The Elderly on Primary-Prevention Statins: No Survival Gains in ALLHAT - Medscape

The Elderly on Primary-Prevention Statins: No Survival Gains in ALLHAT

CHICAGO, IL — Statins for primary prevention do not lower the risk of death, whether cardiovascular or from any cause, when given to people aged 65 years or older with CV risk factors, suggests a secondary analysis of a major trial that caused a stir 15 years ago^[1].
The ALLHAT-LLT trial had randomized >10,000 people aged >55 with dyslipidemia and hypertension but no clinical heart disease to receive open-label pravastatin 40 mg/day or usual care. In its 2002 publication^[2], the trial famously saw no significant mortality reduction for the statin after 6 years, nor an improvement in fatal or nonfatal coronary heart disease events.

The results were similar in the new post hoc analysis of the trial focusing on the 2867 participants aged 65 years and older, as a whole and by the two age groups 65 to 74 years and >75 years, according to a report published May 22, 2017 in JAMA Internal Medicine with lead author Dr Benjamin H Han (New York University Langone School of Medicine, NY).
Although no significant outcomes differences were seen between the two randomized groups in any of the age categories, there was a trend (P=0.07) for increased all-cause mortality on the statin in the oldest age group.

As Han pointed out for heartwire from Medscape, the overall trial had well-recognized limitations. For example, the statin was given on an open-label basis. Also, it has been long noted that the ALLHAT-LLT usual-care group could receive statins at the physicians' discretion, which could potentially blur any differences in treatment outcomes.

Calls for Caution

"I would be very cautious in drawing any real conclusions from this study, as the study was not specifically designed to study statins in older adults, so all of the analyses are underpowered. None of their major conclusions were statistically significant," according to Dr Ann Marie Navar (Duke Clinical Research Institute, Durham, NC), who isn't connected with the ALLHAT-LLT report.
"Most statin trials have shown no difference in mortality, but [they showed] that statins do reduce the risk of coronary heart disease, a trend also seen in this secondary analysis," Navar told heartwire by email.

"The trend toward increasing mortality is certainly provocative but really needs to be explored in a trial specifically designed to test this issue."
The post hoc analysis included 1467 participants who had been randomized to pravastatin; their mean age was 71.3, and 48% were women. Their mean LDL-C level was 147.7 mg/dL at baseline and 109.1 mg/dL after 6 years.
The 1400 participants in the usual-care group had a mean age of 71.2 years, and 51% were female. Their mean LDL-C level was 147.6 mg/dL at baseline and 128.8 mg/dL after 6 years.
For all patients over the age of 65 who took pravastatin, the hazard ratio for all-cause mortality was 1.18 (95% CI 0.97–1.42, P=0.09) compared with the usual-care group. It was 1.08 (95% CI 0.85–1.37, P=0.55) for the 65–74 group and 1.34 (95% CI 0.98-1.84 P=0.07) for those aged 75 and older. Nor were there significant HRs for the secondary CHD end points.

In multivariate analysis, the corresponding HRs were 1.15 (95% CI 0.94–1.39) for 65 and older, 1.05 (95% CI 0.82–1.33) for those 65 to 74, and 1.36 (95% CI, 0.98-1.89) for 75 and older. The prospectively defined covariates included age, sex, race/ethnicity, primary-prevention aspirin use, smoking history, type 2 diabetes, body mass index, and systolic and diastolic blood pressures.

The Issues
"We are seeing a lot more older adults being put on statins for primary prevention, but the problem is, the evidence for doing so is limited," Han said.

"As geriatricians, we emphasize that treatment recommendations really need to be individualized with patients and need to also take into account not just what their cardiovascular risk is, but what their life expectancy is, what other competing risks they may have, and what their functional status and everyday activities are," Han observed.

Moreover, "for older adults, taking another medicine every day for the rest of your life isn't a small thing, especially if you have other chronic conditions, and right now we don't have any evidence that there's any benefit to doing so if you do not have any history of cardiovascular disease."

An editor's note accompanying the ALLHAT-LLC report points out the potential risks of extending statins to groups that may be unlikely to benefit clinically^[3]. For example, statin therapy may be associated with myopathy, myalgias, muscle weakness, and arthropathies, notes Dr Gregory Curfman (Harvard Medical School, Boston, MA).

"These disorders may be particularly problematic in older people and may contribute to physical deconditioning and frailty. Statins have also been associated with cognitive dysfunction, which may further contribute to reduced functional status, risk of falls, and disability," he writes.

"The combination of these multiple risks and the ALLHAT-LLT data showing that statin therapy in older adults may be associated with an increased mortality rate should be considered before prescribing or continuing statins for patients in this age category."

Is There a "Point of No Return"?

"It takes decades for the plaque to build up in the arteries that eventually causes strokes and heart attacks. Data from thousands of adults studied in clinical trials show us that statins, when started early, can interrupt or slow down that process," according to Navar.

But, "we don't know if there is a 'point of no return' where it's too late to start a statin, and ALLHAT was not designed to answer that question. We need a large randomized trial to really know how effective statins are when started in older adults without cardiovascular disease," she said.

"There is a lot of negative press about statins, and I really worry about the effect of studies like these on the public's perception. This study was a secondary analysis of a trial that was not designed to study the effect of statins in older adults," Navar observed.

"Data from thousands of adults in multiple randomized trials have shown that statins prevent heart disease and do not kill people. I hope that the media, in the never-ending search for clickbait, doesn't overemphasize the statistically nonsignificant mortality trend and lead people who are known to benefit to discontinue their statins."

The study was funded by the National Heart Lung & Blood Institute. Study medications were contributed by Pfizer, AstraZeneca, and Bristol-Myers Squibb, and financial support was provided by Pfizer. The study authors and Curfman report no relevant financial relationships. Navar reported research support from the National Institutes of Health, Amgen, and Sanofi & Regeneron Pharmaceuticals and serving as a consultant for Amgen and Sanofi.
Read the full article here.

Cholesterol Paradox: A Correlate Does Not a Surrogate Make

Abstract

The global campaign to lower cholesterol by diet and drugs has failed to thwart the developing pandemic of coronary heart disease around the world. Some experts believe this failure is due to the explosive rise in obesity and diabetes, but it is equally plausible that the cholesterol hypothesis, which posits that lowering cholesterol prevents cardiovascular disease, is incorrect. The recently presented ACCELERATE trial dumbfounded many experts by failing to demonstrate any cardiovascular benefit of evacetrapib despite dramatically lowering low-density lipoprotein cholesterol and raising high-density lipoprotein cholesterol in high-risk patients with coronary disease. This clinical trial adds to a growing volume of knowledge that challenges the validity of the cholesterol hypothesis and the utility of cholesterol as a surrogate end point. Inadvertently, the cholesterol hypothesis may have even contributed to this pandemic. This perspective critically reviews this evidence and our reluctance to acknowledge contradictory information.


Read the complete article here.

Science News

from research organizations

---

Sugar consumption plays greater role in heart disease than saturated fat

Date:

January 13, 2016

Source:

Elsevier

Summary:

Atherosclerotic Coronary Heart Disease (CHD) is responsible for one in every six deaths in the United States as well as being the leading cause of death throughout the developed world. Healthcare professionals have for many years sought to limit and control CHD by focusing on prevention and, from a dietary perspective, on limiting saturated fats.

