. These drugs are now quite inexpensive, as are lovasatin and fluvastatin. Spending several times more for more-potent statins may not be worth it. It's not clear if the 2:1 ratio holds at all levels of cholesterol reduction. In addition, there are also a lot of patients with risk who may have normal cholesterol levels. What do we do about them? Niacin and fibrates are often good strategies.
I can't believe this. Physicians who advocate prescribing toxic drugs to lower numbers, with no proof that changes mortality.
I think physicians who do this should face criminal charges. No protection for willful ignorance.
https://www.statineffects.com/info/
A big point to be borne in mind is the use of long term drug therapy to lower cholesterol levels, where it is unclear what the full effects might be over a 30 year period. In spite of this, the Food and Drug Administration (FDA) gives approval for this class of drugs on the basis of less than 10 years’ clinical trials.
I was fortunate enough to be in graduate school when the first HMG-CoA Reductase Inhibitor, Mevinolin (a natural product BTW) was being studied in dogs in combination with a bile acid binding resin, with extremely impressive results. CV MD is on the right track. The original Framingham data published in the 1960's and 70's showed one impressive fact, among many, that the frequency distribution curve for serum cholestwrol for normals and at-risk patients nearly overlapped, so that we can't use traditional 95th percentiles to define upper limits. Even risk factors are tricky, as the NCEP data go. I do in fact believe that lower LDL cholesterol is better. Even if it were possible to get LDL colesterol levels down to the lower 5th percentile (which defines Heterozygous Hypobetalipoproteinemia), you still wouldn't have severe symptoms.
Mr. Guy-Clarke: The first statin approved by FDA, Mevacor, was introduced 24 years ago and thus proves the excellent long-term safety of ststins. Below is the link to the 1986 landmark paper on Mevinolin in Proceedings of the national Academy of Sciences, the progenitor of Mevacor, the first in the list of these wonderful life-saving drugs. If you were a 48 year old man with coronary heart disease in 1986 and statins hadn't come along, there is a decent chance that you would not be alive to read this thread today, such was the raging epidemic of coronary heart disease in the last half of the 20th century; the Number 1 killer of middle age adults until the life-saving statins came along, aided by the National Heart, Lung and Blood Institute and the National Cholesterol Education Program.
http://www.pnas.org/content/77/7/3957.abstract
I would hope you are aware that Lipitor = atorvastatin has never saved anybody in a clinical trial. Yours truly in a not contradicted letter in this years JACC [no less]: ".. atorvastatin's well-known inability to reduce mortality ... Full text: http://www.health-heart.org/JACC-2010-Vos-IDEAL.pdf
Now, would you really want to be in the lowest group for total cholesterol?? Really? Let's consider the massive Voralberg study, an about 10 year 1 million lab-test population study in white mid European folk. In any age group, the risk for early death was highest for the lowest [your best] cholesterol quartile. Okay, for men under age 50 (only) this finding did not reach p=0.05. In women, the RR for death was +60%, i.e. the same risk as smoking.
My question to you: why would anyone take a drug that will NOT alter one's day of death over the duration of a <5 year study and wind up in that quartile where population studies show has the highest mortality long-term? Just in case you don't know about that study (few 'experts' do), here it is: http://www.health-heart.org/eve-not-adam.pdf
Finally, yes I know that statins in some studies show fewer NON-FATAL CV 'events'. Guess what, that can be explained by their nitroglycerin mimicking action, a pathway NOBODY has ever disputed. Less angina, fewer interventions in a trial [think JUPITER!], no fewer deaths, evidently.
1. They were not clinical endpoints saving dogs from heart disease, and 2. Since an earlier cholesterol-lowering drug made dogs go blind, the Merck people scheduled an eye exam at 11 months in EXCEL and found that [more on statin] dead people don't show up for eye exams and, since dead patients kill drugs, that study was killed by discontinuing the placebo group. How clever!
One of the authors in a mail to me: "and we proved that statin does not cause blindness in people." That too would have killed the drug.
Eddie,
It seems that you'd like evidence-based medicine to go back 25 years. There are multiple landmark trials that demonstrate that a prevention stratgey that includes lowering LDL effectively reduces cardiovascualr events in a variety of populations. If one is a patient with high cardiometabolic risk, it is definitely in your interest to take a statin. The morbidity associated with these events is horrendous. On the other hand, if one is intolerant to statins, there are numerous other strategies that your physician can employ to reduce your risk.
