Cholesterol lowering medicine
 

I received my lab work today from my annual physical. For the last year and half my total cholesterol has been 200-206. My triglycerides went from 316 down to 297, better but still not good. My hdl the good stuff is at 27 which is low. I have decided to go ahead and do the medicine. My major concern is will it affect my riding. Will I not be able to push as hard? I hate taking medicine regularly, so I want to try it for about 6 mo. then stop for a while.

I plan on discussing this with my doctor who is a friend, but he doesn't have any practical experience with it. I want someone's advice that has experience with this type of medicine.

Thanks

One of my best friends was on the medications for high cholesterol, but after changing his diet, he no longer has to take the medication. He was able to exercise, but not bicycle as he didn't like to bike at the time.

It shouldn't slow you down as far as exercise goes.

Best to discuss it with your Dr. I can tell you that Statin drugs will help reduce your total cholesterol, but there is also likely a lot you can do with diet and exercise as well, especially for those triglycerides.

There are also potential side effects with Statin drugs, you'll want to discuss this with your Dr as well so you know what to look for if they do occur. Best advice I can give here.

Analysis and comment
Controversy
Should we lower cholesterol as much as possible?

Uffe Ravnskov, independent researcher1, Paul J Rosch, clinical professor2, Morley C Sutter, professor emeritus3, Mark C Houston, clinical professor of medicine4

1 Magle Stora Kyrkogata 9, S 22350 Lund, Sweden, 2 Departments of Medicine and Psychiatry, New York Medical College, Valhalla, NY, USA, 3 Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver BC, Canada, 4 Vanderbilt University School of Medicine, St Thomas Hospital, Nashville, TN, USA

Correspondence to: U Ravnskov ravnskov@tele2.se

Statins are portrayed as harmless drugs that almost everyone would benefit from, but little is known about the side effects at the high doses now being suggested

People at high risk of cardiovascular disease should be treated more aggressively. This is the message from the American National Cholesterol Education Program published last year.1 By aggressively, it means that low density lipoprotein (LDL) cholesterol concentrations should be lowered to less than 1.81 mmol/l. Recently, Getz et al calculated that in Norway, one of the healthiest nations in the world, about 85% of men and more than 20% of the women over age 40 would be classified as high risk using this criterion.2 If followed, the new recommendations might therefore put most of the Western world's adult population on statin therapy. As the risk to benefit ratio for a more drastic lowering of low density lipoprotein cholesterol is unknown we question the wisdom of this advice.

Are higher statin doses safe?

To achieve this new goal, people at high risk would have to take higher statin doses than currently suggested. This would increase the risk of adverse side effects. In the treating to new targets (TNT) trial, the only study comparing a low and high dose of the same statin, not even 80 mg atorvastatin was able to lower mean low density lipoprotein cholesterol below 1.81 mmol/l.3 Clinical experience has taught us that a dose increase of that size of any drug will inevitably increase both the number and the seriousness of side effects. This apparently did not concern the authors, who concluded, "Intensive lipid lowering therapy with 80 mg of atorvastatin per day in patients with stable CHD [coronary heart disease] provides significant clinical benefit."

However, overall mortality was not reduced because the smaller number of cardiovascular deaths in the 80 mg atorvastatin group was offset by increased deaths from other causes leaving a benefit of 250 (5%) fewer non-fatal cardiovascular events. Because many non-fatal events resolve with little residual damage or discomfort, meticulous recording of all possible adverse side effects is mandatory. However, the authors have not provided adequate information on adverse events.4 5

Deficient information about side effects

The authors failed to elaborate on their criteria for determining whether an adverse effect was considered related to treatment. Surprisingly, that decision was not made by the authors but by the investigator with direct responsibility for the patients. Specific information about the symptoms that were designated as side effects was also incomplete. For instance, only the number of patients with aminotransferase concentrations that were persistently over three times the upper limit of normal was listed (51 more cases in the high dose group). Why not give the number of participants showing any persistent rise as is customary in drug trials?

In the recent incremental decrease in end points through aggressive lipid lowering (IDEAL) trial,6 which compared usual dose simvastatin with 80 mg atorvastatin, no significant difference was seen on the major end points. However, the number of adverse effects were far higher than in any previous statin trial. Almost 90% of participants in both groups had side effects, and in almost half of them they were recorded as serious. The authors of the IDEAL trial did not comment on this alarming finding except by mentioning that "there was no difference between the groups in the frequency of adverse events that were rated as serious"; neither did they inform readers about the nature of these events.