 

---

Atherosclerotic Coronary Heart Disease (CHD) is responsible for one in every six deaths in the United States as well as being the leading cause of death throughout the developed world. Healthcare professionals have for many years sought to limit and control CHD by focusing on prevention and, from a dietary perspective, on limiting saturated fats.

 

In an article published in the journal Progress in Cardiovascular Diseases, Saint Luke's Mid America Heart Institute cardiovascular research scientist and James J.. DiNicolantonio, PharmD, and James H. O'Keefe, MD, examined the question of whether that focus may be misplaced and ask does sugar have a greater impact on coronary heart disease than saturated fat?

The theory of dietary saturated fats as the principal promoter of elevated serum cholesterol and heart disease stems from research beginning in the 1950's by an American scientist Ancel Keys. It was this theory which was embraced by the American Heart Association and the US federal government in the 1960s and 70s. However, at the same time of Keys research, a British physiologist John Yudkin argued that sugar intake was more closely related to incidence of and mortality from CHD.

Both Yudkin and Keys were able to support their theories through observational studies in large part because people eat foods, not isolated food constituents. Dietary sources of saturated fat are also often dietary sources of sugar and people who eat lots of sugar often also eat lots of saturated fat.
Along with co-author, Sean C. Lucan, MD, MPH, MS, from the Albert Einstein College of Medicine, DiNicolantonio and O'Keefe evaluated the evidence to date linking saturated fats and sugars to CHD, considering basic science, epidemiology, and clinical trial data related to CHD risk, CHD events, and CHD mortality. The authors concluded that sugar consumption, particularly in the form of refined added sugars, are a greater contributor to CHD than saturated fats.

"While the original studies upon which the longstanding guidelines were based were largely observational," said DiNicolantonio, "We now have more than a half century of data as well as increased understanding of how nutrition impacts the body and specifically coronary heart disease."
The metabolic aspects of saturated fatty acids (SFAs) are complex but existing research suggests that certain SFAs may actually confer measurable benefits for lipid profiles and CHD risk. For instance, some SFAs increase high-density lipoprotein cholesterol (HDL), which is often referred to as the "good cholesterol" as this lipoprotein is associated with a reduced risk of CHD
Replacing saturated fats, or any other component, from one's diet almost inevitably means replacing it with something else. When carbohydrates, particularly refined carbohydrates like sugar, replace saturated fats, which can have a negative impact on lipid profiles (HDL tends to fall and triglycerides tend to rise).

As stated earlier, people don't eat isolated fatty acids -- they eat foods that are a mix of various fatty acids and other food constituents. While high intakes from processed meats may increase risk of CHD, higher intakes from dairy sources of saturated fat may not only pose no risk but actually decrease risk.

Consuming a diet high in sugar for just a few weeks has been shown to cause numerous abnormalities found in patients with CHD, such as high total cholesterol, triglycerides, LDL, oxidized LDL, uric acid, insulin resistance and abnormal glucose tolerance, low HDL, and altered platelet function. The overall effect of consuming a diet high in sugar on these numerous health markers is likely more detrimental to overall health compared to increased consumption of saturated fat, which can increase LDL but at the same time raise HDL.

Added fructose -- generally in the form of sucrose (table sugar) or high fructose corn syrup (HFCS) in processed foods and beverages seems especially potent for producing harm. Consuming these sugars can lead to resistance in leptin, which is a key hormone in the maintenance of normal body weight. The overconsumption of added fructose undoubtedly increases the risk for obesity, which is also a risk factor for CHD.

Excess fructose also markedly increases the risk for non-alcoholic fatty liver disease (NAFLD) -- the most common liver disease in the US and a strong independent risk factor for CHD. The association between NAFLD and CHD is stronger than the link between CHD and smoking, hypertension, diabetes, male gender, high cholesterol or metabolic syndrome.

Sugars occurring naturally in fruits and vegetables pose no increased risk for CHD. The problem is refined sugars -- with ultraprocessed foods being of greatest concern. Products with added sugars represent 75% of all packaged foods and beverages in the US and most commonly contain sucrose or HFCS, which seem to raise CHD risk even more than other sugars such as glucose.

A diet high in sugar has also been found to promote prediabetes and diabetes. And patients with both of these conditions have a much greater risk for CHD compared to normal healthy patients, particularly a severe narrowing of the left main coronary artery.

Ultra-processed foods also tend to be sources of saturated fats but the harms associated with eating these products may have nothing to do with the fat and everything to do with processed foods themselves. Therefore, best advice is to avoid processed foods rather than to simply avoid SFAs as avoiding SFAs might direct people away from foods that are not only completely benign but actually beneficial (such as dairy foods) but also steer people towards foods that may be harmful -- i.e. low-fat, ultra-processed, with huge amounts of hidden added sugars.

"After a thorough analysis of the evidence it seems appropriate to recommend dietary guidelines shift focus away from recommendations to reduce saturated fat and towards recommendations to avoid added sugars," said Dr DiNicolantonio. "Most importantly recommendations should support the eating of whole foods whenever possible and the avoidance of ultra-processed food."

 

---

Journal Reference:

1. James J. DiNicolantonio, Sean C. Lucan, James H. O’Keefe. The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease. Progress in Cardiovascular Diseases, 2015; DOI: 10.1016/j.pcad.2015.11.006

Read the complete article here.

Does Wheat Cause Coronary Heart Disease?

Introduction

Coronary heart disease (CHD) is the leading cause of deaths worldwide - killing 7 millions people every year. In the following text, we will see that wheat consumption is probably a risk factor for CHD.

Conventional Wisdom on Wheat

Most health organizations currently view wheat as a safe food except for people having celiac disease - affecting up to 1% of the population - and people having non-celiac gluten sensitivity. Also whole wheat - as part of whole-grains - is considered to be one of the healthiest food. In fact a diet rich in whole-grains is considered to be protective against CHD.

Why? Because observational studies consistently find that whole-grain consumption is associated with a decreased risk of CHD. Do these results contradict wheat consumption causing CHD?

Are Whole-Grains Protective Against CHD?

According to this study:

Whole-grain intake consistently has been associated with improved cardiovascular disease outcomes, but also with healthy lifestyles, in large observational studies. Intervention studies that assess the effects of whole-grains on biomarkers for CHD have mixed results.

Indeed many studies show that whole-grain consumption is associated with a decreased risk of CHD. But these studies are observational and can only show correlation but not causation.

In fact there is an health-conscious population bias in these studies: for example people consuming the most whole-grains also exercise more and smoke less:

Data from Majken K Jensen et al., Intakes of whole grains, bran, and germ and the risk of coronary heart disease in men, 2004

Of course researchers adjust the data with these risk factors. But it is very difficult, maybe impossible, to adjust for all risk factors. For example the two previously cited studies did not adjust for important risk factors like socioeconomic status or social support.

A classic example of an occurrence of this bias can be found in hormone replacement therapy (HRT): observational studies had found that HRT was decreasing the risk of heart disease risk while a controlled study finally found that HRT was indeed slightly increasing the risk of heart disease.

