ABC World News reported, “And we have a red flag to tell you about tonight about the most popular prescription drug in the world: statins.” Investigators “at Harvard Medical School” found that “people who take statins to reduce their cholesterol are at slightly higher risk of diabetes.” Sounds scary, right? Not to worry … it isn’t! Continue reading
An easy-to-remember formula for good health (0, 5, 10, 30, 150) is proposed in a wonderful editorial in American Family Physician titled “Preventive Health: Time for Change.” The author suggests this formula to physicians to “help patients achieve healthy lifestyle goals”:
- 0 = no cigarettes or tobacco products
- 5 = five servings of fruits and vegetables per day
- 10 = ten minutes of silence, relaxation, prayer, or meditation per day
- 30 = keep your BMI (body mass index) below 30
- 150 = number of minutes of exercise per week (e.g., brisk walking or equivalent)
The editorial is penned y Colin Kopes-Kerr, MD, from the Santa Rosa Family Medicine Residency in Santa Rosa, California:
It is time to make a decision. Which will be our health promotion strategy—primary prevention or secondary prevention?
Traditionally, the only one available to us was secondary prevention. Medicine consisted of a one-on-one physician-patient relationship, and taking care of patients meant minimizing the impact of any diseases the patient had. We did not have the time or tools to do anything else. More recently, we have been able to reduce a patient’s mortality by 20 to 30 percent by treating heart disease with a statin or beta blocker. These two medications have had the most dramatic effects in secondary prevention.
But now, the way we practice medicine has changed. We have a real choice to make. According to recent literature, primary prevention appears to work better than any other strategy in medicine. So why do some physicians not implement primary prevention? Despite the literature, maybe physicians are not getting the news. We need to keep repeating the message to physicians and patients that primary prevention is simple and effective. Next, we need to take a look at our own behavior as physicians and determine if it makes sense in the context of primary prevention.
There are 10 major studies on the effects of primary prevention.(1–15) These studies demonstrate very large correlations between specific healthy lifestyle behaviors and decreases in major chronic diseases (e.g., diabetes mellitus, heart disease, stroke, cancer) and all-cause mortality.
Although these studies offer a complex array of data to sift through, the elements of a healthy lifestyle are clear: not smoking, regular exercise, healthy diet, healthy body weight, and reduced stress.
Although exercise guidelines vary, I ascribe to the U.S. Department of Health and Human Services’ Physical Activity Guidelines for Americans, which recommends at least 150 minutes of brisk walking or the equivalent per week.(16) For the diet criterion, the Atherosclerosis Risk in Communities study illustrates that merely consuming five servings of fruits and vegetables per day is associated with the same benefits as consumption of a Mediterranean-style diet.(11) A standard of five servings of fruits and vegetables is much easier to remember and adhere to.
There is strong support for at least one weight-related variable in a healthy lifestyle. This may include body weight, body mass index (BMI), waist circumference, or waist:hip ratio. The INTERHEART study showed waist:hip ratio to be the most predictive of cardiovascular disease.(6) However, unlike BMI calculation, measurement of weight:hip ratio has not yet become standard in U.S. practices. I use BMI as the metric, and a value less than 30 kg per m2 as the cutoff between a healthy and unhealthy lifestyle. The goal is to move away from this outer limit toward a more ideal parameter, such as less than 25 kg per m2.
The final variable of a healthy lifestyle, which has strong support from the INTERHEART study, is stress reduction.(7) The INTERHEART study offers useful suggestions for measuring stress—perception of severe stress at home or at work, financial stress, or major life events.(7)
The minimal lifestyle intervention that would be beneficial is not defined. However, 15 to 20 minutes of silence, relaxation, or meditation appears to be a common interval.(17) To be more inclusive of patients, I set the criterion to an even less restrictive amount, about 10 minutes per day.(17) This is enough time to produce a change in biorhythms and is achievable for most patients.
