tag:blogger.com,1999:blog-1629175743855013102.post3710961401022059809..comments2024-03-28T11:29:46.845-07:00Comments on Whole Health Source: New Study Strengthens the Case that LDL Causes Heart DiseaseStephan Guyenethttp://www.blogger.com/profile/09218114625524777250noreply@blogger.comBlogger72125tag:blogger.com,1999:blog-1629175743855013102.post-56635265603079172022016-12-23T07:49:19.956-08:002016-12-23T07:49:19.956-08:00Could someone point me to this 'huge mountain ...Could someone point me to this 'huge mountain of evidence that ldl causes heart disease'<br /><br />Thank youMarkhttps://www.blogger.com/profile/06645183522923868718noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-28414650524446087132015-06-15T23:41:22.940-07:002015-06-15T23:41:22.940-07:00Tim, I don't think the point is that relative ...Tim, I don't think the point is that relative risk isn't scientific. But very fair criticism can be made against relative risk as a way of presenting results. Absolute risk and NNT are also scientifically robust in my understanding, and I feel they are more useful in clearly communicating risk reduction. I think saying that criticizing relative risk is 'inept, misguided and fraudulent' is a deeply inflammatory remark that serves no purpose but to elevate the level of tension in a very controversial subject.<br /><br />On a different note, I'm curious how ezetimibe and cholestyramine factor into the discussion on the direct effect of LDL levels and heart disease. From what I can gather, they both are effective at lowering cholesterol levels, yet both are ineffective are reducing heart disease. If LDL was a direct cause, wouldn't these drugs be effective? Anonymoushttps://www.blogger.com/profile/13013335809575738627noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-66484333182844147842015-06-13T08:00:48.993-07:002015-06-13T08:00:48.993-07:00Of all "arguments" one can contrive agai...Of all "arguments" one can contrive against the significance of some study's results, complaining about the well-established scientific standard of relative risk ratios is certainly the most inept and misguided one.<br /><br />In fact, anyone coming up with such a "last resort" argument against evidence that doesn't fit his preconceptions only reveals his own scientific illiteracy.<br /><br />In the case of Joe Doro's comment above it is not only misguided but outright fraudulent, as he deceptively ommited the context in which the study was conducted by selectively citing parts of the abstract.<br /><br />This is was the methods paragraph states:<br /><br />"We conducted a randomized trial involving 2341 patients at high risk for cardiovascular events who had LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or more and were receiving treatment with statins at the maximum tolerated dose (the highest dose associated with an acceptable side-effect profile), with or without other lipid-lowering therapy."<br /><br />The 48% risk reduction was seen in patiens already on high-dose statin drugs which were ADDITIONALLY given alirucumab in order to get their LDL below 70 mg/dl, compared to those ONLY taking statins and a placebo (any ony trial design would have been unethical anyway). The absolute incidence in CVD events is of course expected to be low in such a collective - the more remarkable it is that alirucumab further cut the risk in half.<br /><br />Of course developing a new drug such as alirucumab is immensely expensive and this cost (plus a generous profit margin for the patent holder of course) is reflected in the actual cost of the medication. However, this is the case with any new drug on the market. Prices go down massively - basically to the mere production cost - as soon as the patent on a drug expires and generics become available.<br /><br />This is why economical objections against a new drug based on its initial market price don't make any sense with regard to the drug's value in the long term.Timhttps://www.blogger.com/profile/13771137905561268666noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-73864268193760995172015-06-01T01:55:26.014-07:002015-06-01T01:55:26.014-07:00Thanks for digging that up Joe Doro. When I see a ...Thanks for digging that up Joe Doro. When I see a "50% reduction" in risk, alarm bells tend to go off in my head. I wonder, where would those numbers would sit if there wasn't a strong bias to only publish positive results?