A proof that this health-conscious bias could explain the seemingly protective effect of whole-grains can be found in randomized controlled studies: many of them fail to find any beneficial effect of whole-grains compared to refined grains.

So according to these randomized controlled studies whole-grains are neutral toward CHD risks. How then can we say that wheat causes CHD?

Are All Grains Created Equal?

Many randomized controlled studies compared wheat with other grains. These trials are usually quite short. So instead of looking at the number of heart attacks, short-term studies focus on risk predictors of CHD like weight gain or markers of inflammations. Apolipoprotein B (ApoB) level is another risk factor. It represents the number of LDL particles - often called “bad cholesterol”. It is now considered to be a better predictor than LDL-C - the amount of cholesterol contained in LDL particles. The lower the level of ApoB the lower is the risk of CHD.

Here are some results of these studies:

• a study concluded that a bread diet may promote fat synthesis/accumulation compared with a rice diet
• wheat increased BMI compared to flaxseed in a 12 months study
• wheat increased ApoB level by 5.4% compared to flaxseed in a 3 weeks study
• wheat increased ApoB level by 7.5% compared to flaxseed in a 3 months study
• wheat increased ApoB level by 0.05 g/L compared to flaxseed in a 12 months study
• oat decreased ApoB level by 13.7% while wheat had no significant effect in a 21 days study
• wheat increased the number of LDL particles by 14% while oat decreased them by 5% in a 12 weeks study
• ApoA to ApoB ratio (a risk predictor similar in efficiency to ApoB alone - here the higher the better) was increased by 4.7% for oat bran and 3.9% for rice bran compared to wheat bran in a 4 weeks study

These studies show that some grains like oat improve the risk factors of CHD compared to wheat. In addition, these studies often show an absolute improvement of the CHD risk profile in groups eating oat and an absolute deterioration in groups eating wheat. Although we cannot say for sure, it would suggest that oat is protective against CHD - which is confirmed by other studies - while wheat increase the risk of CHD.

That could help explaining why people eating more whole-grains are healthier in observational studies since it looks like that they eat more grains like rice and oat and less typically wheat-made food like white bread, pasta and doughnuts:
Data from Andersson A. et al., Intakes of whole grains, bran, and germ and the risk of coronary heart disease in men, 2007

Now let’s have a look at studies linking wheat and CHD.

Observational Studies on Wheat

Some observational studies linked wheat and waist circumference gains - waist circumference being a strong predictor of CHD:

• a study showed a correlation between consumption of white bread and waist circumference gains
• a study concluded that: ”reducing white bread, but not whole-grain bread consumption, within a Mediterranean-style food pattern setting is associated with lower gains in weight and abdominal fat”
• a Chinese study found that ”vegetable-rich food pattern was associated with higher risk of obesity” but as noted by obesity researcher Stephan Guyenet the association between obesity is in fact stronger with wheat flour than with vegetables

A more pertinent result is found in the data of a large observational study in China. Researchers analysed these data and found a 0.67 correlation between wheat flour intake and CHD. They also found a 0.58 correlation between wheat intake and BMI.

From Denise Minger
But this is just a single unadjusted correlation and does not prove much. However blogger Denise Minger thoroughly analysed the data of this study and found that the association held strongly after multivariate analysis with any other variable available like latitude, BMI, smoking habits, fish consumption, etc.

Since it is an observational study it cannot prove anything but it is yet another evidence suggesting that wheat consumption causes CHD. Let’s now have a look at randomized controlled trials.

Randomized Controlled Trials on Wheat

In addition to the previous randomized controlled trials comparing wheat with other grains there are two additional studies suggesting that wheat consumption causes CHD.

The first one is a study involving rabbits. While studies involving animals are not always relevant to humans - especially studies with herbivore animals like rabbit - the results of this study are quite interesting.

The researchers fed rabbits an atherogenesis diet (i.e. promoting formation of fatty masses in arterial walls) with a supplement of cottonseed oil, hydrogenated cottonseed oil, wheat germ or sucrose. And as they concludes:

Severity of atherosclerosis after 5 months was greatest on the wheat germ-supplemented diet, whereas there were no differences among the other three groups.

The second study is the Diet And Reinfarction Trial (DART). In this 2-year randomized controlled trial, people who already had recovered from an heart attack were split into groups receiving various advices. The main result of this study was that the group advised to eat fatty fish had a reduction in mortality from CHD.

One other advice - the fibre advice - was:

to eat at least six slices of wholemeal bread per day, or an equivalent amount of cereal fibre from a mixture of wholemeal bread, high-fibre breakfast cereals and wheat bran

Seeing this advice we can guess that most of cereal fibres intake by this group was from wheat although we cannot be sure.

This advice resulted on a 22% death increase:
From Stephan Guyenet
However this result bordered on statistical significance: the 95% confidence interval being 0.99–1.65.
For people not familiar with statistics, a result is usually defined as statistically significant when there is less than 5% chance that the result is due to luck alone. Here there is a 95% probability that the relative risk is between 0.99 (1% decreased chance of dying) and 1.67 (67% increased chance of dying).

Since the probability that the fibre advice resulted in a protective or neutral effect was a little too high, this result has been quite overlooked. Had the study last a little longer, it would have raised way more suspicion toward whole-grains.

In fact, researchers found this effect to be statistically significant in a follow-up study. After adjusting for pre-existing conditions and medication use, we can see in the table 4 of this study an hazard ratio of 1.35 (95% CI 1.02, 1.80) for the 2-year period of the randomized controlled trial.

These results are quite telling: according to these researchers, a 2 year randomized controlled trial showed that advising people recovering from an heart attack to eat at least six slices of wholemeal bread per day resulted in a statistically significant 35% percent chance increase of CHD compared to people not receiving this advice.

Wheat, Vitamin D Deficiency And Heart Disease

Many studies found that vitamin D deficiency is associated with CHD.
However vitamin D deficiency does not seem to cause heart disease. For example several studies found that vitamin D supplementation did not prevent heart disease.
As this study concludes:

A lower vitamin D status was possibly associated with higher risk of cardiovascular disease. As a whole, trials showed no statistically significant effect of vitamin D supplementation on cardiometabolic outcomes.

Wheat consumption causing CHD could help explaining these results. A study found that wheat consumption depletes vitamin D reserves. That could explain why vitamin D deficiency is associated with heart disease and why it does not seem to cause it: both vitamin D deficiency and heart disease could be consequences of wheat consumption.

Of course this is not the only explanation. For example the DART study shows that fish consumption prevents CHD and fish is a food rich in vitamin D.

Not the Perfect Culprit

To be clear, if it seems likely that wheat consumption is a risk factor of CHD it is not the only one nor the primary one. There are many other factors like smoking, hypertension, lack of exercice or stress. Even among dietary factors wheat is probably not the main one. For example the DART study shows that the protective effect of fish intake is stronger than the adverse effect of wheat.

In addition, deleterious wheat effects might not affect everybody. One study showed that the ApoB level variation following wheat and oat bran intake was different depending on the genotype of the individuals. In another study whole-wheat intake worsened the lipid profile only in people having a specific genotype compared to refined wheat.