Information alone does not lead to behavior change, however. Motivational interviewing or brief negotiation is a new framework that can close the gap between knowledge of available lifestyle interventions and changing behaviors. The framework has already been proven markedly effective for tobacco, drug, and alcohol addiction.(18) Few physicians have received the training necessary to implement motivational interviewing or brief negotiation. Resources for learning about these skills include the Kaiser Permanente Medical Group Web site and the book Motivational Interviewing in Health Care: Helping Patients Change Behavior.(18)
In terms of health, we can have it all. We have the requisite tools to convert knowledge into healthy behaviors. This newfound power to reduce diabetes, heart disease, stroke, cancer, and all-cause mortality with primary prevention strategies should impel us to change how we counsel patients. Research is needed to explore why some physicians are not making this change.
Address correspondence to Colin Kopes-Kerr, MD, at email@example.com. Reprints are not available from the author.
Author disclosure: Nothing to disclose.
- Stampfer MJ, Hu FB, Manson JE, et al. Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med. 2000;343(1):16–22. View here
- Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med. 2001;345(11):790–797. View here
- Forman JP, Stampfer MJ, Curhan GC. Diet and lifestyle risk factors associated with incident hypertension in women. JAMA. 2009;302(4):401–411. View here
- Knowler WC, Barrett-Connor E, Fowler SE, et al.; Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346(6):393–403. View here
- Knoops KT, de Groot LC, Kromhout D, et al. Mediterranean diet, lifestyle factors, and 10-year mortality in elderly European men and women: the HALE project. JAMA. 2004;292(12):1433–1439. View here
- Yusuf S, Hawken S, Ounpuu S, et al.; INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infraction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364(9438):937–952. View here
- Rosengren A, Hawken S, Ounpuu S, et al.; INTERHEART Investigators. Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364(9438):953–962. View here
- Chiuve SE, McCullough ML, Sacks FM, et al. Healthy lifestyle factors in the primary prevention of coronary heart disease among men: benefits among users and nonusers of lipid-lowering and antihypertensive medications. Circulation. 2006;114(2):160–167. View here
- Chiuve SE, Rexrode KM, Spiegelman D, et al. Primary prevention of stroke by healthy lifestyle. Circulation. 2008;118(9):947–954. View here
- Kurth T, Moore SC, Gaziano JM, et al. Healthy lifestyle and the risk of stroke in women. Arch Intern Med. 2006;166(13):1403–1409. View here
- King DE, Mainous AG III, Geesey ME. Turning back the clock: adopting a healthy lifestyle in middle age. Am J Med. 2007;120(7):598–603. View here
- Khaw KT, Wareham N, Bingham S, et al. Combined impact of health behaviours and mortality in men and women: the EPIC-Norfolk prospective population study [published correction appears in PLoS Med. 2008;5(3):e70]. PLoS Med. 2008;5(1):e12. View here
- Ford ES, Bergmann MM, Kröger J, et al. Healthy living is the best revenge: findings from the European Prospective Investigation into Cancer and nutrition–Potsdam study. Arch Intern Med. 2009;169(15):1355–1362. View here
- Lee CD, Sui X, Blair SN. Combined effects of cardiorespiratory fitness, not smoking, and normal waist girth on morbidity and mortality in men. Arch Intern Med. 2009;169(22):2096–2101. View here
- Djoussé L, Driver JA, Gaziano JM. Relation between modifiable lifestyle factors and lifetime risk of heart failure. JAMA. 2009;302(4):394–400. View here
- U.S. Department of Health and Human Services. 2008 physical activity guidelines for Americans. View here.
- Dialogue Partner. View here
- Rollnick S, Miller WR, Butler CC. Motivational Interviewing in Health Care: Helping Patients Change Behavior. New York, NY: Guilford Press; 2008. View here
I have heard from male readers that when they began taking the cholesterol reducing statin medications (such as Crestor, Lipitor, lovastatin, simvastatin, etc.), they have experienced decreased libido (sexual drive).
Now, there is some research that may confirm this.
One study, in 2009, concluded, “the present study suggests that statins may induce or worsen ED (erectile dysfunction) in accordance with other data.”
More recent research shows that statins may interfere with the production of cholesterol and that this may alter hormone synthesis, resulting in reduced testosterone levels, which may decrease the libido (sexual drive) in men on statins.
