To some extent, as long as the statins were working, few people worried too much about why they were helping. But statins are not for everyone. Some people cannot tolerate the drugs’ side effects, including muscle pain and, more rarely, liver damage. Others cannot lower their LDL levels enough simply by taking a statin. In addition, at least one in five people whose LDL levels are well controlled by their medications still experience heart attacks or strokes. “What are we going to do with these people?” asks Christie Ballantyne, chief of cardiovascular research at Baylor College of Medicine.
Thus, by the late 1990s the search was on to find drugs that could supplement the use of statins. One approach was to lower LDL levels using nonstatin drugs such as ezetimibe, which was approved by the U.S. Food and Drug Administration for its cholesterol-lowering ability in 2002. Studies had shown that ezetimibe reduces LDL levels in the body by a different molecular pathway than any that the statins use. Theoretically at least, the combination of a statin and ezetimibe should reduce LDL levels more than either alone. Another option was to raise HDL levels using a drug such as niacin, which is one of the B vitamins. Here again the idea was that a combination of drugs—one to lower LDL and one to raise HDL—should work better at reducing heart disease risk than any single medication.
Crucially, however, neither drug—ezetimibe or niacin—had yet been rigorously tested to see whether it actually reduced the number of heart attacks or strokes in a given population. That kind of investigation is more complicated and takes longer to conduct than does a test of how much LDL or HDL levels change in response to treatment. To determine if a drug actually reduces heart risk or stroke, researchers have to wait until enough study participants develop heart attacks or strokes to make a statistically valid comparison between those who took the trial drug and those who did not.
Clinicians were therefore eager to see the results of a 2008 study named ENHANCE, which compared a combination of ezetimibe and one particular statin drug, simvastatin, against simvastatin alone in people with familial hypercholesterolemia. To everyone’s surprise, ENHANCE found no benefit from the combination treatment, at least with respect to the thickness of the trial participants’ artery walls (thickened walls being a sign of advancing atherosclerosis and another potential indicator of heart disease). This result occurred despite the fact that the LDL levels of the combination therapy group dropped, on average, an extra 51 mg/dL.
Needless to say, the results generated more questions than answers. Did the ezetimibe produce a second effect that negated the beneficial effect of lowered levels of LDL? Or do statins trigger a beneficial anti-inflammatory effect that is the true reason for their benefit? Is LDL lowering as important as most people still think it is? The answers to such questions may become clear in 2013, when results are expected to be released of another study, which is specifically designed to determine whether an ezetimibe-statin combination works better than a statin alone in reducing heart attacks and strokes in test subjects. The clinical results for niacin, the HDL booster, looked more promising at first. A 2009 trial that compared adding either ezetimibe or niacin to standard statin treatment in people with heart disease found that niacin worked better than ezetimibe to reduce trial participants’ artery thickness. Results from this study, combined with those of the ENHANCE trial, looked like bad news for ezetimibe and good news for niacin until this May, when the National Heart, Lung, and Blood Institute stopped its own clinical trial of niacin because researchers found no difference in the numbers of heart attacks and strokes suffered by trial participants taking niacin and a statin compared with participants taking a placebo and a statin.
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36 Comments
Add CommentI recently read an article by Stephanie Seneff.The title: "How Statins Really Work Explains Why They Don't Really Work". I guess you could say her article has pretty much the same conundrum as your article. With numbers like 220 total, 155 LDL, & 50 HDL I was put on a statin. The rare fatigue & rubbery legs side effect stopped me from ever taking the Statins. I'm 80, and blood is still flowing nicely through my carotid artery. Good article Francie & good luck toward getting your master's degree in journalism.
Reply | Report Abuse | Link to thisGeorge Dugdale
Why are these findings perplexing? Many of us in the medical community have long known that cholesterol and even the breakdown between HDL and LDL is insufficient to predict CHD and that statins have an absolutely minor and negligible positive effect, if any, on mortality. All studies have shown a weak link at best. Even the studies touting the benefit of statins need to be read carefully. Their 'benefits' are blindingly small. And LDL numbers are utterly meaningless since even in that subgrouping there are good and bad varieties.
