Showing posts with label Jupiter study. Show all posts
Showing posts with label Jupiter study. Show all posts

Friday, December 5, 2008

Pay No Attention to the Man Behind the Curtain

Vitamin E Reduces Inflammation
but if you want to believe the recent junque science report reiterated from mainstream media in the AARP Bulletin, you are taking your life in your hands.

AARP is doing a grave dis-service to its members by allowing this biased reporting and yet failing to allow for opposing viewpoints that, like one comment on the report on the AARP Bulletin web site. This commenter begins by stating that all participants in the study had a 28.3 BMI and would be considered obese.

And if you read just the last part of this post you'll see AARP has it wrong. All they would have to do is to read the reports on E, C, Selenium and the Jupiter Study on Natural Health News. It's a simple thing to use our search function, and real data. You can even link to our reading site with more about vitamin E.

Or you can read what some other MDs have to say about these faulty studies here: Another push to get cholesterol levels ever lower, but let’s make sure it isn’t killing people first and here.

I'll still side against the cholesterol study and I'll side for vitamin E, C and selenium effectiveness.
Health Discoveries: Selenium, Vitamin E Don't Help After All
By Katharine Greider - December 1, 2008 - From the AARP Bulletin Today

Do vitamin E and selenium help prevent prostate cancer? The answer is no, according to findings from a major trial with 35,000 men. The SELECT study, sponsored by the National Cancer Institute and begun in 2001, was stopped early, in September, after finding no evidence of any benefit from either supplement.

The news disappointed many cancer experts, says Elise Cook, M.D., a study researcher and a cancer prevention specialist at M.D. Anderson Cancer Center in Houston. But it provides important information about what doesn’t work. Cook says many men had been reluctant to join the study because they were already taking vitamin E for heart as well as prostate health. “Since then, other studies have shown that it really didn’t help their hearts, either,” she says.

and they also ran an instant replay of the much touted Jupiter study, falling for the drug company propaganda.
Health Discoveries: By Jupiter! Statins Cut Heart Disease
By Barbara Basler - December 1, 2008 - AARP Bulletin Today

Men and women in their 50s and 60s—with normal cholesterol levels—dramatically cut their risk of heart disease and stroke by taking a statin drug normally used only to lower cholesterol, a new study shows. Published in the Nov. 20 New England Journal of Medicine, the study, dubbed “Jupiter,” could change the basic guidelines for preventing heart disease.

Researchers from Brigham and Women’s Hospital in Boston looked at nearly 18,000 people with no history of heart disease but who did have elevated levels of high-sensitivity C-reactive protein, or hs-CRP, as measured in blood tests. Compared with the group taking a placebo, those on the statin reduced their chances of a heart attack by 54 percent, stroke by 48 percent and the need for bypass surgery or angioplasty by 46 percent. Learn more about the study on bulletin.aarp.org/yourhealth

The December, 2008 issue of the journal Experimental Physiology published the discovery of researchers at the University of Illinois of an anti-inflammatory effect for vitamin E in an animal model of inflammation.

Scientists are becoming increasingly aware of the role of inflammation in a number of diseases and conditions. Chronic inflammation of the skeletal muscles in humans is a cause of significant physical impairment. Antioxidants such as vitamin E have been shown to reduce proinflammatory cytokine expression in cell culture studies, but the vitamin's effects had not been tested in the heart and skeletal muscle of mice with induced systemic inflammation.

University of Illinois kinesiology and community health professor Kimberly Huey and colleagues administered vitamin E or a placebo to mice for three days before injecting the animals with a low dose of E. coli lipopolysaccharide to induce inflammation. A control group received saline injections.

The team found increased levels of the cytokines interleukin-6 (IL-6) and interleukin-1beta (IL-1beta) in the skeletal and cardiac muscle of mice that received lipopolysaccharide, yet among those that received vitamin E, levels of these cytokines were significantly lower than those of the placebo group. The cytokines function as intercellular communicators which assist in immune response, yet can lead to excessive inflammation. Additionally, the researchers observed decreased activation of nuclear factor kappa-beta (another agent involved in inflammation) in mice that received vitamin E.

“The mice were administered vitamin E for three days prior to giving them what amounts to a minor systemic bacterial infection,” Dr Huey explained. “One thing we did – in addition to (looking at) the cytokines – was to look, in the muscle, at the amount of oxidized proteins. Oxidation can be detrimental, and in muscle has been associated with reduced muscle strength.”

Dr Huey revealed that “there was a significant reduction in the amount of lipopolysaccharide-induced oxidized proteins with vitamin E compared to placebo.”