Adverse effects of statins

Many adverse effects are first recognised in the post-marketing surveillance process, and their frequency is likely to be understated because few doctors report them. A request among general practitioners in Rhode Island found that the serious side effects that had been reported from any drug to the Food and Drug Administration included only 1% of those observed.7 Nevertheless, many hitherto unknown potential side effects from statins have already been reported.

Heart failure
All statins inhibit the synthesis of hydroxymethylglutaryl coenzyme A reductase, an enzyme involved in synthesis of the precursor of cholesterol and other important molecules such as coenzyme Q10, vital for mitochondrial energy production. Thus statins lower plasma Q10 concentrations and worsen cardiac function in patients with heart failure, and oral coenzyme Q10 can improve or prevent this serious complication.8-10 Heart failure has not been reported with statins, possibly because it has been seen to be the result of the primary disease rather than an adverse effect but also because patients with imminent or manifest congestive failure are routinely excluded from statin trials.

Myalgia and rhabdomyolysis
Muscle complaints are claimed to occur in less than 1% of patients taking statins, but this is almost certainly an underestimate. In a study of 22 professional athletes with familial hypercholesterolaemia who were treated with various statins, sixteen discontinued the treatment because of muscle side effects.11 Competitive athletes may be more sensitive to muscle pain and weakness, but even mild symptoms may have a deleterious effect on elderly people and others who already have muscular weakness.

In rare cases, myopathy has led to rhabdomyolysis and death from renal failure. In the TNT trial,3 five non-fatal cases of rhabdomyolysis were reported, four of them during the treatment period. To consider them unrelated to the treatment because they were not dose-dependent, as did the authors, seems premature. In a recent review of statin side effects the authors had found 4.2 cases of rhabdomyolysis per 100 000 patient years after atorvastatin treatment.12 If true, and if the five cases observed in the TNT trial (50 000 patient years) were not due to treatment it means that rhabdomyolysis should be twice as common in untreated people than in those treated with statins.

Mental and neurological symptoms
Cholesterol is vital for the development and function of the brain. It is therefore unsurprising that reduced concentrations may produce mental and neurological complaints such as severe irritability, aggressive behaviour, suicidal impulses, cognitive impairment, memory loss, global amnesia, polyneuropathy, and erectile dysfunction.13-19 In many cases the symptoms were reversible and re-occurred after re-challenge. None of these side effects are mentioned on the product labels or information inserts for statins.

Cancer
At least five animal experiments have found that the statins are carcinogenic in amounts that produce blood concentrations similar to those achieved by doses commonly administered to patients.20 Nevertheless, the FDA approved them because cell experiments did not convincingly prove that statins were either mutagenic or genotoxic. But carcinogenicity may be due to the effects of statins on cholesterol because numerous cohort studies have found low cholesterol to be a risk factor for cancer. This may take a long time to surface. No increase of cancer was seen in a 10 year follow-up of participants in the Scandinavian simvastatin survival study, and the authors therefore concluded that 10 years of statin treatment does not induce cancer.21 Neither does 10 years' smoking tobacco.

A significant increase in breast cancer was seen in the cholesterol and recurrent events trial (CARE), with most cases being recurrences.22 Since then patients with a history of cancer have been excluded from statin trials. If statin treatment is carcinogenic it should be seen first in people at high risk such as smokers and old people. As far as we know, no trial has analysed cancer incidence separately for smokers and non-smokers. In the trial of pravastatin in elderly individuals at risk of vascular disease (PROSPER), the only statin trial exclusively in elderly people, the significant increase in cancer mortality neutralised the benefit from fewer cardiovascular deaths (figure).23 This finding was dismissed by referring to a meta-analysis of all statin trials that failed to find an association with cancer, but the authors ignored mentioning that the mean age of participants in these trials was about 25 years lower than in PROSPER.


http://www.bmj.com/content/vol332/is...u306035.f1.gif



Selection bias
The low frequency of side effects in the TNT trial compared with the IDEAL trial may be explained by the way patients were selected for treatment. In the TNT trial more than 3000 people were excluded because they did not fulfil the criteria, already had raised aminotransferase concentrations, cancer, or another disease associated with a limited lifespan, or for "other reasons." After one to eight weeks' treatment with low dose atorvastatin, an additional 5429 patients were rejected, including 197 with non-fatal clinical endpoints, 193 with adverse events, 69 who did not comply with the treatment, 195 who had ischaemic events, 15 with fatal clinical endpoints, and 373 for other reasons. No information was provided on the nature of the side effects or the causes of death. Similarly, it is not clear which side effects later caused 7.2% to stop the treatment.3 Finally, of the 18 468 patients originally screened for the TNT trial, only 10 003 (54%) were selected, whereas for the IDEAL trial the number was 91.7%, meaning that the patients studied in the TNT trial were much healthier than those included in the IDEAL trial and also than those seen in the doctor's office.


