Why I won’t take statins for my high cholesterol - Julianne

Why I won’t take statins for my high cholesterol

In Summary, for those who took the statin for 5 years (with known heart disease):

Benefits in NNT

• 1 in 83 were helped (life saved)
• 1 in 39 were helped (preventing non-fatal heart attack)
• 1 in 125 were helped (preventing stroke)

Harms in NNH

• 1 in 100 were harmed (develop diabetes*)
• 1 in 10 were harmed (muscle damage)

If you have had a heart attack and change your diet to a Mediterranean diet – you will get far more benefit than Statin drugs:

In Summary, for those who adhered to the Mediterranean diet:

Benefits in NNT

• 1 in 18 were helped (preventing repeat heart attack)
• 1 in 30 were helped (preventing death)
• 1 in 30 were helped (preventing cancer)

Harms in NNH

• None were harmed

 

 

And if you want to prevent heart disease the Mediterranean diet is also far more effective than statin drugs:

 

In Summary, for those who ate the Mediterranean diet:

Benefits in NNT

• 1 in 61 were helped (avoiding a stroke, heart attack, or death)

Harms in NNH

• None were harmed (diet effects)

Read the full article here.

How much longer will you live if you take a statin?

"Looking at the Heart Protection Study (HPS) done in the UK, we used a technique for analysing survival time called RMST (restricted mean survival time). I won’t go into the details. The HPS study lasted for five years, and we calculated that the average increase in survival time was 15.6 days. This was at the end of five years of treatment (with a confidence interval of 5 days either side). For 4S, the figure was 17 days."

"Framing this slightly differently, what this meant was that taking a statin for one year, in the highest risk group possible, would increase your life expectancy by around three days."

"However, more recently the BMJ did decided to publish another paper entitled: ‘The effect of statins on average survival in randomised trials, an analysis of end point postponement.’

Results: 6 studies for primary prevention and 5 for secondary prevention with a follow-up between 2.0 and 6.1 years were identified. Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials. The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively."

Conclusions: Statin treatment results in a surprisingly small average gain in overall survival within the trials’ running time. For patients whose life expectancy is limited or who have adverse effects of treatment, withholding statin therapy should be considered

Overall their findings were far less impressive, even, than ours. They calculated, approximately, a single day of increase in life expectancy for each year of taking a statin. Slightly more in secondary prevention, slightly less in primary (people who have not previously had a heart attack or a stroke).

The main take away message I believe, is the following. Statins do not prevent fatal heart attacks and strokes. They can only delay them. They delay them by about one or two days per year of treatment. For those who have read my books you will know that I have regularly suggested we get rid of the concept of ‘preventative medicine’. We need to replace it with the concept of ‘delayative medicine’.

Read Dr. Kendrick's complete article here.

The Cholesterol Myths - Ravnskov

Did you know. . . 

        

. . . that cholesterol is not a deadly poison, but a substance vital to the cells of all mammals? 

               

. . . that your body produces three to four times more cholesterol than you eat? 

                

. . . that this production increases when you eat only small amounts of cholesterol and decreases when you eat large amounts? 

                

. . . that the  “prudent” diet, low in saturated fat and cholesterol, cannot lower your cholesterol more than a small percentage? 

                

. . . that the only effective way to lower cholesterol is with drugs? 

                

. . . that the cholesterol-lowering drugs are dangerous to your health and may shorten your life?

                 

. . . that the cholesterol-lowering drugs, called statins, do lower heart-disease mortality a little, but this is because of effects other than cholesterol lowering? Unfortunately, they also stimulate cancer. 

                

…that you may become aggressive or suicidal if you lower your cholesterol too much? 

                

…that polyunsaturated fatty acids, those which are claimed to prevent heart attacks, stimulate infections and cancer in rats? 

                

…that if you eat too much polyunsaturated oil you will age faster than normal? You will see this on the outside as wrinkled skin. You can’t see the effects of premature aging on the inside of your body, but you will certainly feel them. 

                

…that people whose blood cholesterol is low  become just as atherosclerotic as people whose cholesterol is high? 

        

…that more than thirty studies of more than 150,000 individuals have shown that people who have had a heart attack haven’t eaten more saturated fat or less polyunsaturated oil than other people? 

                

…that old people with high cholesterol live longer than old people with low cholesterol? 

                

…that high cholesterol protects against infections? 

                

…that many of these facts have been presented in scientific journals and books for decades but proponents of the diet-heart hypothesis never tell them to the public? 