For example, Italian researchers have reported a link between statin therapy and hypogonadism (reduced testosterone).
So, if you’re taking a statin and notice a decrease in your libido, DON’T STOP THE STATIN. Rather, talk to your personal doctor about the side effect and possible options.
Some experts say statins help healthier people, but others worry about risks. So, when the U.S. Food and Drug Administration (FDA) approved the use of the cholesterol-lowering statin drug Crestor for some people with normal cholesterol levels, cardiologist Dr. Steven E. Nissen cheered the decision. But, not everyone did. Here are the details in a report from HealthDay News:
“You have to go with the scientific evidence,” said Nissen, who is chairman of cardiovascular medicine at the Cleveland Clinic. “A clinical trial was done and there was a substantial reduction in morbidity and mortality in people treated with this drug.”
But Dr. Mark A. Hlatky, a professor of health research and policy and medicine at Stanford University, has expressed doubts about the FDA move. He worries that more people will rely on a pill rather than diet and exercise to cut their heart risk, and also points to studies linking statins such as Crestor to muscle troubles and even diabetes.
“I haven’t seen anything that changes my mind about that,” Hlatky said.
So, will millions of healthy Americans soon join the millions of less-than-healthy people who already take these blockbuster drugs?
The FDA’s February approval of expanded use of rosuvastatin (Crestor) was based on results of the JUPITER study, which involved more than 18,000 people and was financed by the drug’s maker, AstraZeneca.
People in the trial who took the drug for an average of 1.9 years had a 44 percent lower risk of heart attack, stroke and other cardiovascular problems compared to those who took a placebo — results so outstanding that the trial was cut short.
Based on JUPITER, an FDA advisory committee voted 12 to 4 in December to approve widened use of the drug.
The people in the trial included men over 50 and women over 60 with normal or near-normal cholesterol levels.
However, these individuals did have high levels of C-reactive protein, a marker of inflammation that has also been linked to cardiovascular problems. They also had at least one other heart risk factor, such as obesity or high blood pressure.
For that specific group, Crestor makes sense, Nissen said. “Over a five-year period of time, you prevent one death or minor stroke for every 25 people treated,” he noted.
Whether or not others with normal cholesterol should take Crestor or another statin remains unclear. “Not everyone with normal cholesterol should be treated,” Nissen said. “You should give it to people with a high enough risk.”
And he added that the results applied only to Crestor. Other popular statins include Lipitor, Pravachol and Zocor, as well as some generic versions.
Those statins might not produce the same benefits, Nissen said. “Statins differ from each other in terms of potency,” Nissen said.
Crestor, which is available only in a more expensive brand-name form, is toward the top of the list in terms of potency, he noted, while generic drugs such as simvastatin (Zocor) and pravastatin (Pravachol) have much less powerful effects.
“For patients who need a lot of cholesterol reduction, I use the most powerful drug,” Nissen said. “If I can get a patient there with a generic drug, of course I use a generic drug.”
But Hlatky has his doubts about the advisability of widening statins’ reach. He said he’s reluctant to have people at cardiovascular risk pop a pill rather than change the lifestyle factors that put them in trouble in the first place.
“My view has always been that you start with the basics and do the simple things first before you go to drugs,” Hlatky said. “Lots of people are not doing the sensible things. They’re not eating the right diet, they’re not exercising, they’re still smoking. Most of the people in the JUPITER trial were smack in the middle of that group.”
So Hlatky says he might still prescribe a statin for someone in that group, “but I would have an informed conversation about the long-term risks and benefits and what you need to do to reduce the risks.”
“It is so much easier to prescribe a drug than to change behavior, and that is my worry,” Hlatky said. “We’re heading down that road. Cardiovascular risk prevention is moving in the wrong direction.”
He’s also worried about exposing more people to the rare but still possible side effects that come with statins. The drugs can cause myalgia — severe muscle pain — and a recent study published in the British journal The Lancet found a 9 percent increase in diabetes incidence among people taking statins.