<br /><br />I suppose policy makers perhaps excuse this kind of math by looking at entire populations of a country, thinking that if heart attack rates go down 1.5% they're saving countless thousands of people! Without considering the hundreds of thousands that would be spending fortunes without any statistical chance of benefit while risking significant side effects.<br /><br />It's irresponsible to completely demonize pharmaceutical companies for this kind of shotgun approach to treatment, it can certainly cause one to loose faith in what their real interests are.Anonymoushttps://www.blogger.com/profile/13013335809575738627noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-30380544386616516952015-05-31T12:10:24.441-07:002015-05-31T12:10:24.441-07:00In my comment above I meant Weston Price not Richa...In my comment above I meant Weston Price not Richard. Thank you for your well meaning replies, but my confusion still persists as to cholesterol. It is but a poor consolation that, as much as I can see from the posts, I am not alone. My question remains the same: What is the practical message that this article boils down to? Someone recommends that saturated fat intake should be kept low. An explanation, please. Someone else says ingested cholesterol matters after all. I am still somewhat skeptical about this later opinion, because shrimps (containing lots of cholesterol, don’t ask me if of the good or the bad type) for example have been somewhat of a staple for certain South Sea tribes practically free from western diseases.jewiuqashttps://www.blogger.com/profile/12086623682064078710noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-63582579523951856772015-05-31T08:38:13.466-07:002015-05-31T08:38:13.466-07:00From the study you quote:
Limitations: Results we...From the study you quote:<br /><br />Limitations: Results were derived from study-level data rather than patient-level data, and clinical outcome data are rare.<br /><br />And from one of the studies included in this meta analysis (Efficacy and Safety of Alirocumab in Reducing Lipids and Cardiovascular Events) NEJM.<br /><br />"In a post hoc analysis, the rate of major adverse cardiovascular events (death from coronary heart disease, nonfatal myocardial infarction, fatal or nonfatal ischemic stroke, or unstable angina requiring hospitalization) was lower with alirocumab than with placebo (1.7% vs. 3.3%; hazard ratio, 0.52; 95% confidence interval, 0.31 to 0.90; nominal P=0.02)" Absolute risk reduction 1.6%<br /><br />And from one of the others while showing a decreased overall mortality, did not show a statisitically significant decrease in cardiovascular deaths. <br /><br />Once again,we are being bombarded with relative risks, odds ratios, etc. all of which always sound pretty dramatic. I mean 50% sounds so much better than 1.6 % But when the TV ads come out how many will quote the absolute risk or for that matter, the NNT (number needed to treat), a measure that most clinicians find much more useful.<br /><br />Remember when Jarvik was pitching Lipitor while rowing in a single scull? BTW he wasn't a rower, they had a stand in for him. Anyway, the TV ads shouted a 33% reduction of having a vascular event if you were high risk for a vascular event (primary prevention). Yet if you looked at the package insert and saw the data you found that over a 3 year period the control group had 3 events and the treated group had 2. But through the magic of the relative risk reduction calculation an absolute 1 % risk reduction becomes 33%.<br /><br />So let's look at the NNT<br /><br />Assuuming that the annual absolute risk reduction is near 1.5 % for these new drugs then the NNT will be about 67 so that means at say $10K a patient we as a society will spend about $670,000 a year to prevent 1 vascular event. To put that in perspective, that's my family's health care premium for nearly 56 years.<br /><br />And finally, I wish I could have back the money I have invested over the years in companies that had very promising phase 2 trials only to the have the phase 3 trials fail.<br /><br />No yonder the FDA will probably not give these drugs approval until the clinical data becomes available or at least will have very stricit indications. Remeber the debacle with the statins? In order to get a new one approved all you needed to show was that it lowered cholesterol and was safe. You never had to show they actually reduced clinical events. The LDL itself became the endpoint.Anonymoushttps://www.blogger.com/profile/13928941469746102069noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-39000495592128954082015-05-26T07:23:02.612-07:002015-05-26T07:23:02.612-07:00I forgot to mention dark leafy greens specifically...I forgot to mention dark leafy greens specifically lower the risk of pancreatic cancer, even more so than yellow vegetables. This is something we do not want to get. They are not the only thing I eat. I only recommend adequate to generous helpings in the context of an overall balanced diet.