                

…that the diet-heart idea and the cholesterol campaign create immense prosperity for researchers, doctors, drug producers and the food industry?

"Dr. Ravnskovs contention is that the diet-heart idea is built on sand. He leads us through the history of the concept in an interesting and readable way. His writing clearly demonstrates the enormous depth and range of his reading on this subject. Step by step he examines the evidence for the diet-heart idea, and step by step he shows us how that evidence may be flawed and contradicted by other research that is rarely acknowledged and quoted."

 ~ Michael Gurr, PhD

Terrific response to Uffe Ravnskov's offer to view “The Cholesterol Myths” at  http://www.ravnskov.nu/CM 
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Read the complete article here.

Niacin is/was/will always be the Good One - Penberthy

Laropiprant is the Bad One; Niacin is/was/will always be the Good One

by W. Todd Penberthy, PhD

(OMNS July 25, 2014) Niacin has been used for over 60 years in tens of thousands of patients with tremendously favorable therapeutic benefit (Carlson 2005). In the first-person NY Times best seller, "8 Weeks to a Cure for Cholesterol," the author describes his journey from being a walking heart attack time bomb to a becoming a healthy individual. He hails high-dose niacin as the one treatment that did more to correct his poor lipid profile than any other (Kowalski 2001). Many clinical studies have shown that high doses of niacin (3,000-5,000 mg plain old immediate release niacin taken in divided doses spread out over the course of a day) cause dramatic reductions in total mortality in patients that experienced previous strokes (Creider 2012). High dose niacin has also been clinically proven to provide positive transformational relief to many schizophrenics in studies involving administration of immediate release niacin in multi-thousand-milligram quantities to greater than 10,000 patients (Hoffer 1964; Osmond 1962). Most importantly, after 60 years of use the safety profile for niacin (especially immediate release niacin) remains far safer than the safest drug (Guyton 2007).

Bad Reporting

So why has the media suddenly presented the following niacin alarmist headlines in response to the most recent study in the New England Journal of Medicine?

"Niacin drug causes serious side effects, study says" - Boston Globe, 7/16/14

"Niacin safety, effectiveness questioned in new heart study" - Healthday News, 7/17/14

"Doctors say cholesterol drug risky to take" - Times Daily, 7/16/14

"Niacin risks may present health risks claim scientists" - Viral Global News, 7/17/14

"Studies reveal new niacin risks" - Drug Discovery and Development, 7/17/14

"No love for niacin" - Medpage Today, 7/17/14

"Niacin could be more harmful than helpful" - Telemanagement, 7/18/14

The truth of the matter is that the study quoted and used laropiprant (trade names: Cordaptive and Tredaptive). Laropiprant is a questionable drug and the results say next to nothing about niacin. The study compared over 25,000 patients treated with either niacin along with laropiprant, or placebo. The patients in this study had previous history of myocardial infarction, cerebrovascular disease, peripheral arterial disease, or diabetes mellitus with evidence of symptomatic coronary disease. The side effects observed in those who took the laropiprant-niacin combination were serious and included an increase in total mortality as well as significant increases in the risk for developing diabetes.

For responsible reporters, this should have raised the question of which compound, the drug laropiprant, or the vitamin niacin, is the culprit.

Such side effects have not been seen in over 10 major clinical trials of niacin involving tens of thousands of patients, not in over 60 years of regular usage of niacin in clinics across the country. However, niacin causes a warm flush on the skin. Some people find the warm niacin flush uncomfortable, although many people enjoy this temporary sensation. In this study, niacin was given in combination with laropiprant, a drug that prevents the niacin flush. By including a dose of laropiprant along with the niacin to eliminate the flush, the thought was that more patients could benefit from niacin without complaint. But in fact the niacin flush is healthy. A reduced flush response to niacin is a diagnostic for increased incidence of schizophrenia, and this assay is now widely available (Horrobin 1980; Messamore, 2003; Liu 2007; Smesny, 2007).

Problems with Laropiprant

So what about the other half of the combo, the drug laropiprant?

• Laropiprant has never been approved by the FDA for use in the USA and when taken alone has been shown to increase gastrointestinal bleeding. *
• Laropiprant interferes with a basic prostaglandin receptor pathway that is important for good health.
• Last year Merck announced it would withdraw laropiprant worldwide due to complaints from continental Europe. Therefore the clinical trials in this most recent study could only be performed in the UK, Scandinavia, and China.