Reply | Report Abuse | Link to thisI disagree. I love statins and think their advantage to the pt goes beyond affecting the LDL/HDL. More importantly though is the role of proper diet, exercise and nonsmoking play in ones overall health. Statins are useless (maybe) in those individuals that do not make important lifestle changes. Physicians need to tell pts that stAtins will not help you unless you change those nasty habits.
Reply | Report Abuse | Link to thisI was on statins for a while for "prophylactic care" but I quit them after doing a bit of research. Even if I hadn't got the nasty side effects I would have quit taking them. Why take a drug if there is no real evidence for their benefit prophylactically.
Reply | Report Abuse | Link to thisI find this bewildering.
Reply | Report Abuse | Link to thisDon't you guys follow the science at all? This is an important area!
LDL cholesterol is made up of large particles (GOOD) and small particles (BAD.) In order to get any useful information from your LDL level, you need a VAP test that differentiates between these two particle types. Adding them together is like counting eggs and golf balls together because they're both vaguely similar looking... Many people with high LDL have low levels of the bad small, dense particles, so it's FINE. The large fluffy particles being counted as LDL are not a problem.
Second, it's the ratios that matter more. Triglycerides are VERY important, and they have an almost linear relationship to carbohydrate intake. If your triglycerides are too high, you can lower them in just a few days by lowering your carb intake significantly.
Third, statins have only been proven to prevent death in men under 65 with a previous heart attack. There is no evidence they help women, people over 65, or men without a history of heart attacks. Whatever they are doing to lower these TEST NUMBERS is not lowering risk of heart problems. Just say no.
I'm happy to see some realistic reporting on this matter. Those of us actually following these studies have known that (outside of familial hypercholesterolemia) total LDL is overblown as a risk factor and statins are even a bit overblown as a risk-reducer.
Reply | Report Abuse | Link to thisWe need to use these numbers to identify help issues instead of prescribing drugs to normalize lab ranges.
Atherosclerosis affects only herbivores.
Reply | Report Abuse | Link to thishttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1312295/
Why take a drug? From the pharmaceutical company's point of view: They can't very well sell them if you don't take them. I'm not trying to cast them as villains, I'm just stating their bottom line motivation. That's the way a free market works. It's up to doctors and patients to balance these forces.
Reply | Report Abuse | Link to thisIt's my understanding that all of the current osteoporosis drugs only increase your reading on bone density tests, by blocking the shedding of dead bone cells. These dead cells don't add to the bones' strength, they just don't 'flake' off. So here are drugs you pay to take, so you can pay to take a test to say they are working. You get it on both ends, and yet you receive no actual improvement in health.
I'll second what ravenrose said. The single biggest thing you can do to control triglycerides is to cut down on the carbs. Many people can cut down on their statins and insulin if they cut down on carbs which will also help them lose weight and lower their blood pressure.
Reply | Report Abuse | Link to thisThe (now) conventional wisdom to cut down on dietary cholesterol and salt are misleading. I eat 3 eggs and bacon or sausage every morning and my lipid profile is the best it's ever been.
Your right! Some people always fail to use commonsense.
Reply | Report Abuse | Link to thisUnless a person changes the "nasty habits", it's just a matter of when...the consequences will occur.
I read some where, "Dreams are my reality". Lots of luck to that kind of thinking.
The cholesterol-heart hypothesis is dogma, not science. This shows up when considering the results of statin trials. The modest effects seen do not correlate with the degree of cholesterol lowering. This should make researchers aim to new hypothesis, but because of the dogmatic (and economic) aspect of the subject, they keep beating a dead horse.
Reply | Report Abuse | Link to thisThe idea that LDL just floats around in the bloodstream and sticks wherever it wants its appealing, but physiologically not plausible.