<br /><br />Dark leafy greens are an excellent addition to any diet- even one that does pretty well without them. Variety is essential. I am neither low carb, nor high carb. I eat as much variety as possible, until we know more. And we have MUCH to learn about nutrition. This may well be the most complicated area in biology or one of them.Anonymoushttps://www.blogger.com/profile/11913377210298291464noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-50931513718072392372015-05-25T13:41:14.967-07:002015-05-25T13:41:14.967-07:00Taylor
You are bang on - the 'LDLp as main ca...Taylor<br /><br />You are bang on - the 'LDLp as main cause of atherosclerosis' is a lucrative farce...<br /><br />Ivorfffhttps://www.blogger.com/profile/03594222216394266705noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-2421348679993284592015-05-24T10:10:04.332-07:002015-05-24T10:10:04.332-07:00It doesn't really seem that there is a scienti...It doesn't really seem that there is a scientific consensus about what the precipitating factor of an atherosclerotic lesion is : http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2796.2000.00655.x/full<br /><br />The risk associated with high LDL-p would exist if LDL contributed only to the progression of the disease or only to the initiation of the disease or to both.<br /><br />I must admit that I find the idea that LDL particles start to tear through the arterial wall when the concentration of them increases by 50% or so to be somewhat dubious.TCO348https://www.blogger.com/profile/15972478226700429070noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-34555519726844078582015-05-23T10:29:44.938-07:002015-05-23T10:29:44.938-07:00Richard Nikoley:
They are anti-inflammatory, and ...Richard Nikoley:<br /><br />They are anti-inflammatory, and extremely nutrient dense. They are a great addition to anybody's diet likely. Far too little is known about nutrition for the Blogosphere's certitude and dietary tribes.<br /><br />We want as much VARIETY in our diets as possible until we know more- much more. Nutrition is not rocket science, it is FAR worse. Far more complicated.....<br /><br />You might know who I am. We have met before I believe. ;)Anonymoushttps://www.blogger.com/profile/11913377210298291464noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-84207989812712206202015-05-22T17:11:52.266-07:002015-05-22T17:11:52.266-07:00Yep it's a no brainer. I lowered my cholestero...Yep it's a no brainer. I lowered my cholesterol to 112 mg/dL on a starch based diet. Below 150 is considered heart attack proof woohoo! You can get omega 3 from flax and fats from nuts, seeds, avocados without the toxins that reside in the fats of fish, etc.<br /><br />Amazing people think if you eat cholesterol it doesn't affect your cholesterol but they make exceptions for iron, protein and calcium from meat and dairy that they eat. You are what you eat, it's common sense. Our biology points to us being herbivores from teeth, saliva, stomach acidity, intestines, jaw, etc.Will Kriski (Potato Strong)https://www.blogger.com/profile/14249601752461194413noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-2029069892840899402015-05-18T09:46:51.473-07:002015-05-18T09:46:51.473-07:00Richard S:
Where does all tis "leafy greens&...Richard S:<br /><br />Where does all tis "leafy greens" stuff come from? It's basically rabbit food and they're coprophagic.<br /><br />For instance, consider the Ugandan diet. Lots of various starches, and meat. No leafy greens in sight.<br /><br />http://freetheanimal.com/2015/05/prebiotic-probiotic-mercenaries.htmlRichard Nikoleyhttps://www.blogger.com/profile/08479556896882145179noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-20292451188204501852015-05-17T07:14:09.173-07:002015-05-17T07:14:09.173-07:00Jewiuqas,