So why did so many media outlets and even some MDs conclude that niacin was the problem? Simple: none of the headlines mentioned laropiprant, which is quite clearly the real culprit that caused the side effects reported. The simplest way to put it is to say that sensational stories promulgated by the media are quite often completely wrong. This suggests a hidden agenda.

Confusing and fantastical headlines can increase readership for hysteria-based business models. Which headline is likely to garner the greatest attention: "Laropiprant is a Dangerous Medication that has Not Been Approved by the FDA" or "Niacin Causes Serious Side Effects"? The correct headline would be, "Niacin doesn't cause serious side effects; drugs do."

Why the B Vitamins Are So Important

The B vitamins were discovered due to terrible nutritional epidemics: pellagra (niacin/vitamin B3 deficiency) and beriberi (thiamine/vitamin B1 deficiency). We are very sensitive to a deficiency of niacin. Over 100,000 people died in the American south in the first two decades of the 20th century due to a lack of niacin in their diet. It was perhaps the worst nutritional epidemic ever observed in modern times, and was a ghastly testimony to how vulnerable the human animal is to niacin deficiency. The pellagra and beriberi epidemics took off shortly after the introduction of processed foods such as white rice and white flour. Poor diets, mental and physical stresses, and certain disease conditions have all been proven to actively deplete nicotinamide adenine dinucleotide (NAD) levels, causing patients to respond favorably to greater than average niacin dosing.

How is it possible that niacin can be useful for many different conditions? It seems too good to be true. The reason is that niacin is necessary for more biochemical reactions than any other vitamin-derived molecule: over 450 different gene-encoded enzymatic reactions (UniproKB database of the Swiss Institute of Bioinformatics; (Penberthy 2013)). That is more reactions than any other vitamin-derived co-factor! Niacin is involved in just about every major biochemical pathway. Some individuals, who have a genetically encoded amino acid polymorphism within the NAD binding domain of an enzyme protein, will have a lower binding affinity for NAD that can only be treated by administering higher amounts of niacin to make the amount of NAD required for normal health. Genetic differences such as these are why many individuals require higher amounts of niacin in order for their enzymes to function correctly (Ames 2002).

It is a deadly shame that the media so often ignores this information. Fortunately, many physicians will see through the recent headlines that give misinformation about niacin, having already personally witnessed how effective high dose niacin therapy is for preventing cardiovascular disease.

Nutrients are the Solution, Not the Problem

So what is the solution? At the end of the day the data on patients with problem cholesterol/LDL levels still support 3,000-5,000 milligrams of immediate-release niacin as the best clinically-proven approach to maintaining a healthy lipid profile. Niacin in 250mg to 1000mg doses can be purchased inexpensively from many sources. Extended-release niacin is the form of niacin that is most frequently sold by prescription, but it has more side effects than immediate release (plain old) niacin. . . and it costs much more.

Tangential to niacin but pointed to cardiovascular disease, conventional medicine is finally beginning to respect chelation therapy as an approach owing to the recent unparalleled positive clinical results for cardiovascular disease patients with diabetes - up to 50% prevention of recurrent heart attacks and 43% reduction in death rate from all causes (Avila 2014). Some times chelation therapy can be expensive. However, there are other inexpensive approaches include high dose IP6 therapy that are yet to be conventionally appreciated. Other supplements desirable for any ideal cardiovascular disease: a nutritional regimen include additional vitamin C, magnesium, coenzyme Q, fat soluble vitamins (A, D, E, and K2), and grass-fed organic butter. Your ideal intake varies with your individuality.

Nutrients such as niacin you need. Media misinformation you don't.

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Read the complete article here.

FDA Approves Dangerous and Worthless Cholesterol Drug - Brownstein

FDA Approves Dangerous and Worthless Cholesterol Drug

by Dr. David Brownstein

On May 3, 2013, the FDA approved a Big Pharma Cartel founding member Merck drug Liptruzet.  Liptruzet is a combination drug of Zetia and Lipitor.  I wrote to you about the failure of Zetia in three separate blog posts.  They can all be found by clicking here:  http://blog.drbrownstein.com/?s=zetia.
Zetia is a failed drug.  It should never be prescribed and should have been pulled from the market years ago.  There is no excuse for any doctor prescribing Zetia for any condition.  Zetia works by blocking cholesterol absorption in the gut.  Conventional doctors believe that drug therapies that lower cholesterol levels reduce the risk of heart disease.  However, Zetia, which has been around for over 10 years, has never been shown to lower the risk of developing a heart attack or stroke.  Furthermore, Zetia has never been shown to prolong life.