Summary points

US recommendations for low density lipoprotein cholesterol concentrations could put most of the Western world's adult population on statins

Doses of statins would have to be more than eight times higher than currently used

Increasing the dose of atorvastatin by eight times does not lower total mortality

Adverse side effects in clinical trials are under-reported

Any reduction in non-fatal events may be outweighed by more numerous and more severe adverse effects


Contributors and sources: All authors have published extensively in this and similar areas for decades in the scientific press and elsewhere. This article arose from discussions between the authors. UR wrote the first draft; MCS, PJR, and MCH revised the manuscript. UR is the guarantor.

Competing interests: UR, PJR, and MCS have argued in the scientific press and elsewhere that high cholesterol is not the cause of atherosclerosis and coronary heart disease.

References

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2. Getz L, Sigurdsson JA, Hetlevik I, Kirkengen AL, Romundstad S, Holmen J. Estimating the high risk group for cardiovascular disease in the Norwegian HUNT 2 population according to the 2003 European guidelines: modelling study. BMJ 2005;331: 551-4.[Abstract/Free Full Text]
3. LaRosa JC, Grundy SM, Waters DD, Shear S, Barter P, Fruchart J, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med 2005;352: 1425-35.[Abstract/Free Full Text]
4. Ravnskov U, Rosch PJ, Sutter MC. Intensive lipid lowering with atorvastatin in coronary disease. N Engl J Med 2005;353: 94.
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6. Pedersen TR, Faergeman O, Kastelein JJ, Olsson AG, Tikkanen MJ, Holme I, et al. High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction: the IDEAL study: a randomized controlled trial. JAMA 2005;294: 2437-45.[Abstract/Free Full Text]
7. Scott HD, Rosenbaum SE, Waters WJ, Colt AM, Andrews LG, Juergens JP, et al. Rhode Islands physicians' recognition and reporting of adverse drug reactions. R I Med J 1987;70: 311-6.
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I've taken Niacin in large doses. Unfortunately, I've had reactions to it, so I don't take the 500 MG that's recommended to boost HDL. Aside from getting nervous and jittery, I didn't find it interfered with riding.

Are you sure you don't have any information.

Wow, thanks for the research.

My Dr. told me we would try and control it with diet and excercise about 3 yrs ago. Thats when I started riding seriously. I have seen an improvement and I haven't really changed my diet as much as I should. We learned my son was Type 1 diabetic so that changed my diet a lot over night but I admit I could be doing better. At what point do you decide to try the meds just for a while.

My Dr. is not one to give medicine for everything and tries his best to keep you off of them. But the last time I took my results to him, he mentioned we may have to try.

I am still looking for someone who currently takes them for input.

I was on Statins, and I hated it. Liver function tests every 6 months and no energy and aches all the time. Apparently I was in the sensitive category.

Thanks

You don't think it affects your stamina any?

My concern is dad had a 5 bypass and they had him on something for a while and he said he felt weak all the time. He is no longer on it and is doing fine. I just don't want it to be something that gets me off the bike.

Niacin is a B Vitamin. It won't slow you down, it'll actually amp you up, hence the jitteriness the Historian mentioned. ;)

Was it bad enough to keep you from riding? Would it be worth it to try and get your levels to a better range and then start working on your diet again or not worth the pain?

I've been on Lipitor (a statin) for about 5 years with no adverse effects (your results may vary) and it did what it was supposed to in terms of lowering my cholesterol. It wasn't until I got serious about diet and exercise that I really changed my numbers for the better though. I should be off the meds in 5 months if I maintain what I've been doing. I take it before bed in order to minimize side effects and I have noticed none, but your doc will likely seek occasional liver screening to look for normal function.

It also might cause you to get flushed, feel your heart race, get headaches, and break out in hives. Ask me how I know this, Tom. :-)

Couldn't say. I'd discontinued it by the time I was seriously training for my century ride. But I doubt it affected anything.

Thanks,
This has been helpful. I plan on talking with the Dr. a lot about this. It is just nice to get input from people who have actually been there instead of someone who has only studied it.

"The Historian"
Just wanted to let you know you are an inspiration. I hated to hear about the spinning class incident but you have total respect from me. I probably won't get to join you in part of your ride next year due to work, but I will try my best.