What is your bias?
CV MD
"I am a 64 year old material sciences engineer with no sign of the diseases I write about. I work close to Montreal, just North of the Vermont border. My work is to determine the causes of technical failures. I go on location, establish physical data and facts and add those up in a report --and try to do the same with some of the disease conditions that have popped up in the last century .. and why arteries corrode and fail."
You should recognize the above, Eddie. It's verbatim from your website. Somehow you neglected to include where you went to medical school or where you obtained your doctorate in pharmacology.
Let's have your creds pharmavet.
I once worked at an agency that provided analytics to a major NJ-Based biopharmaceutical company. I did some field rides with their reps and they ignored me.
Saving lives, I submit, is the primary function of a CV Medic, and that is where statins have failed. I obviously agree with you that a non-fatal event can be life changing. However, simply having a nitroglycerin mimic causing fewer non fatal events to be logged in a trial is arguably similar a cohort an low dose VIOXX in an arthritis trial having fewer interventions recorded. Who would expect differently? Indeed, the majority of the 'benefit' in JUPITER was in revascularizations + hospitalizations, neither, so show the data, of any cardiovascular mortality benefit in that group of 8900 after 1.9 years of taking Crestor/rosuva. My bias? About 30 years of independent research as to the causes of arterial and cardiac decline. Also, I am a specialist in structural failures .. and the heart and artery are in most part structural proteins. In heart, the structure building cells out number the muscle cells and that is where my interest /bias lies.
Pharmavet. At least I don't hide behind a fake name like you do and if the only thing you can do is attack my person, it will be obvious to anyone reading this blog that you find attacking someone with >20 references about the topic on Medline [see the same page on my website that you quote] and a more than minimal knowledge of the cardiology field more important than answering his concerns.
It does not take someone with a degree in anything to read the mortality numbers in a clinical trial ... if anything, it should NOT be doctors but actuarial types and those folk have not published on the issue to my knowledge. If, by any chance you have a degree in pharmacology [who knows] how come you have not dealt with my concerns: start with the factoid that statins have no mortality benefit in women [RR 1.00 in those 2 meta analysis]. Sorry you missed that mortality bit.
I've done ride-alongs with cops. That doesn't make me one.
You post with an pseudonym, Vos uses his name. You won't give your credentials, Vos has his on the Cardiology Journal site and his own site, both linked in his comments. You name-drop some researcher you were introduced to/passed in the hallway about 50 year's ago. Vos is searchable on PubMed.
You dismiss him based on his profession.
We still haven't heard what yours is, where it was obtained, and what the date of that was.
Okay, riv. Here goes:
-Undergraduate degree, 1970. Major in Zoology, minor in Chemistry. Summa Cum laude, Phi Beta Kappa.
-Graduate/Medical. MD/PhD program, 1977. Completed in seven years. Graduated 7th in class of 127.
- National Heart, Lung and Blood Institute Post-Doctoral Fellow, 1979-1981.
- Director, Clinical Research Pharmaceutical Industry, 1981-present with specialization in CV/metabolic sieases.
I'd list my publications but i don't wish to waste any more bytes. I'm sure that my publication list would be even longer if I wrote a lot of review articles and commentaries instead of the original research papers that I have published in peer-reviewed journals.
Since having a pharma degree seems important to some, my upcoming critical letter about Crestor in an AHA journal was jointly written with a cardiologist and a pharma prof. There is little disagreement [privately] even among the 'statin opinion leaders' that they have not made a dent in mortality.
Regarding riv's comment. I have no problem with you having zero or massive credentials, my problem is that you don't answer concerns and, in my humble opinion, that you appear have missed the most crucial failure of statins and, despite of that, propose that they are marvelous. Moreover, they have side effect but no cardiologist [or pharmacologist] reads obscure journals that deal with some of them, like Glia. Cardiologist do not examine brain or colons, and that is where the long-term damage [if low total cholesterol is an issue and if statins affect the nervous system] may well lie.
I'll go with the engineer. At least he's not got a heart-stopping list of conflicts of interest that had to be dragged and shamed out of him.