Whenever a lifestyle change results in improved health, it is often attributed to lowering of cholesterol levels. However, most don't realize that LDL and HDL both form part of the innate immune system. Stress, infection (mainly prokaryotic) and inflammation rise cholesterol levels, as it rises cytokine levels. Its just the normal response. This holds true for atherogenesis. Cholesterol recruitment to the site of endothelial damage is part of the immune response triggered by the insult, not the other way around. Thus, the logical intervention is to prevent the damage of the endothelium by reducing inflammation, not reducing cholesterol levels per se. This is why statins show some benefits in some patients: its pleiotropic (antiinflammatory) effects.
Your statement that "statins have an absolutely minor and negligible positive effect on mortality" is not true. Two large meta-analyses of statins in persons with pre-existing cardiovascular disease or at high risk for same showed substantial reduction in mortality with use of statins (Lancet 366:1267, 2005, and British Medical Journal 338:b2376, 2009). The key is the extent to which the person is at risk. For those at low risk, it is hard to show a benefit since the risk is low to begin with. But for those at high risk, there is substantial benefit.
Reply | Report Abuse | Link to thisKeep stuffing your face, sitting on your butt and enriching the pharma's and you'll see the pills won't help. I took them long enough to feel the side effects, after that I lost the 50lbs and got back to exercising and quit taking the statins. I have more confidence in nature/evolution and myself to control my levels.
Reply | Report Abuse | Link to thisMy total cholesterol is 636. My LDL is 535. I'm a 65 year old male and by standard orthodoxy I should be long dead. Instead, by EBCT my arteries are whistle clean. I eat a diet extremely high in saturated fats and cholesterol (3 dozen eggs a week, for starters.)
Reply | Report Abuse | Link to thisThere are enough people like me that the Harvard, Yale, and other cardiologists I've contacted recognize "there are some families with FH that don't develop vascular disease. It is probably genetic." That is just another way of saying they haven't the vaguest idea why someone can have enormous amounts of lipoprotein circulating for a long lifetime and not develop the disease that "everybody knows" is caused by excessive cholesterol. What is most disappointing to me is the utter lack of interest in figuring out what is different. Seems akin to saying "because there are so few people that spontaneously eliminate the HIV virus from their bodies we aren't interested in figuring that out, either."
Regarding the VAP breakdown, the conventional wisdom that types I and II are "light and fluffy" and don't "migrate into the endothilial walls" and types III and IV are "small and dense" and therefore can enter into the artery wall, doesn't seem logical. The difference in particle sizes in is a very small fraction of the overall sizes of the particles. A claim that it is physical size, rather than some as yet undiscovered difference, seems unwarranted. Especially since HDL particles are much much smaller and contain much more cholesterol by weight.
Pehaps I'm being overly cynical, but I am extremely disappointed in the medical community's enthusiasm for finding the next profitable pill at the expense of deeper understanding of disease.
Oh yeah, my longest living relative was an FH carrier. She died of a broken hip at 93 after a lifetime of a high fat diet.
Reply | Report Abuse | Link to thisNot sure you should conclude from your experience that the medical community is not interested in learning why somce persons like yourself with very high LDL don't get cardiovascular disease. I suspect you just haven't connected with investigators who are working in this specific area. You might try contacting the NHLBI in Bethesda MD to see if there are any researchers interested in you as an experimental subject.
Reply | Report Abuse | Link to thisBy the way, the HIV research community has been very interested in why some people exposed to the virus don't get infected, and why some who get infected don't get AIDS. By studying this question they have come up with important new insights into the pathogenesis of HIV infection and AIDS.
A review of NHLBI and clinical trials.gov current research tends to support my thesis. Only one current NHLBI study involves FH and that is for homozygous FH. (Heterozygous FH is to homozygous FH as having one kidney is to having no kidneys.) In a quick scan of the 93 clinical trials studies involving FH I could find only drug studies, mostly to lower cholesterol.