How the wheat is cooked may have a role too. Studies show that sourdough bread improve mineral bioavailability (such as magnesium, iron, and zinc) compared to yeast bread or uncooked whole-wheat. Also content in proteins with potential adverse consequences like gluten or wheat germ agglutinin differs depending of the food type.

Conclusion

There are strong evidences that wheat consumption is a risk factor for CHD. People at risk of CHD should avoid wheat as should those trying to lose weight. In all cases, stopping wheat consumption for a month for example to see how one feel without wheat is always a good idea since there is currently no available method to diagnose non-celiac wheat sensitivities and that even for celiac disease the average delay in diagnostic is 11 years in the US.

More studies looking at the links between wheat and CHD are urgently needed since CHD is the leading cause of deaths while wheat is the second most widely consumed food and whole-wheat is often advised to lower risk of CHD. Studies considering grains as a whole are bound to give inconsistent results since different grains seem to have opposite effects in the case of CHD. So as much as possible future studies should treat grains separately and consider things like type of wheat products and genetic variability.

===============================================================
Read the complete article here or here.

Wake Up CALL

Wake-up call for sleep related CVD risk

 

Geneva, Switzerland - Those who sleep badly, and not for long, have a 65% increased risk of cardiovascular disease—and an even greater risk of coronary heart disease—compared with normal sleepers, according to new research presented at the EuroPRevent 2011 meeting this past weekend.

 

Researcher Marieke Hoevenaar-Blom (National Institute for Public Health and the Environment, Bilthoven, the Netherlands) explained that several investigations have found an increased risk of CVD in short sleepers compared with normal sleepers, but this is the first study to take into account whether people rise feeling rested. The results should help confirm that suboptimal sleep is a risk factor for cardiovascular disease, something she says is not widely appreciated in the cardiology community.

 

Hoevenaar-Blom, who is studying for a PhD in primary prevention of cardiovascular disease by lifestyle, reported her findings from 12 years of follow-up in a Dutch cohort during an oral session; she was nominated for a young investigator award for her research, which has also been accepted by the journal Sleep for publication [1].

 

"The message is that you have to assess sleep, and especially sleep quality, when you see a patient, because it might be a risk factor for cardiovascular diseases," Said Hoevenaar-Blom "When a patient is sleeping poorly, you can very easily fix that," she noted, although she acknowledged that this involves figuring out what is causing the sleep disturbance. However, simple advice—such as restricting intake of caffeinated drinks after a certain time and not watching TV late—can often be useful, she suggested.

 

Is sleep quality a modifying factor in association with CVD?

 

In the Monitoring Project on Risks Factors and Chronic Diseases in the Netherlands (MORGEN) study, Hoevenaar-Blom and her colleagues explored the combined associations of sleep duration and quality with CVD and CHD incidence.

The message is that you have to assess sleep, and especially sleep quality, when you see a patient, because it might be a risk factor for cardiovascular diseases.

Information on sleep duration and quality was obtained by a self-administered questionnaire filled in by 20 432 participants (9217 men and 11 215 women aged 20 to 65 years) between 1993 and 1997. Over 10 to 15 years of follow-up, data on morbidity and causes of death were obtained through linkage with several national registries.

 

Average sleep duration was assessed by asking participants how many hours of sleep they usually got in a 24-hour period. Short sleep duration was defined as six hours or less, while long sleep duration was sleeping for nine hours or more per 24-hour period. Sleeping for seven to eight hours was designated "normal." Sleep quality was assessed in the first two years of baseline measurements with the question, "Do you usually rise feeling rested?"

"Our research questions were: 'What is the association between sleep duration and cardiovascular disease and coronary heart disease? And is sleep quality a modifying factor in this association?' " Hoevenaar-Blom explained.

 

After 10 to 15 years of follow-up (mean 11.9 years), 1486 participants developed CVD, of whom 177 had a fatal event. After adjustment for multivariate confounders, short sleepers had a 15% higher risk of incident CVD compared with participants with normal sleep duration, a finding that was significant, and short sleepers had an even stronger, 23% higher risk of CHD compared with normal sleepers.

 

It's not just quantity, but quality, that is important

 

On its own, no association was found between sleep quality and CVD incidence, but when assessing quality in combination with sleep duration, short sleepers with poor-quality sleep had a 65% higher risk of CVD and an 85% higher risk of CHD than participants with a normal sleep duration and good sleep quality.

 

The investigators found no association between long sleep duration and CVD, a finding that contradicts previous studies, said Hoevenaar-Blom. She noted that there has never been any biological mechanism to explain why people who sleep longer have increased risk, but she hypothesized it could be due to reverse causality—that these people were perhaps ill in the first place and therefore slept longer.

 

Asked whether psychosocial stress could be contributing to poor sleep quality and short duration of sleep, she acknowledged that, of course, this was likely. "We do need more research," she observed.

 

"In conclusion, short sleepers have an increased risk of total CVD and CHD; the risk in short sleepers is the largest when they are not rising rested; it's really the combination" that is important, she said.

=============================================================================

Read the complete article here.

More Misinformation from the British Press - Smith

More Misinformation from the British Press

Friday, December 28, 2012 Justin Smith

 

Yesterday, an article was published on the front page of a national newspaper in the UK, claiming “proof that statins save millions” and “wonder pill halves heart attack deaths”.

The article was published in the Daily Express newspaper on 27 December 2012, written by Giles Sheldrick. I have formally complained to the editor about the gross inaccuracies the article contains.
The article is based on data published in a recent report from the British Heart Foundation (BHF). The title of this report is Coronary Heart Disease Statistics 2012.

The article in the Daily Express claims that the reduction in heart disease deaths / heart attacks is mostly due to cholesterol lowering statins.

The recent BHF publication (available here) does clearly show that deaths from heart disease have continued to fall, however, nowhere in this publication is there any data to support the claim that statins have played a significant part.

The BHF publication references only one study; a 2004 study referenced on pages 14 and 15 of the publication. This referenced study is freely available here:
http://circ.ahajournals.org/content/109/9/1101.long

It is absolutely clear from this study that the vast majority of the reduction in heart disease deaths was from the reduction in the number of people smoking and improvements in emergency treatments. It had very little to do with statin medications. In fact, if you look at Table 1 of this study, we can see that statins, at best, contributed less than one percent to the reduction in deaths.

The first line of the Daily Express article reads “THE use of statins has halved the number of deaths from heart attacks”. There is no data to support this statement anywhere in the BHF publication or the 2004 study referenced by the BHF.

There are a number of additional points to consider.

The graph below is from another publication from the British Heart Foundation (Coronary Heart Disease Statistics 2008, available here) . If we look at figure 1.4 from page 25, we can see that heart disease deaths have been reducing since the 1970s, but there is no significant change in the graph around 1995. This is important because statin medications first started to be widely prescribed in 1995. If statins were having a significant impact, we would of course expect to see a more dramatic reduction around 1995, but we do not. In fact, some age groups have seen a slowing down of the reduction since the widespread introduction of statins in 1995.