But Nissen believes the benefits of expanded use of Crestor outweigh possible risks. The study that found an increased incidence of diabetes did not find that it was accompanied by any increase in cardiovascular problems and deaths, he noted.
“The is one example where the FDA got it exactly right,” Nissen said.
And, from my perspective, I agree.
Some of you are wondering about my response to this news. First of all, you should know that I’m on Vytorin. My doctor had recommended a statin, along with omega-3 fatty acids for my increasing triglycerides and decreasing LDL (lethal) cholesterol. When my cholesterol particle counts (we don’t just follow my lipid profile) didn’t meet goal, my doctor added Zetia (using the statin and Zetia combination drug of Vytorin). Voilà, my particle counts are way normal.
Does this new information change my view about the reasonableness of adding either nyacin or Zetia to a statin as add-on drugs? Absolutely not. You can read my previous blogs on Zetia here:
- Cholesterol Drug Controversy Continues
- A trusted expert speaks out on the Vytorin fiasco (for doctors)
In the meantime, for the many doctors who read this blog, I’ve solicited the opinion of a friend and internationally-recognized lipidologist, Tom Dayspring, MD. Here’s his response to the newest study data. It’s a long, and complex read, but well worth it for medical professionals:
By now you have likely heard something about the ARBITER-6 HALTS trial which was just presented at the AHA and published in the New England Journal of Medicine. Basically this is a trial designed to show what happens to carotid intima–media thickness (IMT) when either Zetia or Niaspan is added to a long term statin use.
For those who do not know, I am a consultant and National Speaker for both Abbott Labs and Merck (Schering Plough). I educate professionals all the time about aggressive use of lipid drugs to achieve goals.
I believe Niaspan, Zetia, fenofibrate, Trilipix, and Lovaza are grossly under prescribed. They are all potential “statin-helper” drugs.
Without outcome data (data on heart attacks, strokes, deaths), no one can ever state one combination is superior to another.
Readers of my newsletters know by now that statins have serious residual risk in all their trials and only get a minority of patients to apoB or LDL Particle Count (LDL-P) goal. Per all guidelines combination therapy is indicated to achieve goal.
There is zero Level One outcome data with any of the potentially available combination therapies that are out there right now.
So the only sane way to know what drugs to add to a statin is will the combo help me get to lipid goals (non-HDL-C) or lipoprotein goals like apoB or LDL-P and perhaps an emerging goal – HDL-P (not always the same thing as HDL-C)).
I happen to very much like both Niaspan and Zetia as wonderful statin-helping therapies.
I personally take 2000 mg of Niaspan as well as Zetia 10 mg every day (along with TriCor) along with once weekly statin (because of myalgia). And, I prescribe Zetia and Niaspan a lot in my practice to help achieve goal.
Based on multiple existing angiographic trials and now the ARBITER-6 HALTS trial it is my belief that if you have coronary heart disease (CHD), I want to know why Niaspan, unless it is not tolerated, is not part of your regimen to help achieve goal (except for unusual circumstances I never use niacin or Zetia monotherapy).
The ARBITER-6 HALTS trial was small, open-label (impossible to do a blinded trial with niacin) randomized trial enrolled CHD patients (with high or very high risk) who were on a statin for several years (mostly atorvastatin with some simvastatin) at or near LDL-C goal (all < 100 mg/dL).
They then received either Niaspan (extended release niacin) titrated to 2000 mg (a dose rarely used in the real world) or Zetia (ezetimibe) 10 mg daily. As expected there were more Niaspan dropouts due to drug side effects in the trial compared to Zetia.
The endpoint was change in carotid IMT over a year.
Unfortunately the trial was stopped prematurely, for no good reasons (both of the editorialists [see the editorials here and here] in the NEJM and the discussants at the AHA meeting agreed on that). Premature stoppage likely means whatever findings occurred are over-exaggerated.
Furthermore, the morons in the press are running around telling people they can take an over the counter vitamin for CHD. Niacin at 2000 mg or more mg per day is way beyond the vitamin dosage: it is a major pharmacological dose of a vitamin B3 and cannot be considered a vitamin at that dose and certainly has issues that must be followed.