This below? It'll do. As I said, I know who you are. But this at least gives readers some idea of how much credibility you have on this issue.
From my opinion, you have none.
You think this is impressive. I think this is qualification for being excluded from discussion of the benefits of statins.
- National Heart, Lung and Blood Institute Post-Doctoral Fellow, 1979-1981. FAIL
- Director, Clinical Research Pharmaceutical Industry, 1981-present with specialization in CV/metabolic sieases. (sic) FAIL
Use tiny url. Give us a PubMed link. And exclude any that were industry funded, otherwise yes, I'd have to agree with the latter part of this statement.
"I’d list my publications but i don’t wish to waste any more bytes."
This person clearly has has an enviable history in the field but, just possibly, there is the sad reality that drugs rarely if ever deal with the causes of "CV/metabolic diseases", his/her field. The very idea of a metabolic disease being fixed by a drug [mainly inhibitors of biochemistry] is strange. How can a drug fix something to do with what we do or do not put into our mouths? Remember, Pfizer announced a couple of years ago that they abandoned the field of CV research.
Cardiovascular disease is primarily a decline of structure --and thus function-- and the solutions to that decline are elsewhere, for example in minimizing life-long damage from homocysteine with a multivitamin [a 'metabolic' approach], by limiting AGEs and by optimizing omega-3 fatty acids and some electrolytes, like magnesium and potassium, to maintain heart beat when it counts.
Before people jump on my neck about homocysteine: lowering it does not repair an atheroma damaged artery or shrink an over stretched left ventricle. However, homocysteine can be a major cause of that damage as per ~10 avenues of research. On the other hand, there are no obvious endogenously made [i.e. pure] cholesterol pathways for damage to our structural proteins. Pfizer was right to give up research in CV drugs.
Dr. Vos, I assume for the sake of discussion that you would consider the United States Centers for Disease Control as reasonably unbiased source of information. The attached link to the CDC website explains the reasons for the great decline in cardiovascular disease mortality and morbity in the 20th century in the United States:
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm4830a1.htm
Extracting the principle reasons from the article:
"1) a decline in cigarette smoking among adults aged greater than or equal to 18 years from approximately 42% in 1965 to 25% in 1995 (13). Substantial public health efforts to reduce tobacco use began soon after recognition of the association between smoking and CVD and between smoking and cancer and the first Surgeon General's report on smoking and health published in 1964. 2)a decrease in mean blood pressure levels in the U.S. population (11,13,14). 3)an increase in the percentage of persons with hypertension who have the condition treated and controlled (11,13,14). 4)a decrease in mean blood cholesterol levels (12-14). 5)changes in the U.S. diet. Data based on surveys of food supply suggest that consumption of saturated fat and cholesterol has decreased since 1909 (15). Data from the National Health and Nutrition Examination surveys suggest that decreases in the percentage of calories from dietary fat and the levels of dietary cholesterol coincide with decreases in blood cholesterol levels (16). 6)improvements in medical care, including advances in diagnosing and treating heart disease and stroke, development of effective medications for treatment of hypertension and hypercholesterolemia, greater numbers of specialists and health-care providers focusing on CVD, an increase in emergency medical services for heart attack and stroke, and an increase in coronary-care units (13,17). These developments have contributed to lower case-fatality rates, lengthened survival times, and shorter hospital stays for persons with CVD (1,17)."
My question is: do you dispute the conclusions of the foremost public health agency in the United States that pharmacotherapy for hypercholesterolemia, as well as other interventions has played a role in improvements in coronary mortality and morbidity?
My fuller comment is hung in moderation so to conclude:
Dear Pharmavet: to answer your question directly [and I am NOT talking morbidity or 'other interventions']: NO, I don't believe that pharmacotherapy has numerically or visually affected the mortality curves of your CDC figure. BP drugs may lower stroke deaths but increase deaths from other causes while cholesterol-lowering drugs, I submit, have not reduced mortality. Moreover, population wise, it is low cholesterol that is the greatest risk for early death, certainly in anyone over age 50 [see Vorarlberg].
Pharmavet
Eddie Vos is a member of The International Network of Cholesterol Skeptics (THINCS).
http://www.thincs.org/members.htm
Pharmavet, I have a cholesterol level of nearly 500. I don't have cardiovascular disease.