I would recommend a balanced style of e...Jewiuqas,<br /><br />I would recommend a balanced style of eating with plenty of leafy greens, berries, citrus fruit and supplementation with chia seeds and fatty fish or fish oil. This is because your cells need these fats in small amounts. A top researcher who studies the endothelium told me this. Stephan has a quality article here exposing hucksters.Native newly formed LDL does not appear atherogenic, but the endothelial cells themselves have the ability to modify LDL. Oxidized and altered LDL lipoprotein is a problem and the greater the levels of LDL the more risk and potential there is for modification. Of course, many other things matter-blood sugar, elevated blood pressure.Anonymoushttps://www.blogger.com/profile/11913377210298291464noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-54465888033329424462015-05-16T17:31:44.424-07:002015-05-16T17:31:44.424-07:00As to refined carbs, I got no worries because I ha...As to refined carbs, I got no worries because I have almost totally excluded them from my diet apart from some white rice flour that I use as thickener in shepherds pie and suchlike dishes. But I use very little, so that a 250 g pack lasts for 6 months.<br />So, the Richard Price devotees are proved to be wrong with their saturated fat rich regime ? But saturated fats are more stable, it is the PUFA-s that get oxidized and turned into trans fats, is it not the case?jewiuqashttps://www.blogger.com/profile/12086623682064078710noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-71410282187964877352015-05-16T14:38:19.970-07:002015-05-16T14:38:19.970-07:00@jewiuqas: For authorative, science-based and larg...@jewiuqas: For authorative, science-based and largely ideology free information on healthy eating - including CVD prevention - you should consult the Harvard Nutrition Source:<br /><br />http://www.hsph.harvard.edu/nutritionsource<br /><br />Regarding dietary cholesterol: unless you carry some rare genetic polymorphism, dietary cholesterol won't have much effect on your cholesterol levels. What is more likely to raise your LDL cholesterol is saturated fat and refined carbohydrates.Timhttps://www.blogger.com/profile/13771137905561268666noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-90726572116754522652015-05-14T16:32:53.312-07:002015-05-14T16:32:53.312-07:00Sorry for interrupting the sophisticated scientifi...Sorry for interrupting the sophisticated scientific exchange of views. I am just a down-to-earth guy somewhat at a loss as to which school of nutrition to adhere to with the view to escape the lamentable fate of many of my ancestors of both sexes who died in their early sixties, or even in their fifties of various diseases termed “of civilization”. So, does anyone have a recommendation as to what I should exclude from my diet in the light of the subject discussed in this post? I never cared a fig for cholesterol because someone knowledgeable said once that it was one of the biggest mistakes of the 20th century to accuse dietary cholesterol with causing cardiovascular issues. LDL and HDL, discussed in this post, are not the same as cholesterol, as much as my understanding goes. So, should I avoid eating cholesterol or LDL, or both? If so what foods contain them?jewiuqashttps://www.blogger.com/profile/12086623682064078710noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-28769273937832971712015-05-10T22:43:47.249-07:002015-05-10T22:43:47.249-07:00Just a few random comments.
I recently saw a vide...Just a few random comments.<br /><br />I recently saw a video put out by Ray Kurzweil (narrated by Edward James Olmos) that made the claim that it really is oxidized LDL that causes atherosclerosis. LDL particles normally get into the artery wall and macrophages clean them out. But the oxidized particles "kill" the macrophages which leads to the formation of foam cells and starts the process. Too many LDL particles circulating for too long tends to make more of the oxidized. The video didn't cite any references as far as I could find.<br /><br />Also, some have speculated that one of the ways statins work is by increasing the number of LDL receptors in the live, much like PCSK9. The body notices that there is less cholesterol being produced so it increases production of some protein that promotes LDL receptor creation. I think researchers should try to figure out if something is nuking our LDL receptors, something that was not around until the early 20th century. Seed oils, vaccines, electricity, sugar, whatever.<br /><br />And, as Dan said a few posts up, blood sugar seems to be a better predictor of risk than LDL (C or P).<br /><br />Sorry no links or references for any of this, just recalling what I have seen recently.E. Hosewaterhttps://www.blogger.com/profile/03952660610191473905noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-81518552612963272892015-05-07T23:31:44.016-07:002015-05-07T23:31:44.016-07:00Tim, yes everyone has an opinion.