Patients in the study had at goal or near goal LDL-C and borderline low HDL-C at the lower end of normal (remember baseline HDL-C was assayed while on a statin – not in a drug naive state).
Tragically the author did not see fit to measure the far more important parameters apoB or LDL-P or apoA-I or HDL-P. That is a mind boggling oversight in 2009 and it also makes it much more difficult to truly interpret what are the benefits of statin/Zetia (Vytorin) or statin/Niaspan (Simcor).
Most of these patients were on statins for over 5 years and thus their carotids have many years of statin therapy. Over the very short 14 month period of this trial the carotid IMT (CMIT) changes regressed on Niaspan/statin while statin/Zetia caused non-progression or miniscule regression (just like Crestor, a proven outcome therapy, did in METEOR).
Thus neither combination therapy failed, but Niaspan/statin induced what certainly seem to be more favorable changes than the statin/Zetia.
However there is no data that event reduction would be any different in patients with no progression versus regression. So until we have outcome trials, no one can conclude which combo therapy is in reality the best therapy.
Both editorialists and all discussants at AHA made that clear. However, let’s be also be very clear that based on CIMT changes statin/Niaspan was the winner.
However, because of the lack of data correlating therapy-produced, precise imaging changes to outcomes, there are no guidelines advising us to judge the efficacy of our drugs by performing repeat imaging procedures (including IMT).
Does everyone remember that estrogen, raloxifene, Fosamax and torcetrapib all have positive CIMT data and NONE have been shown to reduce cerebrovascular disease (CVD) events? Indeed both estrogen and torcetrapib also raise HDL-C.
Statin data on IMT changes are all over the map (positive and negative) yet all statins reduce outcomes. There does not seem to be much linkage. Pravachol reduces outcomes in its trials but was associated with plaque progression in an IVUS study (REVERSAL).
The lipids concentrations and presumably lipoprotein were beneficially altered with the addition of either Zetia or Niaspan. Zetia helped LDL-C more than niacin and niacin helped TG and HDL-C more than Zetia (no surprise there). Both drugs helped non-HDL-C.
My guess is the LDL-P (apoB) was fairly well controlled by the several years of statin use in this trial and both Zetia and Niacin further improved that crucial parameter (LDL-P or apoB). My guess is also that niacin improved apoA-I and total HDL-P and the Zetia did not. That would likely be a benefit in the Niaspan column.
- We grossly under treat our patients.
- Statin monotherapy, usually nontitrated is the routine therapy in the US.
- Stents, strokes, bypass and deaths are way too high despite statin monotherapy.
- We desperately need to get more aggressive to achieve all goals, especially lipoprotein goals.
Want to help lower apoB (LDL-P):
- Use statins — if not at goal add Zetia, Welchol, or Niacin in no particular order although if there are not TG or HDL issues, I prefer Zetia first because of ease of use.
- However if HDL-P (HDL-C) is low in the face of an elevated apoB or LDL-P then Niacin becomes my first add on (which is the exact recommendation made by ACC and ADD position statement published last year).
- If the TG are an issue (> 200 mg/dL) or TG/HDL axis is abnormal then a fibrate, niacin (or high dose or omega-3) is the likely best choice.
So, if I take a drug like Niaspan and can help a statin achieve better apoB levels and raise HDL-P levels, I think I have a great add on. Simcor would save be a copay, but Crestor/Niaspan would be the more potent therapy.
The ARBITER-6 HALTS trial certainly supports Niaspan/statin use. I prescribe Niaspan as they did in the study: get all patients to 2000 mg ASAP. I suggest you do the same. You cannot expect lower doses of Niaspan to achieve these results.
With proper advice, and perseverance Niaspan use is easier done than commonly believed. Abbott also offers a nice program to help patients properly take Niaspan. Talk to your reps.
This study does not change the fact that apoB (LDL-P) reduction is the primary goal, but it enforces the belief that raising HDL-P should be the secondary goal (by the way, fibrates raise HDL-P more so than niacin, yet fibrates, because of what they do to LDL size, do not raise HDL-C anywhere near what niacin does). This is one reason HDL-P is more informative than HDL-C.