P.S. Can you tell me pharmavet: What's the definition of Munchausen by Proxy?
Riv, if you seriously have a cholesterol level near 500 mg/dl, you may have Heterozygous Familial Hypercholesterolemia, even if you are asymptomatic. Non amount of non-drug therapy will lower this level.
So, if you were my physician would you advise me to take a statin?
Oh and P.S.
What are the symptoms of "Heterozygous Familial Hypercholesterolemia" I should look for.
To all, a larger posting got blocked by a spam blocker -- probably because it had a very long URL to Pharmavet's figure in it. I'll try and post it tomorrow although I've asked our host to post it for me.
To riv: FH people lived longer in the 1850's than the one population that was looked at. The authors, including a man I admire, Kastelein, concluded: the condition has a large 'environmental component'. .. and where drugs cannot help you, only your biochemical environment.
Dr. Vos, we may differ on treatment approaches, but I would suggest that if a patient voices a real or potentially significant medical problem, that we should all try to refrain from giving or even suggesting medical advice on this site. There are other, more appropriate venues for that.
Thanks Eddie. I have no concern whatsoever for my cholesterol level. I do however, continue to try to recover from the life-altering harm caused me by statins. I do this alone, because the physicians who don't question edicts handed out to them by agencies (CDC, WHO, FDA, Health Canada, CIHR) whose mandate it is to protect the public from graft, greed, and predatory prescribing, are themselves in conflict of interest.
And by the way pharmavet, you shouldn't be diagnosing anyone on the internet. FH!!! I might have FH??????
Oh my GOD? Will I die? What should I DO!!! How much longer do I have?!! Will this affect my 97 year-old mother? My 80 year-old brother? Perhaps this is why my father died young.
. . . . . . .
Oh wait, he died in a hunting accident.
Dear Pharmavet, I did not give medical advice that I recall, I simply stated the trial results about mortality and statins, a failure certain in women.
P.S. the figure in your CDC link shows an epidemic, the topic of my blocked posting but accessible from your link. Regards, EV
Dear Eddie: I did not mean to imply that you were recommending medical advice, but as you can see from some of these posts, there are some people who seem to be seeking such advice. Since we have no way of knowing whether these folks are sincere, or whether they are simply trying to provoke an opinion one way or another, it seems prudent to me to avoid giving medical advice in all cases. For me, it's more of a general principle. I would never give medical advice without seeing the patient in my office. The only reason that I even suggested that someone with a serum cholesterol of 500 mg/dl might have Heterozygous FH is that in my clinical experience there are no other disorders, even profound hypothyroidism, with cholesterol levels that high.
BTW, "industry insider" is my alter ego to Pharmavet-R. Now that my "cover" has been blown, I changed my handle because some other people were expropriating the Pharmavet-R moniker. I don't know why this has happened, since I seem to be so thoroughly disliked by many folks on these boards.
My cholesterol level isn't a disorder. I don't want or accept medical advice from the likes of you. And I think you are dangerously, and possibly, willfully ignorant on this issue.
www.whp-apsf.ca/pdf/statinsEvidenceCaution.pdf
www.ti.ubc.ca/pages/letter48.htm
This is a reposting of something bounced by a spam filter; I took out the 1st URL and I split it in 2:
Dear Pharmavet aka “industry insider” , I accept the title of Dr. in the sense that it means 'teacher'. I was very well aware of that CDC article in particular of its Figure 1 that starts well above near zero for [non infectious] coronary disease. No change in intake from fat, a 50% increase in obesity, an insignificant drop in blood pressure and an 8% drop in total cholesterol explaining a 50% drop in coronary mortality?? Not likely.
I personally have that curve start [as per AHA and just continue the red line to the left in your figure] not far from zero near Herrick's first description of MIs in 1912.
So, we agree there is a mortality epidemic; the ideas over what causes it differ. Epidemics cannot be caused by genetics and this one not by microbes or cholesterol in the diet, let's agree on that.
Now, if one only looks at say 5 factors they all are made to fit to explain the rise and fall [CDC, INTERHEART]. The curves clearly do not follow the use per person of cigarettes but that evidently can cause an attack. They are also unrelated to the existence of statins, that's a given.