It is important to note that even if statins do very slightly reduce the risk of suffering a heart attack (typically less than one percent reduction in risk), at the same time, these medications increase the risk of dying from other serious diseases. This is particularly the case when statins are used for 'prevention'. All of the clinical trials, where statins have been used for 'prevention' have failed to show any increase in life expectancy. The potential very slight reduction in heart attack risk has always been off-set by an increase in deaths from other causes due to the statin.

Not to mention the fact that around 20 percent of people who take statins experience considerable adverse effects, which in many cases have ruined peoples' lives.
=====================================================================
Read the complete article here.

Track Your Plaque - Davis

Track Your Plaque

In addition to writing, speaking, and practicing preventive cardiology in Milwaukee, Wisconsin, Dr. Davis is the Medical Director and founder of the Track Your Plaque program for heart disease prevention and reversal. This program was described in the book, Track Your Plaque: The only heart disease prevention program that shows how to use the new heart scans to detect, track, and control coronary plaque, as well as the online program. Wheat elimination, along with the nutritional principles articulated in Wheat Belly, serve as the cornerstone of the heart disease prevention efforts used in the Track Your Plaque program, as well.

An Introductory video.

Low-Fat Diet a Dud for Women's Heart Disease - Jancin

Low-Fat Diet a Dud for Women's Heart Disease

By: BRUCE JANCIN, Clinical Endocrinology News Digital Network

ESTES PARK, COLO. – Perhaps the least-known finding of the landmark Women’s Health Initiative was the complete failure of a structured low-fat diet intervention to lower the risks of coronary heart disease, stroke, or colon cancer.

 

"This has gotten very little press. But the results made me very happy because it gave me one less thing to worry about, which is eating a low-fat diet. It doesn’t seem to have the same magnitude of effect in women as it does in men," Dr. Nanette Santoro said at a conference on internal medicine sponsored by the University of Colorado.

Dr. Nanette Santoro

The Women’s Health Initiative Randomized Controlled Dietary Modification Trial involved 48,835 postmenopausal women aged 50-79 at 40 U.S. centers who were randomized 40/60 to a low-fat diet intervention or a control group.

 

During a mean follow-up of 8.1 years, the diet intervention and control groups didn’t show any significant differences in rates of coronary heart disease (hazard ratio, 0.97); stroke (1.02); or cardiovascular disease (0.98) (JAMA 2006;295:655-66).

 

Similarly, the event-rate curves for cardiovascular outcomes as well as for colon cancer in the intervention and control arms were virtually identical the entire time, with no hint of either early or late benefit for the low-fat diet (JAMA 2006;295:643-54).

 

There was a nonsignificant trend for less invasive breast cancer in the low-fat diet group, where the annualized incidence rate was 0.42%, a 9% relative risk reduction compared with the 0.45% rate in controls (JAMA 2006;295:629-42).

 

"So if there’s any possible benefit to a low-fat diet, there might be some for breast cancer," commented Dr. Santoro, professor and chair of the department of ob.gyn. at the university.

The diet intervention entailed an intensive behavioral modification program with 18 group sessions during year 1 and quarterly maintenance sessions thereafter, with supplemental individualized contact. The goal was to reduce dietary fat intake by boosting consumption of fruits and vegetables to at least five servings daily, along with at least six servings of grains daily. Weight loss goals weren’t part of the study, which was designed in the 1990s before the obesity epidemic was apparent.

 

The intervention was effective in terms of accomplishing lasting dietary change. At baseline, fat accounted for about 38% of total daily energy intake. After 1 year, this figure dropped to 24% in the diet intervention arm. At year 6, fat accounted for 29% of daily energy intake in the diet group compared with 37% in controls, a difference Dr. Santoro called "huge" in light of the enormous number of participants and the women’s diverse ethnicities and backgrounds.

 

The intervention group averaged 3.6 servings per day of fruits and vegetables at baseline and 4.9 by year 6, compared with 3.8 in controls. Efforts to increase consumption of grains were unsuccessful, however. The intervention group averaged 4.7 servings per day at baseline and 4.3 at year 6, compared with 3.8 in controls.

 

The Women’s Health Initiative Randomized Controlled Dietary Modification Trial was funded by the National Heart, Lung, and Blood Institute. Dr. Santoro reported that she has a research grant from Bayer.

=========================================================

Read the full article here.

Genetic studies lay the foundations for anti-inflammatory drugs to prevent heart disease

Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies

Original Text

IL6R Genetics Consortium Emerging Risk Factors Collaboration

Summary

Background

Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling.

Methods

In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6.

Findings

The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4—38·2) and of interleukin 6 by 14·6% (10·7—18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9—9·1) and of fibrinogen by 1·0% (0·7—1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8—5·0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes.

Interpretation

Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease.

Funding

British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation.

==================================================================

View the article here.
See also this article in theheart.org.

Wheat Belly

Tom Naughton just reviewed the book Wheat Belly by Dr. William R. Davis cardiologist. See that review here.

I just received my Kindle e-book copy and will read it soon.

I stopped consuming wheat products about two years ago at the recommendation of Dr Davis for the treatment of lipid disorders (it has a dramatic effect on small LDL) )and heart disease. Since I have a history of CAD that has resulted in 6 heart attacks I am of course interested in finally doing something to reduce the progression of plaque growth. The only advice I have received previous to this is to reduce my serum cholesterol i.e. take a statin and eat a low fat diet. But in the process of doing that I had my first four heart attacks. I treated that 'risk factor' (cholesterol) over the course of many years and while doing so had my first 4 heart attacks. Clearly it was not attacking the disease, only a non-significant risk factor in my case.

I am now following the Track Your Plaque regimen of measuring plaque using a heart scan, advanced lipid testing (VAP NMR, Berkley) , treating lipid disorders shown to be correctable in clinical trials and observations, following the TYP diet and monitoring blood glucose levels. I have only been on board fully with this approach since Feb 2011 so it is a work in progress.

I first began learning about this approach to actually treat the disease rather than a single risk factor back in 2006 or so but it took my skeptical self a while to become convinced. After all it was not exactly Main Stream Medicine. Was it quackery or something more. It took a couple more heart attacks and the realization that MSM had not served me well other than to patch the damage but not to treat the disease, to push me over the edge. I began blogging some of what I was finding in early 2007 to, if you will, document and share my findings, and keep track of what I think is Credible Evidence leading me to where I am now.

The Kindle version of Wheat Belly is only ten bucks. It is not the whole answer, but it does, I think, point to what is a significant piece of the puzzle.

Thanks Tom for the review.

Enjoy eating saturated fat but preferably from grass-fed animals.

In an article taken from a talk given by Donald W. Miller, Jr., MD at the 29^th Annual Meeting of the Doctors for Disaster Preparedness in Albuquerque July 19, 2011, he stated

 "Enjoy eating saturated fat but preferably from grass-fed animals."

Read the full article here.