“So that’s a good thing,” she noted. “Potentially, if you reduce the oxidized proteins, that may correlate to increased muscle strength.”

In previous research conducted by team member Rodney Johnson, an association in mice between vitamin E supplementation and reduced brain inflammation was observed. Inflammation in the brain is associated with Alzheimer’s disease in humans.

Dr Huey concluded that vitamin E “may be beneficial in individuals with chronic inflammation, such as the elderly or patients with type II diabetes or chronic heart failure.”

“This is clearly an animal model so whether it would translate to humans still requires a lot more research,” she remarked. “Vitamin E is a supplement that is already approved, and these results may suggest an additional benefit of taking Vitamin E beyond what’s already been shown.”

And consider that Chronic Inflammation will respond well to vitamin E and some other natural substances as mentioned in this report -
In aged people with multiple degenerative diseases, the inflammatory marker, C-reactive protein, is often sharply elevated, indicating the presence of an underlying inflammatory disorder (Invitti 2002; Lee et al. 2002; Santoro et al. 2002; Sitzer et al. 2002). When a cytokine blood profile is conducted on people in a weakened condition, an excess level of one or more of the inflammatory cytokines, e.g., TNF-a, IL-6, IL-1(b), or IL-8, is usually found (Santoro et al. 2002).

Scientists have identified dietary supplements and prescription drugs that can reduce levels of the pro-inflammatory cytokines. The docosahexaenoic acid (DHA) fraction of fish oil is the best documented supplement to suppress TNF-a, IL-6, IL-1(b), and IL-8 (Jeyarajah et al. 1999; James et al. 2000; Watanabe et al. 2000; Yano et al. 2000). A study on healthy humans and those with rheumatoid disease shows that fish oil suppresses these dangerous cytokines by up to 90% (James et al. 2000).

Other cytokine-lowering supplements are DHEA (Casson et al. 1993), vitamin K (Reddi et al. 1995; Weber 1997), GLA (gamma linolenic acid) (Purasiri et al. 1994), and nettle leaf extract (Teucher et al. 1996). Antioxidants, such as vitamin E (Devaraj et al. 2000) and N-acetyl-cysteine (Gosset et al. 1999), may also lower proinflammatory cytokines and protect against their toxic effects.

Friday, November 14, 2008

Cholesterol and Statins: Another physician reviews the Jupiter study

UPDATE: 21 April, 2010 -
Cholesterol Drugs May Lower Men's Sex Drive
Some new studies believe that low testosterone is associated with prostate cancer.
Eating your way to lower cholesterol Note that we do not support the use of plant sterols as they are mainly sourced from GMO soy and canola oil

ORIGINAL POST
In addition to the many posts (136) here on Natural Health News, there is a selection of related articles on our main website.
Statins reduce cardiovascular disease in healthy people, and why this study is a poke in the eye for the cholesterol hypothesis

By Dr John Briffa On November 10, 2008

It’s been going this way for a while: even healthy people should be on the cholesterol-reducing drugs known as statins. That, in a nutshell, is the verdict of a study published over the weekend which found that even in people deemed to be at low risk of cardiovascular disease, treatment with rosuvastatin (Crestor) at a dose of 20 mg per day almost halved the risk of ‘vascular events’ (such as heart attack, stroke, and death from these conditions) in middle-aged and elderly men and women. Overall risk of death was down too in those taking the rosuvastatin, to the tune of 20 per cent. Average length of treatment was a shade under two years.

These results look impressive, but it does need to be borne in mind that the study population were essentially healthy. And, because of this, the risk of things like heart attacks and strokes is generally low in this population. Just to put this in perspective, the risk of vascular events was 2.2 per cent in the group taking the statin, but 2.8 per cent in those on placebo. In other words, what is known as the absolute risk reduction (as opposed to the relative risk reduction) was a little over half a percent.

It is perhaps also worth reflecting on the fact that treatment with rosuvastatin was associated, compared with placebo, with a significantly increased risk of developing diabetes. Curiously, the authors of the study say this effect could “reflect the play of chance.” In other words, even though there was a statistically significant enhanced risk of diabetes in those taking the statin, it may have nothing to do with the statin, and everything to do with bad luck. Curiously, the authors are not similarly circumspect about the positive effects of statins seen in this study.

But the reason for writing about this study is not so much to put the results in this context, but more to explore what these results say about the widely accepted context that cholesterol causes cardiovascular disease. On the face of it, this study strengthens this concept. But I’m not so sure.