I have never took them so I can't give you any information on my experience.

The reason I posted the info is because I am going to do a descriptive lit review on the effects of cholesterol, and hopefully a meta analysis in the future. I saw the article above around the same time that I saw your post, so I though you would like to see it, so you could have an opposing view to the conventional.

Personally, I believe atherosclerosis is much more complicated than cholesterol levels, and aggressively lowering levels is not always prudent. Safe cholesterol levels are constantly being lowered so now 90% of people over 50 are considered candidates for cholesterol lowering drugs.

It is good that you have changed your diet, and I hope you son is doing well, DM is a hard disease to deal with. I always enjoy talking to people with DM 1, it is interesting to see how the disease came about. Do you think that poor eating habits caused your sons DM1?

Thank you.

I'm going to take a wild guess and say you're one of those that experiences discomfort from high doses of B complex vitamins? ;) It can happen. Your threshold dose is lower is all. ;)

Me, I get a flush, and then the metabolism takes off like I'm doing a gram or so of crank.......:D

I really appreciate the article.

My son's diabeties is a mystery. No family history, they say it doesn't really play apart though. My wife has kept the kids diet exremely healthy. My son was 8 before he had his first candy bar. He was pretty much a vegetarian until about 5. In fact, when the dietician talked to us the first time and asked him what his favorite food was, he said, asparagus. She said, ya'll wont have any troubles with this. We never let them have soda's mostly water and 2% milk. He wasn't overly sick as an infant, and he was breast fed no formula. He did have a lot of ear infections around 2-3.

They told us they look for a certain imune cell that attacks the pancreas. He did not have it. He falls into an extremly small % that they told us they really do not understand why he has it. Any theories you have, I would like to hear.

I have been using statins in relatively low doses for years now. Originally Zocor and more recently Lipitor, with either one I am very responsive to the medication and my cholesterol levels are in the normal range, without the medication I am many times the norm.
My high cholesterol is a hereditary condition and diet changes made no difference at all. As a point of reference, I have never been over weight, am currently 6’7”, 230 lbs, commute by bike approximately 140 miles a week, run, and race BMX. I don’t fit the stereotype that most people associate with high cholesterol.

While on Zocor I experienced more frequent cramping after exercising so I was switched to Lipitor and have had no noticeable side effects. My older brother had the opposite experience and prefers Zocor. Neither medication had any impact on my energy levels or endurance.
As much for my own piece of mind as anything, I have voluntarily participated in a number of studies at one of the local research hospitals. Being involved in studies gives you the opportunity to have tests run that you would not normally have access to. For me this has been excellent as I have found out that I am very healthy and that I have almost no measurable plaque build up.

While the reported numbers are low regarding the muscular cramping issues related to statins, the effects can be severe in some cases. My fiancee was on Crestor for about 3 weeks before starting to get some very serious muscle pains. With accident related injuries, it's already difficult for her to walk unassisted. Compounding that with the side effects of the statin nearly put her back in a wheelchair.
The good news is that these effects are not permanent, and when you stop taking them and the meds wear out of your system, your muscles will start to feel better.
Keep a close monitor of how your muscles are feeling, and if you start to get pains and/or cramping then talk to your doctor about either adjusting dosage or switching medications. I'll say this about Crestor: In the 3 weeks she was on it, my fiancee's total cholesterol dropped by 17%. That's more than dietary changes had been able to do in the previous 12 months.

Cholesterol
 

i had a M.I. in 2004 as a reward for forty years of cycling so needless to say I'm on statins. I don't feel they effect me negatively. (Beta blockers are a dead loss they turn me into a slug). I have an appointment next week with a cardiologist who is an ancien of P-B-P and I will ask him his opinion. For what its worth my opinion is that I would do what it takes to get cholesterol to well below 200 and if it can't be done by diet etc do it with statins.

Its unusual to see muscle aching etc with Crestor - it, like Pravachol, bypasses the P450 cytochrome which contributes to the muscle problems we see with statins. Crestor is not usually a first line statin in people without CV disease. It's a super statin and for the most part is reserved for those who need VERY aggressive lipid lowering. The other "lab test" getting attention is hCRP. It is an inflammatory marker and being investigated as to whether it is a risk factor like high chilesterol and inproper diet is....

Thanks, lots to think about.

Green tea
 

natural solution Green tea and more green tea, I use mega t green tea pills

People have said that, I really don't like it. But, I guess I need to get use to it.

What changes have you seen as a result of it?