Krauss is in the HOUSE: 'Low-fat Message Was a MISTAKE'

"Everybody I know in the field -- e v e r y b o d y -- recognized that a simple low-fat message was a mistake," says Dr. Krauss, as interviewed in the latest Men's Health magazine, see below. Why is Men's Health interviewing Krauss?! What is this revolutionary MH reporter saying? Don't. S-W-A-L-L-O-W . . . ! ? ? *haa!!* Men's Health, Your Unstoppable Heart: Before you swallow what your doctor prescribes, we suggest you read this article By: Paul Scott CHOLESTEROL IS A NATURAL SUBSTANCE your body produces for a variety of uses. It is carried through the body in three containers -- LDL, HDL, and VLDL -- that deliver it to cells along with triglycerides. The average man reasons that the cholesterol in his scrambled eggs must surely end up in his arteries somehow, and this makes him do things like order egg-white omelets for breakfast. There is indeed a link between the cholesterol you eat and the cholesterol in your arteries. It's just not the "eat more, have more" worry that's been drummed into you for years. In fact, your body's production and uptake of cholesterol is highly regulated; eat a six-egg omelet and your body simply produces less cholesterol because of the dietary onslaught. "There is a very weak connection between the LDL cholesterol we measure and dietary cholesterol," Dr. Krauss says. "I spend a lot of time talking to reporters and trying to explain that dietary cholesterol is not the same as blood cholesterol." He adds that the 200 milligrams of cholesterol most people eat every day is NOTHING compared with the 800 milligrams their bodies produce [my EMPHASIS]. But you don't have to take his word for it. "It is now acknowledged that the original studies purporting to show a linear relation between cholesterol intake and coronary heart disease may have contained fundamental study design flaws," wrote the author of a recent review in the International Journal of Clinical Practice. [ HERE . Jones PJ citing Hu et al] The author suggests to lower small dense LDL, the actual heart disease culprit Targeting the Killer LDL Small changes, fewer small particles "Small, dense particles of LDL are much more inflammatory than larger particles," says Paul Ziajka, M.D., Ph.D., a clinical lipidologist with the Southeast Lipid Association. Here's how to snuff the little devils. Crack an egg Down an omelet every morning and you may lower your small-particle count, University of Connecticut researchers recently found. People who ate three whole eggs a day for 12 weeks dropped their small-LDL levels by an average of 18 percent. Choose your meds wisely A class of drugs known as fibrates, which includes Tricor, specifically targets small, dense LDL, says Dr. Ziajka. The effect is significant only when your triglycerides are also elevated, he says. [Note: no statin mentioned...*haa*; actually low carb, sat fats and fish oil omega-3 work far FAR better than fibrates, PPAR drugs] Pop some niacin "Most drugs shift particle size after the cholesterol is made," Dr. Ziajka says. "Niacin causes the liver to produce larger particles." Try a no-flush variety (Dr. Ziajka recommends Slo-Niacin) starting with 500 milligrams a day and building to 2,000. There are side effects, so talk to your doctor first. [Note: no-flush doesn't work; slo-niacin is a lower-flush type of niacin] Lighten your load Deflating your spare tire may reduce your small, dense LDL cholesterol, say scientists at Children's Hospital Oakland Research Institute. The majority of overweight men who were pattern B (mostly small LDL) switched to pattern A (mostly large LDL) after they lost an average of 19 pounds. Have a glass That nightly beer does more than relax you -- it may also lower your small, dense LDL, a recent Journal of Clinical Endocrinology Metabolism study found. Men who drank 7 to 13 alcoholic drinks a week had 20 percent fewer small-LDL particles than men who didn't drink at all. [Note: beer aint paleo] Previous animal pharm: Men's Health interview with Mozzafarian MD on benefits of dietary saturated fats Read more about Krauss et al's newest research that redeems the role of saturated fats at my fave peeps and playgrounds: Tourgeman, holymoly ur so funny Nephropal Seth Roberts my Berkeley bud... Animal Fat Peter Hyperlipid Stephan WholeHealthSource Don Primal Wisdom Chris Masterjohn Daily Lipid Dr. Mike Eades THANKGODFORYOURSANENESS

Statin Drugs linked to rise in Diabetes

from Mercola.com

By Suzy Cohen, R.Ph.

Coronary heart disease is a leading cause of death in the United States, killing one in five adults, and doctors are very quick to prescribe statins. In fact, statin drug sales rank in the billions each year globally.

These drugs are so pervasive that they are no longer just indicated for hypercholesterolemia, they are also being prescribed for elevations in C reactive protein, and are promoted for kids as young as eight years old.

Heart disease is so pervasive that some have boldly suggested that we should put statins in our water supply as some kind of protection.

This is very disturbing.

Do You Really Need a Statin Drug?

By far, statin drugs are the most popular cholesterol-lowering drugs available today. They work in your liver by preventing your body from making cholesterol. The drugs block an enzyme called HMG-CoA Reductase. This can be helpful, but only if you are one of those people who happen to produce too much cholesterol.
It doesn’t do a good job at removing it from your clogged arteries, contrary to what most people think.
Physicians and health experts now agree that statins seem to offer more benefit through their ability to reduce dangerous inflammatory chemicals in your body, rather than by reducing production of cholesterol, which usually leads to uncomfortable, unwanted and dangerous side effects. One study found that lowering cholesterol too much actually backfires.
Cholesterol is good for you; it’s one of your body’s most powerful antioxidants, it makes important neurotransmitters and sex hormones so this madness to lower it as much as possible really concerns me. Plus, I believe the indiscriminate use of statins has contributed to the staggering rise in diabetes…

The Statin—Diabetes Connection Few People Know About

I watched this happen to my mom who was given a statin, and then told months later she suddenly had diabetes. All of a sudden? This happened many years ago, and it began my search to understand the connection. It also prompted me to write a book on the subject entitled “Diabetes Without Drugs” (Rodale, 2010).
It typically happens like this:
Many statin users come back to see their physician for a routine visit and after the blood work is drawn, they find their cholesterol ratios may be improved, but now they have high blood glucose.
It’s entirely possible that some physicians then mistakenly diagnose their patients with “Type 2 diabetes” when in fact they just have hyperglycemia—a side effect, and the result of a medication that was prescribed to them months earlier.
Do you think you have type 2 diabetes?
I will provide more information so you can see for yourself that so-called “diabetes” diagnosis might not really be genuine diabetes. It may just be hyperglycemia (high blood sugar)—the result of your cholesterol medication, and for some people, it may be reversible with drug discontinuation. Whether or not you are able to discontinue your medication is between you and your physician.