You see this study was done in individuals whose cholesterol levels were not deemed to be risky. Individuals had to have LDL cholesterol levels of less than 130 mg/L (3.37 mmol/L) to qualify. However, to qualify for the study individuals did have to have elevated levels of a substance known as C-reactive protein (CRP). CRP is a marker for inflammation in the body, and inflammation is believed to be a key underlying process in the development of cardiovascular conditions such as heart disease and stroke.

Significant benefits were seen individuals who had elevated CRP levels, but no other major risk factors for cardiovascular disease (and LDL cholesterol levels of 100 mg/L or less). This inevitably throws up the possibility that in this study, the benefits of rosuvastatin came, at least in part, through its ability to reduce CRP levels. CRP levels actually dropped by 37 per cent on average in this study.

Cholesterol levels dropped too (LDL levels actually halved), but as the authors point out, the clinical benefit associated with this was much larger than expected. This finding also adds weight to the idea that rosuvastatin’s benefits may have been less to do with bringing cholesterol levels down, and more to do with an anti-inflammatory and/or other actions.

Previously on this site I have cited a 2006 review of the evidence regarding the relationship between cholesterol and cardiovascular outcomes such as heart attacks and strokes [2]. Having reviewed a broad range of available evidence, the authors of this review stated that: ‘…no clinical trial subgroup analyses or valid cohort case control analyses suggesting that the degree to which LDL cholesterol responds to statin independently predicts the cardiovascular risk reduction.” In other words, there is no robust relationship between cholesterol levels and degree of risk of cardiovascular disease.

This is not the only review that has found this. In another from the same year, researchers reviewed 13 studies in which statins were used in individuals who had suffered from ‘acute coronary syndrome’ (i.e. heart attack and angina). Statin therapy was found to reduce risk of cardiovascular disease, but this was independent of LDL cholesterol reduction. The authors concluded that there is no significant evidence that reduction in LDL cholesterol level explains the clinical benefits seen with statin therapy on cardiovascular disease risk [3].

And what of studies that have assessed the relationship between CRP and cardiovascular outcomes? The lead author of the recent NEJM paper was also the lead author of a paper published in 2005 that assessed data from another large statin study (the so-called ‘PROVE-IT’ study) [4]. The study concluded: “Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol.”

From the same year, comes another study in which the relationship between LDL cholesterol and CRP levels and development of the process which narrows the coronary blood vessels in heart disease (atherosclerosis) in individuals treated with a statin. Atherosclerosis actually regressed in patients with the greatest reduction in CRP levels, but not in those with the greatest reduction in LDL cholesterol levels [5].

Another way of unpicking the role of cholesterol in health would be to go beyond statins, and look at the effectiveness of other cholesterol reducing drugs or strategies on overall risk of death. This latest study, and others (particularly in those at high risk of cardiovascular disease) found statin therapy is associated with a reduced risk of death. A review from 2005 assessing the impact of cholesterol reducing therapy on overall mortality. Here are the results:

Statins – statistically significant reduction in risk of overall mortality

Fibrates – NO statistically significant reduction in risk of overall mortality

Resins – NO statistically significant reduction in risk of overall mortality

Niacin – NO statistically significant reduction in risk of overall mortality

Diet – NO statistically significant reduction in risk of overall mortality

Some people argue that the failure of other cholesterol-reducing strategies is because they don’t reduce cholesterol enough. I suppose that’s one potential explanation. Here’s another: cholesterol reduction doesn’t have broad benefits for health.

References:

1. [1] Ridker PM, et al. Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein. New England Journal of Medicine. Epub 9th November 2008.

2. Hayward RA, et al. Narrative review: lack of evidence for recommended low-density lipoprotein treatment targets: a solvable problem. Ann Int Med 2006;145:520-530

3. Hulten E, et al. The effect of early, intensive statin therapy on acute coronary syndrome: a meta-analysis of randomized controlled trials. Archives of Internal Medicine. 2008;166:1814-1821

4. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. New Engl J Med 2005;352:20-8.

5. Nissen SE, et al. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease. N Engl J Med 2005;352: 29-38
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Article printed from Dr Briffa’s Blog: http://www.drbriffa.com
URL to article: http://www.drbriffa.com/blog/2008/11/10/statins-reduce-cardiovascular-disease-in-health-people-and-why-this-study-is-a-poke-in-the-eye-for-the-cholesterol-hypothesis/
URLs in this post:
[1] Ridker PM, et al. Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein. New England Journal of Medicine. Epub 9th November 2008.: http://content.nejm.org/cgi/content/full/NEJMoa0807646