Reply | Report Abuse | Link to thisA while back I found a study using heterozygous FHers that examined if aggressive serum cholesterol lowering over 26 months would alter artery stenosis. The results showed very, very modest improvement (<1% per year) with massive intervention, but only in the body of the text was it mentioned, completely in passing, that a full 20% of the study candidates had to be excluded "because they had little or no stenosis."!!
For anyone really interested in cholesterol read Uffe Ravnskov, MD, PhD, books "Fat and Cholesterol are Good for You" and "Ignore the Awkward, How the Cholesterol Myths are Kept Alive."
Reply | Report Abuse | Link to thisAnd for those still thinking statins are harmless, read Duane Graveline, MD, book "Statin Drug Side Effects and the Misguided War on Cholesterol"
Can one of you please tell the rest of us what 'FH' stands for? Interesting discussion and clarification of what homo- versus -hetero zygotic inheritance mean, but we also need to know what is being inherited! With a smile :)
Reply | Report Abuse | Link to thisSorry! FH stands for familial hypercholesterolemia, ie, an inherited condition that causes very high serum cholesterol. Wikipedia has a pretty good discussion. The most important disagreement I have with the Wiki article is the statement regarding increased mortality. Conventional thought is that it has a big negative impact on average life expectancy. Better thinking recognizes that most such analyses suffer from selection bias (Most FHers are found because a relative had heart disease, those of us in families that have no heart disease are only rarely discovered.) A fascinating Dutch study looked back across more than a century and found decades during which FH was actually beneficial, presumably because LDL is important for immune systems. Again, for the best discussions, read Ravnskov. His books are incredibly informative
Reply | Report Abuse | Link to thisSorry! FH stands for familial hypercholesterolemia, ie, an inherited condition that causes very high serum cholesterol. Wikipedia has a pretty good discussion. The most important disagreement I have with the Wiki article is the statement regarding increased mortality. Conventional thought is that it has a big negative impact on average life expectancy. Better thinking recognizes that most such analyses suffer from selection bias (Most FHers are found because a relative had heart disease, those of us in families that have no heart disease are only rarely discovered.) A fascinating Dutch study looked back across more than a century and found decades during which FH was actually beneficial, presumably because LDL is important for immune systems. Again, for the best discussions, read Ravnskov. His books are incredibly informative
Reply | Report Abuse | Link to thisSorry! FH stands for familial hypercholesterolemia, ie, an inherited condition that causes very high serum cholesterol. Wikipedia has a pretty good discussion. The most important disagreement I have with the Wiki article is the statement regarding increased mortality. Conventional thought is that it has a big negative impact on average life expectancy. Better thinking recognizes that most such analyses suffer from selection bias (Most FHers are found because a relative had heart disease, those of us in families that have no heart disease are only rarely discovered.) A fascinating Dutch study looked back across more than a century and found decades during which FH was actually beneficial, presumably because LDL is important for immune systems. Again, for the best discussions, read Ravnskov. His books are incredibly informative
Reply | Report Abuse | Link to thisAfter my angioplasty I went to the University/Hospital's medical library and came across an article that said people from a Dutch background had (as far as I remember) 50 times the incidence of hypercholestemia as people of English origin. This was from a study done in South Africa, where these populations lived side by side. I am half and half, so looks like the Dutch side got me.
Reply | Report Abuse | Link to thisI'm sure sorry that you needed angioplasty. Hope all is better now. I'd be highly skeptical of any study that found a 50x difference between populations. Can't imagine there is much genetic difference between any populations much less Dutch and English; the English Channel isn't that big. The paper I referenced, from JG Silbrands, et al, out of the April 28, 2001 BMJ, looked at 6950 person-years of FHers, in a way that specifically reduced the risk of selection bias, and found "mortality was not increased in carriers [of the FH] mutation during the 19th and early 20th century; it rose after 1915, reached a maximum between 1935 and 1964 (standardized mortality ratio 1.78...)and fell thereafter..."
Reply | Report Abuse | Link to thisSo, even during the worst interval mortality risk was only 1.78x normal, and during a much longer earlier period there was no increased mortality risk.