Research Suggesting Raised Blood Sugar is a Side Effect of Statin Use

Several studies have indicated that statins can cause high blood sugar, which can be mistaken for “diabetes.” For example, researchers in Glasgow, Scotland conducted a meta analysis, known as the JUPITER trial, which took into account 13 statin trials that each included 1,000 patients or more. The participants were followed for over than a year. The conclusion was there was indeed an increase, albeit small, in the development of Type 2 diabetes.
It should be considered that some of the patients in this meta analysis already had symptoms of insulin resistance or metabolic syndrome, so it could be said that they were on their way to diabetes anyway.
Now consider another meta-analysis published in the Lancet Here, the researchers reviewed randomized controlled trials beginning in 1994 and ending in 2009, for a total of 91,140 participants who took either a statin or a placebo.
They found that people treated with statin drugs showed a nine percent increase for diabetes. They did not evaluate other factors however, which would be considered pre-diabetes, so I suspect their nine percent number to be on the low side.
Insulin is a pancreatic hormone that reduces blood sugar. You want some insulin to maintain blood glucose levels, but too much of it is bad—it’s an inflammatory compound in your body when it is elevated. And guess what? The use of statin drugs appears to INCREASE your insulin levels! High insulin is extremely harmful to your health.
For starters, elevated insulin levels lead to heart disease, and isn’t that the reason cholesterol drugs are prescribed in the first place?
The ratio of glucose to insulin should be less than 10:1, this ratio is far more important than the levels of glucose or insulin alone. Keep that in mind if you seek a complete recovery. For more information about the harmful effects of elevated insulin levels, see my article on dearpharmacist.com, or my book Diabetes Without Drugs.
You want to keep insulin normal, to protect yourself from heart disease and high blood pressure. Chronically elevated insulin causes a cascade of inflammatory chemicals and high cortisol which lead to belly fat, high blood pressure, heart attacks, chronic fatigue, thyroid disruption, plus major diseases like Parkinson’s, Alzheimer’s and cancer.
Unfortunately, the most popular cholesterol drugs in the world seem to increase insulin levels. However, that’s just one mechanism by which these drugs can raise your risk for diabetes.

How Statins Raise Your Insulin

Keeping things simple, you might imagine it like this: When you eat a meal that contains starches and sugar, some of the excess sugar goes to your liver, which then stores it away as cholesterol and triglycerides. Now stay with me — when you have a statin on board, it’s like a message to your liver saying, “No! Don’t make any more cholesterol, please stop.”
So your liver sends the sugar back OUT to your bloodstream. As a result, your blood sugar goes up.
In 2009, it was proven that statins could directly raise blood sugar, whether or not you have diabetes. Over 340,000 people were included before this conclusion was made. The people who did not have diabetes but took statins experienced a rise in blood glucose from 98 mg/dl to 105 mg/dl. Those who already had diabetes and also took statins experienced a rise from 102 mg/dl to 141 mg/dl.
After adjustments for age and medication use were considered, researchers concluded that both diabetic and non-diabetic statin users showed a statistically significant rise in blood sugar.
Why take all these risks, just to get the convenience of taking a pill instead of eating a better diet and exercising?
It’s been scientifically discussed and even published in JAMA that eating a better diet could lower cholesterol as well as the statin drug lovastatin.
And of course, there are so many other benefits to eating a healthier diet that consists of fruits, vegetables, nuts, seeds, and lean meats. Besides feeling better and increasing lifespan, you can squeeze into those skinny jeans you’re hiding in your closet.
Another way statins can affect your blood sugar is via their “drug mugging” effect. A drug mugger is my term, and the title of my newest book, which describes how a drug can rob your body’s warehouse of a valuable nutrient. In the case of statins, they rob your body of two different nutrients, both of which are needed to maintain ideal blood sugar.

Two Important Nutrients Decimated by Statins

The first nutrient that is mugged is vitamin D. There have been mixed studies regarding the D-depletion effect of statins, but statins reduce your body’s natural ability to create active vitamin D called 1,25-dihydroxycholecalciferol, shortened to “calcitriol” when it is eventually converted to its active hormone form.
This happens because statins reduce cholesterol, and you need cholesterol to make vitamin D! It is the raw material that exposure to UVB from sunlight will convert to vitamin D.
It is well documented that D improves insulin resistance, so needless to say, when you take a drug mugger of vitamin D (like statins), then you increase your risk for diabetes.
More specifically, a 2004 study published in the American Journal of Clinical Nutrition determined that raising a person’s serum vitamin D levels (from 25 to 75 nmol/l) could improve insulin sensitivity by a whopping 60 percent.
Compare that to the blockbuster diabetes drug metformin, one of our pharmaceutical gold-standards, which can dispose of blood sugar by a meager 13 percent according to the New England Journal of Medicine.
Now, statins also suppresses your natural coenzyme Q10— also called “ubiquinol” in its active form; it makes energy for every cell in your body, and it’s produced mainly in your liver.
This powerful antioxidant just so happens to also play a role in maintaining blood glucose. When you deplete levels of CoQ10 by taking a drug mugger of it, like a statin drug, then you lose that benefit. You also raise your risk for heart failure, high blood pressure and heart disease as CoQ10 deficiencies can contribute to those conditions. A study by Hodgson et al, published in 2002 found that 200mg CoQ10 taken daily caused a 0.4 percent reduction in hemoglobin A1c.
Moreover, CoQ10 protects your body from oxidative stress, a strong contributing factor in the development of diabetes, metabolic syndrome and heart attacks. You want to make sure you have enough CoQ10 (or ubiquinol) on board to protect every cell in your body. The take home point is that statins annihilate this compound and you need it for good health.
In summary, if you take a statin medication and you’ve been told that you have diabetes, it may be drug-induced, and it’s possible that it can be reversed over the course of time. However, you will have to eat right, exercise, and take supplements that help to lower your risk for heart disease naturally.
About the Author
Suzy Cohen, R.Ph., has been a licensed pharmacist for 22 years, and has had a weekly syndicated health column for the past 13 years which you can get for free by signing up at her website Widely recognized as “America’s most trusted pharmacist,” she has appeared on The Dr OZ Show, The View, Good Morning America Health and The 700 Club.
Cohen is also the author of three books: The 24-Hour Pharmacist, Diabetes Without Drugs, and Drug Muggers: Keep Your Medicine from Stealing the Life Out of You.
For more information, see www.SuzyCohen.com.

Sources:
Journal of the Federation of American Societies for Experimental Biology May 1, 2004; 18(7): 805-815
Journal of Investigative Medicine March 2009; 57(3): 495-499
About.com February 20, 2010
The Lancet February 2010; 375(9716): 735 – 742
The Lancet February 27, 2010; 375(9716): 700 – 701
Reuters March 10, 2011
International Journal of Obesity February 8, 2011 [Epub ahed of print]
American Heart Journal (ENHANCE trial) February 2005; 149(2): 234-239
Lancet February 27, 2010; 375(9716): 735-42
Journal of Investigative Medicine March 2009; 57(3): 495-499
JAMA 2003;290(4):502-510
=====================================
Read article with comments here  http://articles.mercola.com/sites/articles/archive/2011/03/28/the-stealth-drug-cause-of-diabetes.aspx

New study adds to the growing evidence that cholesterol reduction has dubious benefits for health

Dr. Briffa's 'A Good Look at Good Health', which I subscribe to and follow, has a good article about the growing evidence against low cholesterol and use of statin drugs.