Though a lot of...Tim, yes everyone has an opinion.<br /><br />Though a lot of us formed these opinions with help from previous posts on this very blog so I'm sure you can appreciate the confusion.Anonymoushttps://www.blogger.com/profile/13013335809575738627noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-29499812049418926362015-05-06T02:20:15.002-07:002015-05-06T02:20:15.002-07:0050 comments and counting. No surprise, really. Som...50 comments and counting. No surprise, really. Somehow on the blogosphere everyone whose cousin's friend is on statins and who has understood the difference between LDL and HDL seems to consider himself an expert on cholesterol, knowing about the "real causes" of atherosclerosis all medical experts have missed for decades (because they are only fostering their dogmas without commiting any empirical research). Well, sure!<br /><br />Is the oxidative state of the LDL particle the key factor to atherosclerosis? Very unlikely, otherwise the vitamin E trials wouldn't have failed so badly. Does a pro-inflammatory milieu promote the progression of atherosklerosis? You bet! But LDL tearing though the artery wall remains the initiating factor, and the less LDL the less atherosclerotic lesions. Thank you, Stephan, for once again confronting people with the actual scientific evidence.Timhttps://www.blogger.com/profile/13771137905561268666noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-43614049156589352912015-05-04T21:03:33.833-07:002015-05-04T21:03:33.833-07:00Nawp:
I may have used your post as the beginning o...Nawp:<br />I may have used your post as the beginning of a point I wanted to make, but your question does not strike me as a real question. There is no doubt that dietary saturated fat consumption is a minimal factor in increased "cholesterol " levels. But there is little evidence that increased LDL actually "causes" anything like heart or arterial problems. Now it may be that LDL increases correlate with such issues, which raises some issues regarding the cause for the increase, but it does not necessarily show anything like "cause."<br /><br />As Suzee points out, the reality is that LDL increases may be the body's reaction to arterial damage, not a cause in itself. Statins may "work" because they might function as an anti-inflammatory, but they also seem to have some undesirable effects. But why take a drug (or medicine?) that does not actually do what it is advertised to do? Calcium in the wrong place (in soft tissue) is a possible cause of arterial damage, and is not addressed by statins. <br /><br />Better to eat some kimchee or natto or cheese on a regular basis and avoid statins. As if they do any good.Richardhttps://www.blogger.com/profile/13579689230767618822noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-79386972806624595432015-05-04T09:10:31.078-07:002015-05-04T09:10:31.078-07:00Well well.
I love the pure exercise of iconoclasm...Well well.<br /><br />I love the pure exercise of iconoclasm, of challenging beliefs that reach bromide and slogan proportions. Stephan, you've always been good at that, and the fact that you are now saying "wait a minute" with respect to those things you were posting about way back is testament to your underlying honesty. This is independent of being right or wrong. Honesty finds a way.<br /><br />Personally, I suspect it's rather a U or J curve thing, where most people are in reasonable ranges. Probably, the standard industrial health BUSINESS wants the range of "probably OK," to be as narrow as possible. It's unrealistic to hold them to higher standards than auto-manufacturers and marketers. It's their business to sell drugs. OTOH, just as in cars, you really have to benefit the consumer long term (economics is all the same, whether cars or pills).<br /><br />I also suspect that modern lifestyles and food engineering serve to either push people out of normal C ranges they would otherwise have, or, exacerbate somewhat out-of-normal that in an HG setting would not be any problem. Chronic widespread inflammation is--to my opinion--probably the most underlying factor and C exploits this. So what if treating C is treating a downstream symptom. Would people complain about a drug with low side effect that reduced MI 50% independent of other factors?<br /><br />My HDL remained near 100 and my LDL went way down by focussing on feeding my gut, primarily beans.<br /><br />Finally, it's really difficult for me to see what Stephan politely suggested in terms of the marriage of LC and Paleo in terms of super high C in so many as anything more that irrational denial and justification.