Continued: CDC concentrates on blood pressure. But, is it a cause of heart attacks or a result of a declining responsiveness of the vascular system? I believe the latter, and suggesting that lowering a marker [BP] is a 'cause' of the 50% reduction in coronary deaths is bizarre. Anyone knowing anything about BP drugs knows that they do not reduce deaths vs placebo, and even less to to change an incidence curve such as in your article.
As you know, it is easy with a drug to lower a marker, just like one can lower a fever, marker for an infection, by sitting in ice water, something that will clearly not deal with the cause of the problem, being a microbe.
Moreover, the CDC did not control for homocysteine, red-cell omega-3 [the 'omega 3 index'] and other variables. But here the CDC deserves kudos: they document the major rate reductions in deaths following the introduction of only one homocysteine lowering B vitamin: http://circ.ahajournals.org/cgi/reprint/113/10/1335.pdf
The cause of arterial decline can be lack of nutrients causing homocysteine over 7 µM; the cause of heart disease cannot be lack of circulating statin. Teacher Eddie signs off.
Eddie, I have read of a theory that states that atherosclerosis may be an autoimmune reaction triggered by a virus, which attacks the lining of blood vessels. Since inflammation, i.e. CRP, homocysteine has now been linked to vessel wall changes such as mononuclear cell infiltration, the autoimmune theory seems like it may have some plausibility. I also believe that the lipid hypothesis also explains only a part of the process, although how much of a role I suppose is up for discussion.
Hopefully you and I can have a high level scientific discourse on this subject without being subjected to more bile from people without the scientififc background to put forth a cogent argument without devolving into inflammation of a different and unseemly sort.
http://www.health-heart.org/CardiacMortalityUS1900-96.gif was the DCD gif I was referring to. I extend the red curve to the left to 1912 Herrick in JAMA. How can any cause explain this rise and fall, and drop for strokes, over 96 years, if not simply 'environmental', our biochemical environment. I take this as lack of B-vitamins via the corrosive agent of homocysteine, of a drop in antiarrhythmic magnesium from refined grains, and removal of omega-3's by food choices and hydrogenation as of 1911.
Microbes can figure in [and did] but can they explain such curves and that have different epochs in different parts of the world. Think the former Soviet Union / East Block.
About C-RP, it's elevated in or marker of obsity / metabolic syndrome / diabetes, and lowering it for 1.9 years in 8900 people with Crestor did not drop CV mortality. So lower an inflammatory agent [and there are at least 6 ways to drop C-RP] for that long seems to have no effect. Antibiotics do not decrease the incidence of CVD in our current setting. Also, which virus? And why not the same curves across the planet if it's a virus?
I believe 'monoclonal' myocyte migration into the intima should not happen when the elastin that defines the media remains intact and is well regenerated [again, B-vitamins / homocysteine can be causal].
I believe The Lipid Hypothesis can only be rescued by looking at the nutritional and toxic composition of the LDL particle [carotenoids, tocopherols, omega-3s or, on the other hand, trans fat, ox-cholesterol and homocysteine, other]. That is where statins cannot play a role, they can only reduce the amount of endogenously produced cholesterol of which ~48% is needed to make stable LDL emulsion particles. We have to improve the QUALITY of what LDL transports, not its amount. If it carries bad stuff, we have 'bad LDL'.
To me, CV disease is structural decline and taking care of our structural proteins is biochemistry 101. Best, EV
Sounds good to me, Eddie. Sounds like you might also subscribe to the idea of the damaging effects of oxidized LDL on the vessel wall, which I happen to agree with, since otherwise, macrophages would have little other reason for being there, as these cells are not primarily involved in LDL cholesterol transport in the first place.
I think that many people were sold on the lipid hypothesis early on by the dietary studies in susceptible species, such as rabbits, where they were fed diets abnormally high is cholesterol and saturated fats. This led everyone, including me chasing down the same road. With discoveries about oxidized-LDL as a damaging agent, people began to look elsewhere, as well as to the importance of different particle sizes, not just holo-LDL. I always believed that the story was much more complicated, as you've pointed out, than just the "bad cholesterol" vs the "good cholesterol". I think that the NCEP framed the public education program in this manner as a means to get people to get their lipids checked, so that people could be able to know "their numbers". I would say at the end of the day that "knowing your numbers" may not be such a bad thing if it is considered in the context of other risk factors. Sadly the biggest risk factor in my judgement, obesity, has been sadly neglected in the US.