========================================
New study adds to the growing evidence that cholesterol reduction has dubious benefits for health


Posted By John Briffa On 28 January 2011 @ 2:40 pm In Cholesterol and Statins

Statins reduce cholesterol-levels and have the ability to reduce heart disease risk. However, some researchers have asked if the primary mode of action of statins is cholesterol reduction. After all, statins have several effects in the body which might reduce the risk of heart disease in ways that have essentially nothing to do with cholesterol. For example, statins enhance nitric oxide production (this helps dilate blood vessels), have anti-inflammatory effects (see below), and also have the ability to reduce clotting in the blood (e.g. reduced fibrinogen levels and inhibition of platelet adhesion and aggregation).
Today saw the publication of a study which reinforced this idea. It involved the treatment of individuals deemed to be at high risk of cardiovascular disease with a statin (simvastatin) or placebo [1]. This research was designed to assess whether the effect of statin therapy was in any way influenced by levels of a substance known as C-reactive protein (CRP) in the body. CRP is a marker of inflammation, and inflammation is a key underlying process in heart disease. Statins are anti-inflammatory. Could it be, therefore, that statins work between in individuals with raised CRP levels. In short, this study found that risk reduction was essentially the same across different levels of CRP. In other words, in the study, CRP levels did not appear to help identify individuals who might benefit most from statin therapy.
But an interesting finding from this study, I think, is the fact that statin therapy appeared to reduce cardiovascular events (such as heart attack and stroke) in individuals with low LDL-cholesterol (supposedly ‘unhealthy’) levels. Now, low levels of cholesterol are not a risk factor for cardiovascular disease. So, if statins broadly help individuals with low LDL levels, that does suggest their main mode or modes of action here do not relate to cholesterol reduction.
This is not, however, the first time research has found statins reduce cardiovascular disease risk in individuals with ‘normal’ or even ‘low’ cholesterol levels [2]. It is also interesting to note that statins substantially reduce the risk of stroke, despite the fact that raised cholesterol levels are a weak or non-existent risk factor for stroke [3,4]. Also, more intensive cholesterol reduction does not necessarily lead to improved outcomes [5].
All of this also calls into question the wisdom of cholesterol reduction generally. If cholesterol reduction does indeed have broad benefits for health, we would expect to see positive effects from cholesterol-reducing strategies in terms of risk of total mortality. However, in a meta-analysis (pooling together of several similar studies) of a variety of cholesterol-reducing strategies including drug treatments [6], neither fibrates nor resins (two forms of cholesterol-reducing drugs) were found to reduce overall mortality. In fact, in this meta-analysis, other than statins, no cholesterol-reducing strategy analysed was found to reduce overall mortality.

Some argue that other cholesterol-reducing strategies fail to reduce cholesterol enough compared to statins. However, in this meta-analysis statin therapy was found to reduce cholesterol by 20 per cent on average, and this was associated with reduced mortality. This level of cholesterol reduction was matched by resin therapy in those with a prior history of cardiovascular disease, yet there was no reduction in overall mortality here.

In 2002, a new type of cholesterol-reducing drug – ezetimibe – was licensed for use. The basis for this decision was ezetimibe’s proven cholesterol-reducing effect. However, to date, no studies have been published which show that this agent has the capacity to reduce CVD risk or mortality.

Moreover, one trial found that treatment with ezetimibe actually increased thickening in the wall of the arteries (carotid artery intima thickness). Most importantly, ezetimibe use was associated with five times the risk of cardiovascular events (e.g. heart attacks, stroke) compared to another treatment (niacin – a form of vitamin B3) [7]. Such findings clearly call into question the view that cholesterol reduction, through whatever means, is beneficial to cardiovascular and general health.

The reason that this is important is because that we are generally encouraged to drive our cholesterol levels to ever-lower levels, and there is good evidence which questions the fundamental assumptions on which this approach is based. Research suggests that cholesterol reduction, per se, does not have broad benefits for health. Though I do admit the drugs companies and the researchers in their pay have done a generally very good job of persuading us otherwise.
References:


1. Heart Protection Study Collaborative Group. C-reactive protein concentration and the vascular benefits of statin therapy: an analysis of 20 536 patients in the Heart Protection Study. The Lancet, Early Online Publication, 28 January 2011


2. Ridker PM, et al, JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359(21):2195-2207

3. Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration. Lancet 1995;346(8991-8992):1647-53.

4. Imamura T, et al. LDL cholesterol and the development of stroke subtypes and coronary heart disease in a general Japanese population: the Hisayama study. Stroke 2009;40(2):382-8
5. Kastelein JJ, et al, ENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med 2008;358(14):1431-1443
6. Studer M, et al. Effect of different antilipidemic agents and diets on mortality: a systematic review. Arch Intern Med 2005;165(7):725-30
7. Taylor AJ, et al. Extended-Release Niacin or Ezetimibe and Carotid Intima–Media Thickness. N Engl J Med 2009; 361:2113-2122]

--------------------------------------------------------------------------------

Cost of cardiovascular disease to triple by 2030

Exerpts of an article from Prevention's The Heart.org. I do not know too much about Prevention' position on heart disease relative to mine (which should be quite obvious if you have read much of what I post here on Credible Evidence), but I thought there was some interesting observations made by Michael O'Riordan.

Please avail yourself of the link to the full article and their site for further insite from their perspective.

=========================================================



Cost of cardiovascular disease to triple by 2030


January 25, 2011
Michael O'Riordan

Dallas, TX - In the next 20 years, more than 40% of the US population is expected to have some form of cardiovascular disease, and this will triple the total direct medical costs of caring for hypertension, coronary heart disease, heart failure, stroke, and other forms of cardiovascular disease from the current $273 billion to more than $800 billion, according to a new policy statement from the American Heart Association (AHA) [1].

In addition, the AHA estimates that the prevalence of cardiovascular disease will increase by approximately 10% over the next 20 years given no changes to prevention and treatment trends. If some risk factors, such as diabetes and obesity, continue to increase rapidly, cardiovascular disease prevalence and associated costs might increase even more, write Dr Paul Heidenreich (Veteran Affairs Palo Alto Health Care System, CA) and colleagues in the report, published online January 24, 2011 in Circulation.

At present, cardiovascular disease is the leading cause of death in the US and accounts for 17% of overall healthcare expenditures. In the past, the medical costs of cardiovascular disease increased at an average annual rate of 6%, and this growth in costs has been associated with an increase in life expectancy. That said, there are "many opportunities to further improve cardiovascular health while controlling costs," according to the AHA.

Cardiovascular disease is largely preventable (emphasis by Bill Davis)

The latest 2030 prevalence estimates for hypertension, coronary heart disease, heart failure, and stroke are derived from the 1999-2006 National Health and Nutrition Examination Survey (NHANES) and Census Bureau population estimates for the years 2010 to 2030. Projections of the medical costs associated with cardiovascular disease used the 2001-2005 Medical Expenditure Panel Survey (MEPS) and did not double count expenditures resulting from individuals with multiple conditions.

By 2030, the prevalence of cardiovascular disease is expected to increase 9.9%, with the prevalence of heart failure and stroke increasing approximately 25%. Total direct costs will increase to $818 billion by 2030, according to the AHA estimates, and the total indirect cost to the US in terms of lost productivity is close to $275 billion.
.
.
.
.
.
Offering up a glass-half-full take on the data, Heidenreich and colleagues write that it is "fortunate that cardiovascular disease is largely preventable,"(emphasis by Bill Davis) and the healthcare system needs to focus on prevention and early intervention.
.
.
.


Jan 25, 2011 15:30 EST Source

1.Heidenreich PA, Trogdon JG, Khavjou OA, et al. Forecasting the future of cardiovascular disease in the United States. Circulation 2011; DOI:10.1161/CIR.0b013e31820a55f5. Available at: http://circ.ahajournals.org.