To my way of thinking, if a cohort of people that have extremely high cholesterol only just barely have extra mortality risk, sometimes, and sometimes not, why are all those people with slightly elevated cholesterol even giving it a second thought? Don't misunderstand, cardiovascular disease is nothing to mess with, but the weak relationship with cholesterol is no reason to automatically take statins to lower it.
One do not have to conclude on these new studies showing no benefit of LDL or HDL change, it must be compared with older studies. An example is the breakthrough trial with cholestyramine lasting for 7 years, and showing reductions in Cardiovascular disease in the treatment group. Cholestyramine is not absorped from the intestine and can for thatt reason have no systemic effect. Another important trial is the helsinki heart study, where the highest reduction in CAD was in the participants that had both a reduction of LDL and a rice in HDL. As we are dealing with statistics one study is not sufficient for any conslusion. It is necesseary to preform a meta analysis, of all cholesterol reducing studies done during the last 35 years of clinical cholesterol trials. It is vital, and that goes for all science, that you alwayes remember to take into account what has been done before. If new studies contradict old studies, one should be looking for the errors or misinterpretations in one of the trials, and not just conclude on one of them.
Reply | Report Abuse | Link to thisAnother issue that comes to mind when I read the article is that the incidense of heart disease must be very low in the two groups compared, as both is taking a statin. This normally means that you need a very large sample of patients to show a statistical significant difference. On top of that comes the ages of the patients. The rate of heart diease is low in the population under 65 years of age. If most of the participants is below that age, it will be even more difficult to show a statistical signifincant difference. In Denmark the total amount of AMI in the population under 65 is around 10-15 %, the rest happens in the older population. It follows from that fact, that a real reduction in CAD and mortallity is easier to reach in the older population than in middle aged men and women.
Reply | Report Abuse | Link to thisI assume you are referring to the Lipid Research Center (LRC) study. I remember when that study came out. Only men in the highest 0.8% for serum cholesterol took part. After seven years, when the results were analyzed the difference in the number of heart attacks was so small that it did not reach statistical significance. Ten percent of the study group had non-fatal heart attacks as opposed to 11.1% for the controls. For fatal heart attacks the numbers were 1.7 and 2.3 percent. The paper study did not present the data this way. They said that the "relative risk" was lowered by 19% and 30%. The use of relative risk is simply a way of fooling the less informed. For those considering cholesterol lowering, a more meaningful way to state these results is a) the study did not reach statistical significance so there may be no benefit to cholesterol lowering even if you are in the top 0.8% of serum cholesterol, and b) even if the study results were significant, it took screening of half a million men to prolong the life of twelve individuals. And twelve is optimistic, because the difference in all cause death was just five. Seven more people taking Cholestyramine powder died by violence or suicide.
Reply | Report Abuse | Link to thisIf you are referring to the earlier MRFIT (Multiple Risk Factor Intervention Trial) study, another massive attempt to reduce heart attacks by multiple interventions (diet, cholesterol lowering, smoking, weight loss, and blood pressure control), after seven years of active intervention, the number of deaths from all causes in the intervention group was 265 as compared to only 260 for the control group. Oops. But the project directors, not to be undone, after the fact decided to manipulate the data by dividing the one large group into select subgroups and showed that some, not all, of the subgroups had marginally better outcomes. Hmmmm.
Isn't it interesting that, as you point out, that most (85%?) of heart attacks occur in those over 65, and at the same time it is well established that serum cholesterol levels do not associate at all with heart attack risk for those over 65. In other words, some argue that cholesterol levels correlate with risk, and yet for the period in which most events occur, the correlation is gone.
Uffe Ravnskov, MD, PhD, wrote of the Helsinki Trial that there were two parts to the trial, a primary prevention and a secondary prevention. In the secondary (patients with prior heart disease) seventeen individuals who took Gemfibrozil died while only eight in the control group died. Even worse, the category "unwitnessed deaths" was included as a heart attack although that is not necessarily correct. If those deaths had been excluded from the results there would have been three times as many deaths in the Gemfibrozil treatment group as the control group (15 vs. 5).