If a patient on statin/Zetia is still not at LDL-P goals of therapy, Niaspan can help even if the HDL-C is not low. Also, if I have a patient on statin/Niaspan and LDL-P is not at goal I add Zetia. There is published data that statin/Zetia/Niaspan is a great lipid modulating triple therapy.
- we all need to use a lot more Niaspan (all CHD patients should be on it along with whatever else is needed to get to goal).
- No one needs to stop Zetia in anyone and no one needs to be afraid of using Zetia to help achieve goal.
- For your Vytorin users: if HDL-P is not normal or LDL-P is still high: please add Niaspan AND PLEASE TITRATE IT TO TWO GRAMS.
I want to conclude some of the what I consider outrageous statements made in the paper by the author.
- Is it plausible that Zetia is harmful to atherosclerosis: that is the conclusion by the author speculating on lipid issues that I do not believe have any support? The paper hints Zetia impairs reverse cholesterol transport. I can supply several studies show it improves RCT (start with Arterioscler Thromb Vasc Biol. 2008;27:1296-1297). I also hate to remind everyone: a serum HDL-C has no relationship what so ever to the dynamic process called reverse cholesterol transport. Macrophage RCT (removing cholesterol from the arterial wall) has no influence on serum HDL-C levels. Niacin raises HDL-C by increasing apoA-I production, inducing hepatic lipidation of HDLs, reducing CETP activity, inhibiting hepatic lipase (thus making HDLs large) and reducing the apoA-I beta synthase hepatic holoparticle receptor.
- ACAT (the enzyme that esterifies free cholesterol into cholesteryl ester) inhibition is bad and Zetia is thus bad because it reduces ACAT. ACAT inhibitors, which have failed in clinical trials prevent esterification of cholesterol and the free cholesterol accumulates in macrophages. Zetia reduces ACAT activity and expression because by reducing cholesterol delivery (absorption) ACAT downregulates. There is no cellular cholesterol accumulation on Zetia. In the study quoted, the dose of Zetia that impacted ACAT, was infinitely larger than we use to treat lipids.
- The author states Zetia affects SRB1 and thus impairs RCT. The study referenced was looking at SRB1 in intestinal cells has nothing to do with reverse cholesterol transport. Niacin inhibits ApoA-I beta chain synthase the hepatic holoparticle (HDL catabolism) receptor which decreases hepatic uptake of HDL trafficked cholesterol and potentially decreases RCT. Yet niacin sure works. Statins downregulate ABCA1 the main HDL lipidation enzyme involved with macrophage RCT yet they work.
- Amazing the NEJM published a nonsensical post hoc analysis showing too much LDL-C lowering with ezetimibe worsens CIMT. This trial is not empowered to examine such an endpoint in a univariate analysis. Shame on the NEJM and their reviewers for allowing such speculation. This has outraged many respected lipidologists. The author was taken to task by the discussants on the podium for this type of analysis.
- Implying that Zetia increased CV endpoints in a trial that has no such power to do so is the worst kind of fear mongering analysis and no one should pay any attention to such a statement. The author again was taken to task big time by the discussants on the podium for stating such a thing. The main discussant John Kastelein firmly stated that mortality data has NO MEANING. Shame on the NEJM for letting such statements appear.
In conclusions: FACTS:
- There is no outcome data for Zetia of any kind.
- There is no level one evidence for Niacin: there is secondary endpoint data from CDP.
- There is no outcome data relating what a drug does to HDL-C benefits CVD outcomes, but there is level 2 evidence that raising HDL-P is beneficial (see VA-HIT).
- There is no data relating specific drug induced imaging benefits (including IMT) to CV outcome benefit. Crestor, a drug proven to significantly reduce CV outcomes failed to induce regression in a big CIMT trial (METEOR) but rather inhibited progression (exactly what statin/ezetimibe did in this trial. Yet in an angiographic trial regression occurred with Crestor.