Check here Monday:
------- DO STATINS HAVE A ROLE IN PRIMARY PREVENTION? AN UPDATE. LETTER 77 --
Therapeutics Letter #48 (April-June 2003)1 concluded that “statins have not been shown to provide an overall health benefit in primary prevention trials” based on the 5 RCTs8-12 available at that time. More RCTs are now available and 5 systematic reviews2-6 designed to answer this question have been published since 2003. Unfortunately, these reviews do not answer the question “Do the benefits of statins outweigh the harms in people without proven occlusive vascular disease?” This question is critically important to patients, physicians and health care resource utilization.
Read more here: http://ti.ubc.ca/letter77
Sadly, all your "high level scientific discourse" achieved nothing. Statins were prescribed based on marketing, not science.
In a fairer world, pharma vets and other insiders would be in prison. We may yet achieve that.
So, IF it is the nutritional composition of the LDL droplets that matters [including ox-chol from extra crispy bacon et al] we have to conclude that lowering THE NUMBER is pointless. That has been shown by every NUMBER lowering technique ever used on women [fact certain] and men [fact probable]. I don't blame the scientists for having explored non productive paths, I blame each doctor for placing his/her signature on a script for statin without knowing the lack of benefit and understanding the harms; THAT is the problem, there is the blame.
The tragedy is that the marketing types have promoted garbage and people like riv have been permanently damaged by statins. Therefore her understandable anger and outrage. Also, millions are and will be damaged [financially and physically] by statins based on zero science, and in the mistaken belief they'll avoid a fatal heart attack.
Anecdote: last week our 63 year old neighbour on Lipitor suffered a FATAL bleeding stroke. Guess what: SPARCL showed Lipitor causes that kind of strokes vs placebo, a trial that ended with numerically more deaths on that statin.
The tragedy to researchers [who all were well paid to follow non productive paths] is that they came up with no solutions to deal with the actual causes of arterial decline. It would have been simple if science had not be hi-jacked by the Lipid Hypothesis, declared dead by George Mann in NEJM in the early 70's. It would have been dead if not given life support by the 10s of billions now made yearly off statins.
Obesity: send people to eat more carbs and it's like cows in a grain feed lot: they get fat, another Evil result of the NCEP idiocy: see http://www.health-heart.org/links.htm#INSIDER
Eddie, we could continue the statin debate ad infinitum. I could probably come up with my share of success stories on Lipitor, which my own mother takes for ischemic cerebrovascular disease, and on which she has shown remarkable improvement. Such would be the non-productivity of such a dialogue.
Riv, I am thankful that I'm not in prison, or I would not have been able write the Rx the Lipitor that has improved my dear mother's life. I'm sure, however, that you think that it's all part of my evil plot to kill my own mom so that I can inherit her money, of which she has very little.
Hence the folly of continuing on this thread. Eddie I will look you up off line so that we can discuss arterial wall pressure dynamics and the like, that are of mutual interest. If I self-identify off line, I only ask that you respect confidentiality, as I will respect yours.
Over and out.
Insider, my email is eddie{at}vos.qc.ca with the promise I'll never reveal your name. I'd be interested seeing your Medline / publication record.
Statins MUST be debated, and that is easy when sticking to the RCTs. There are many other ways slowing ischemia. My mother was killed through a now withdrawn OTC addictive kidney toxin [phenacetin] that was OTC for >100 years. That'll never happen to statin. Hoping your mother will do well. I trust you know the NNTs in SPARCL. Cheers, EV
Best to stick to science when you offer up Lipitor success stories.
Just the facts please. You don't have any.
This is the problem Eddie. You and the suit here can exchange pleasantries and niceties all you like. All you're doing is confirming his thinking that status take the game.
And the people die.
Statin survivors, about 400 who have not recovered, and some who have died: stopped_our_statins.webs.com/
NIH funded study in to statin negative effects: Over 1,000 study participants, all statin injured: www.statineffects.com/info/
For those impressed by cvs: www.statineffects.com/bgolomb/
Thanks Ed for leaving these in. For the lurkers.
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