<br /><br />Keep on clashing with icons, Stephan.Richard Nikoleyhttps://www.blogger.com/profile/08479556896882145179noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-59974536822057276632015-05-04T03:25:27.510-07:002015-05-04T03:25:27.510-07:00Responding to Paul Darrigo, about my other markers...Responding to Paul Darrigo, about my other markers & dosage of Berberine:<br /><br />I've been taking 500mg 3 times daily with meals. For the past two years, My HDL has been steady at 60, triglycerides stay right at 149. The only change has been the LDL going down. That and I lost 15 pounds, about 7% total bodyweight. I know losing weight can lower cholesterol, but I don't think it would be to the extent it has. (LDL dropping 50 points)Jerryhttps://www.blogger.com/profile/15641211463328140432noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-25338740118611121612015-05-03T19:26:58.165-07:002015-05-03T19:26:58.165-07:00I tend to be leery of statins because it seems tha...I tend to be leery of statins because it seems that bile has a role in transporting excess dietary cholesterol out of the body. Since bile is synthesized from cholesterol, reducing it would seem to reduce our ability to remove dietary cholesterol from our body. It often seems as if the elements necessary for digestion and processing of nutrients are included in the foods we eat (if they are not processed).Suzeehttps://www.blogger.com/profile/16352039641179232628noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-18853508945106481072015-05-03T19:22:41.422-07:002015-05-03T19:22:41.422-07:00There may be a role for menaquinones in prevention...There may be a role for menaquinones in prevention of arteriosclerosis. Menaquinones are needed for the carboxylation of Matrix-Gla-proteins which are responsible for inhibiting calcification in arteries. Our normal source of menaquinones is fermented cheeses, milk and some meat. Alteration of meat and milk production via grain feeding rather than grass may be the cause of many cases of arteriosclerosis and bone loss. It may be more important to prevent the calcification than to change the particles that are clustering. There are many new studies looking at the role of K2 in CVD and other illnesses.<br /><br />http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648716/Suzeehttps://www.blogger.com/profile/16352039641179232628noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-45867610502723544282015-05-03T12:11:17.060-07:002015-05-03T12:11:17.060-07:00In science, truth is gained through replication. ...In science, truth is gained through replication. All that we have in this area are studies funded by pharmaceutical companies that have never been independently replicated. <br />In addition, the best study we have, that is rather independent, is the Framingham Heart Study. Well, what did that study tell us: 1. Over 50 percent of people having a cardiovascular event had LDL in the optimal ranges, 2. the best predictor of heart disease was triglyceride levels and HDL levels (LDL was not a good predictor at all).<br />Then we have the French paradox. A group of people with high cholesterol and LDL levels with low levels of heart disease. I am not going to debate why but only to demonstrate object information about a group of people and their rates of heart disease. <br />Then we have the fact that oxidized LDL occurs when glycemic load increase. That is, to create large fluffy pattern A LDL you lower your glycemic intake. To lower triglycerides you lower your glycemic intake. To increase HDL you lower your glycemic intake. Do you see a pattern? Oh yeah, to lower HS-CRP, you might want to try lowering your glycemic intake. <br />In addition, even the best run pharmaceutical funded studies on statins show that 100 people have to be treated to maybe reduce 1 non-fatal heart attack. None of these studies are a slam dunk proof of anything. <br />In addition, and no one can deny this, is the fact that statins are being given out for “preventive care.” As such, all studies done on them are short, no longer than three to four years. Yet, statins are given to people to take for decades. There are no long term studies demonstrating the efficacy and safety of these drugs for such a long period of time.<br />In fact, what studies do show is that statins, when the outcome is reduction of all cases of mortality, do nothing to extend a person’s life.<br />I would also add, when doing a study, the longer it goes, the harder it is to keep a hold of the benefit you are studying. That is, these pharmaceutical companies know to end these studies because the effect they might have demonstrated, all but low, would disappear over time and might actually demonstrate harm when statins are taken for long periods of time. <br />Ask yourself, if statins are such wonderful drugs, why would a pharmaceutical company end the study instead of keeping it going, if the outcomes were so promising? A study cost nothing in the grand scheme of things as far as the billions they make off these drugs. There is a clear reason why they end these studies early.Danhttps://www.blogger.com/profile/10474662524451464770noreply@blogger.com