- Fact: every guideline wants you to get to lipid/lipoprotein goal using lifestyle and FDA approved drugs. Statins first line if TG are < 500 mg/dL. In patients with cardiometabolic risk, niacin is the preferred first add on drug (ADA/ACC consensus statement).
- NIASPAN is a great statin helper drug and needs to be prescribed much more frequently than it is.
- Zetia is a great statin helper drug and needs to be prescribed much more frequently.
- No one should be stopping Zetia, no one should be afraid to use Zetia to get to goal and for sure we need to use a lot more Niaspan at 2000 mg.
- Guess what: I am not stopping my Zetia – I surely and happy to continue my Niaspan and I’d ask you all to review the great John Guyton study: Lipid-Altering Efficacy and ”Safety of Ezetimibe/Simvastatin coadministered With Extended-Release Niacin in Patients With Type IIa or Type IIb Hyperlipidemia: (J Am Coll Cardiol 2008;51:1564–72.
Conclusion: Combination treatment with E/S plus N showed superior lipid-altering efficacy compared with N or E/S in type IIa or IIb hyperlipidemia patients and was generally well tolerated aside from N-associated flushing. This combination offers an effective, broad, lipid-altering therapy with improvements in lipid effects beyond LDL-C in these patients.
Tom Dayspring, MD
There’s good news for men concerned about developing prostate cancer. The AP reports, “Men may protect more than their hearts if they keep cholesterol in line: Their chances of getting aggressive prostate cancer may be lower.” Want to learn more? Then, read on as scientists at two institutions have detailed the research that led them to that conclusion in Cancer Epidemiology Biomarkers & Prevention.
According to the AP report, even though the papers “are not definitive and have some weaknesses,” they do “fit with plenty of other science suggesting that limiting fats in the bloodstream can lessen cancer risk.”
HealthDay reported that NCI investigators reviewed “data from a study that has followed more than 29,000 Finnish men for 18 years,” finding that “cholesterol levels below the generally recommended 200 milligrams per deciliter were associated with an 18 percent higher overall risk of cancer.”
Two studies looked at cholesterol in cancer finding that low cholesterol is a symptom rather than a cause and that low cholesterol may actually lower a man’s risk of high-grade prostate cancer.
In the first study, researchers observed over 29,000 men for 18 years for cancer and found no association unless they included men who were diagnosed right away after enrolling in the trial.
These men likely already had cancer and their low cholesterol was an effect and not a cause, since all the other men didn’t develop cancers at a rate different from men with normal or high cholesterol.
The second study found an association between low cholesterol and lower than average risk for high-grade prostate cancer, however we need to see the results of a clinical trial looking at the effects of lowering cholesterol on cancer risk before there will be recommendations for drugs like statins to be used preventively.
An editorial in same issue of Cancer Epidemiology, Biomarkers & Prevention concluded, “Results from the two analyses of cholesterol and risk of cancer published in this issue . . . clearly show that low total cholesterol is unlikely to increase risk of cancer.”
The editorial also makes this interesting observation: “If results of such observational studies support the hypothesis that low cholesterol inhibits prostate cancer progression, then it would raise the question of whether prostate cancer patients choosing active surveillance, rather than immediate treatment, could reduce their risk of disease progression by using statins or other cholesterol lowering drugs. This question, however, would need to be answered by a randomized trial.”
So, the bottom line?
Guys, get a lipid profile and if it’s abnormal do what you must do to get it normal — whether that’s changing your nutrition, increasing your physical activity, or using cholesterol lowering drugs.
Ladies, get the guys you love to have a lipid profile. If it’s abnormal, follow the advice above.
On March 31, 2008, pharmaceutical giant AstraZeneca trumpeted the early closing of its so-called JUIPITER trial of a cholesterol-lowering drug (statin), Crestor. The results after only two years yielded “unequivocal evidence” of the drug’s effectiveness, the trial concluded, and the company argued that it could not be withheld from anyone who was well and had normal cholesterol levels but had an elevation in another normal blood constituent, the C-reactive protein (CRP). But, what’s the “other side” of this story?
More Information: Continue reading