Reply | Report Abuse | Link to thisWith respect to the primary prevention group there was a reduction in the number of nonfatal heart attacks but not in the number of deaths. In other words, even this study did not lower mortality from coronary heart disease. There were, however, a few more deaths in the treated group from all causes than in the control group.
To the Editor:
Reply | Report Abuse | Link to thisThe article “Cholesterol Conundrum” by Francie Diep is presented, at least initially, in an unfortunate manner, suggesting that there is a problem with the Cholesterol Crusade. This is only true in one aspect: it DOES make a difference how one lowers LDL-cholesterol or raises HDL-cholesterol. I am in print to that effect (on theheart.org website) and I have proposed that no new cholesterol medication be used unless it can be shown to stabilize/regress coronary artery plaque. The article cites the ENHANCE trail to show that, despite further lowering LDL, ezetimibe did not lead to further reduction of carotid intima-media thickness (CIMT). CIMT, however, is not the ideal method of testing a medication’s effectiveness since a number of factors besides cholesterol influence CIMT. However, the ILLUSTRATE trial, which used torcetraib, also lowered LDL and had no effect on coronary artery plaque. On the other hand, torcetrapib raised HDL by a great amount, and as noted earlier failed to have an effect on plaque. I have seen alcoholics with very high levels of HDL sustain cardiovascular events, albeit they were all cigarette smokers. Similarly, Dilantin users have very high HDL levels, but I have seen cardiovascular events occur in these patients even without any current cigarette smoking. AIM HIGH, however, took patients with optimal LDL levels and then added niacin to see if any further reduction in cardiovascular events would occur—and there was no further decrease in cardiovascular events. AIM HIGH is therefore not a fair trial with which to judge niacin—after all in HATS, which used a statin and niacin versus stand-alone statin, the angiograms were better in the niacin-statin group than in the statin group. Angiographic improvement leads to a marked reduction in cardiovascular disease events. (The therapeutic strategies were different in HATS and AIM HIGH, so one needs to be careful in comparison of the two trials.)
Remember that cardiovascular disease is a multi-factorial process and concentrating solely on cholesterol will not eliminate cardiovascular disease. The chief risk factor is cigarette smoking, followed by cholesterol disorders, and trailed by hypertension. Uncontrolled diabetes can inflame the artery walls and poison the heart muscle cells, leading to heart failure. Inflammation, as it relates to cardiovascular disease, is simply a response to these risk factors, and is not per se a risk factor—otherwise cardiovascular disease would be rife in sub-Saharian Africa where people have widespread malaria and high levels of inflammation. (Please see my letter to the editor of the 15 October 2011 issue of the American Journal of Cardiology. Also, my Guest editorial in the summer issue of The Lipid Spin.)
W.E. Feeman,Jr,MD
Dr. Freeman, this is very interesting! You note trials that have altered both LDL and HDL without benefit to plaque burden and propose that cholesterol medications should not be approved unless they also have a positive effect on plaque. That seems to me to be a major step in the right direction. But, why talk about cholesterol lowering at all? If a medication has a beneficial effect on plaque it seems that is a stand alone positive. Conversely, serum cholesterol modification for its own sake may well be of no value. And as you and I discussed inprevious emails, there are a significant number of us who have outrageously high lifelong LDL to no detriment (as you said,"something else is going on").
Reply | Report Abuse | Link to thisI read this article with great interest as I had surgery on my carotid arteries more than 14 years ago. I was put on a Statin and have been on it since. However, I did have a heart attack in 2003 even with the cholesterol lowering medication. Having a vested interest in this subject I have since learned that the real cause of CHD or any other arterial disease is inflammation. With that said I have read many other books and articles on this very conundrum. My own due diligence on the subject has brought me to the conclusion that the cholesterol story is a myth. The real culprit in CHD is inflammation and the direction I have taken is simple. I have decided to take inexpensive, OTC vitamins and minerals that have a proven track record in combating CHD. These are the ones I take daily: Niacin, B6, B12, Folate, Omega 3, Magnesium, selenium, CoQ10, and aspirin. I am sure there are experts out there that will take exception to those OTC medications; especially drug companies that don't make any money off of them. When the statins patents expire I believe you will see fewer doctors pushing them.
Reply | Report Abuse | Link to thisThe Fancie Diep's comment in "Cholesterol conundrum" that changing HDL and LDL levels does not always alter heart disease or stroke risk is not accurate. It is more correct to indicate that the results from clinical trials available to date show that the use of statins to reduce LDL cholesterol levels with the subsequent addition of a drug to increase HDL cholesterol levels (niacin) is a more effective treatment to reduce coronary heart disease risk than the addition of a drug to achieve a higher LDL-cholesterol reduction (ezetimibe). Clinical trials have shown than statins alone reduce LDL cholesterol levels and the risk for coronary heart disease and stroke.
Reply | Report Abuse | Link to thisI'm a statin survivor. In 2002 I took Lipitor, first 10mg then 20mg when 10mg made no difference to my LDL reading. After a short while on 20mg I started getting sciatic type pains and discomfort in lower back and buttocks. I started researching on the Internet and stopped the Lipitor. I was off for about 6 or 7 months, then Crestor was allowed to be sold in Canada. My MD suggested that perhaps I was allergic to Lipitor so why not try Crestor, only 10 mg dose was available in 2003. After about 5 or 6 weeks I went to bed early one night, not feeling very good. I awoke in about 2 hours and could hardly move, immense sciatic pain. I needed 2 crutches for about 4 weeks to get around, then a walking stick for 6 months. Now I can move, but my balance is not good and I still have a dropped foot, 8 years later. My diagnosis is that the myelin sheathing around my nerves was not being repaired because of a lack of cholesterol. Overtime that was corrected of course but I had suffered nerve damage, unprotected nerves on bone.
Reply | Report Abuse | Link to thisYou need to talk to a lipid specialist. A VAP test will measure 2 components of HDL (HDL-2 most protective & HDL-3 least protective) and 3 components of LDL (LDL-R, Lp(a), & IDL) directly. Also, the VAP measures pattern density. Patern A indicates large, boyant LDL particles (desirable). Pattern B indicates small, dense LDL prticles and is most atherogenic (less desirable). Niacin and exercise raises HDL-2. Statins will lower total LDL but not Lp(a) which they call the widow maker. Lp(a) is genetic. The best course of action is to raise your HDL-2 as much as possible and limit carbs as they will cause you to go into pattern B. Statin wont hurt as they will lower total LDL and reduce inflamation.
Reply | Report Abuse | Link to thisWe need more facts and evidence than a comparison between 2 articles funded by the drug industry. Master's level reporting requires an in-depth literature review.
Reply | Report Abuse | Link to thisHalf of all heart attack victims have normal cholesterol levels, and independent research has shown that inflammation is the real cause of cardiovascular problems. In its natural form, cholesterol is blameless. The system however, continues to push cholesterol lowering drugs called statins, without exploring the real physiological effects of statin drugs.
Statin drugs have been found to limit the manufacture of brain cholesterol in glial cells resulting in aggressive behavior, irritability, depression and rage. Cholesterol is essential for nerve endings, or synapses, and thus for the proper function of the nervous system. Neuromuscular damage often leads to symptoms misdiagnosed as multiple sclerosis, ALS and Parkinson's disease. We also have to wonder about the growing number of cases of dementia! It's not all due to age. How many cases are related to prescribed drugs ...?
Surely, high LDL cholesterol level can cause serious arterial plaque in heart. To live healthy cholesterol free life, you should follow a special diet which can <a href="http://www.cholesterolverlagen.nu/bloedcholesterol-verlagen/cholesterol-verlagen.php/">lower cholesterol</a>
Reply | Report Abuse | Link to thisvery easily.