Why the FDA would approve this combination of Zetia and Lipitor is beyond belief.  The previous combination of Zetia and Zocor, known as Vytorin, was proven to be a colossal failure in multiple studies—see my previous blog posts.

FDA’s action is a perfect example of why we spend more money on health care than any other people on the planet.  Liptruzet will cost $5.50 per pill.  This means a patient prescribed Liptruzet will spend over $2,000.00 per year on a worthless drug that will be associated with side effects such as muscle aches and pains, memory loss, and neurological disorders.  We take too many ineffective drugs that are too expensive.  Do all of these drugs translate into better healthcare outcomes?  Heck no.  As compared to every other wealthy Western country, we finish last or near the bottom on every single health indicator.  In Liptruzet’s case, there is no justifiable reason for the FDA to approve it.  This is another example, amongst many, of why the FDA should be disbanded.  The FDA gives false credibility to Big Pharma.

If you are on Zetia, I suggest talking to your doctor about stopping it.  Ask him/her for any studies showing a clinical benefit such as a significantly lowered risk for heart disease, heart attack, stroke, or increased longevity.  I can assure you that you won’t be getting any articles from your doctor since they don’t exist.   More information about cholesterol-lowering medications can be found in my book, Drugs That Don’t Work and Natural Therapies That Do. 
=======================================================Read the complete article here.

Published on Dec 30, 2013
          

Heart disease prevention and reversal pioneers Dr. William Davis and Dr. William Blanchet meeting for the first time to have a frank discussion on how to beat heart disease and heat attack. This is the first of a multi-part series documenting this historic meeting.

http://www.youtube.com/watch?v=hYiZtfNBI80

The controversial study that started the War on Cholesterol - Watson

The controversial study that started the War on Cholesterol…

      

Alan Watson | June 14, 2012   

Revisiting the Coronary Primary Prevention Trial (CPPT) – 1973 to 1984

Using "relative risk statistics" and changing the study's design, the CPPT researchers declared success and the War on Cholesterol began in earnest

 

Launched in 1973 by the National Institutes of Health, the Coronary Primary Prevention Trial (CPPT) set out to prove that lowering blood cholesterol with a drug and a low cholesterol, low saturated fat diet would reduce the risk of coronary heart disease and extend the lives of the study participants.

(As part of the study, twelve new Lipid Research Clinics were set up by the Heart Institute at large universities throughout the country including Baylor, Stanford, Johns Hopkins and the University of Washington in Seattle.)

The researchers were looking for middle-aged men with total cholesterol levels exceeding those of 95 percent of Americans. (Only men with the highest 0.8 percent total cholesterol qualified.) The CPPT researchers screened 480,000 applicants in order to select 3,806 high risk men between the ages of 35 and 59.

This meant that many of the participants had familial hypercholesterolemia, a rare genetic defect in cholesterol metabolism present in about 1 percent of the population. The trials chance of success was therefore greatly increased by focusing on this particular group of presumably vulnerable men.
In their preliminary report, CPPT researchers announced that they would study two separate outcomes:  (1) Nonfatal heart attacks and (2) fatal heart attacks or deaths from coronary heart disease. The CPPT directors emphasized that they would be satisfied with nothing less than the strongest statistical proof of their findings; they had to be “99 percent certain that the results were not due to chance.”

The researchers also announced their goal of reducing blood cholesterol in the treatment group by 25 percent and reducing the risk of heart disease in the treatment group by at least 50 percent.
Approximately half of the 3,806 men were provided low cholesterol, low saturated fat dietary advice and were treated with cholestyramine, a cholesterol-lowering bile acid resin (Questran).

(Cholestyramine lowers cholesterol by interfering with digestion. Statins such as Lipitor, Mevacor and Zocor were not available yet.)

The control group was provided the same dietary advice and an unpleasant tasting placebo – an indigestible mixture of sand, sugar and food coloring. Both trial groups suffered with moderate to severe gastrointestinal distress. There were eight gastrointestinal cancer deaths in the treatment group (out of 21 cases) and one in the placebo group (out of 11 cases).

(There were more deaths from cancer, intestinal disease, stroke, violence and suicide in the group taking the cholesterol-lowering drug, and overall mortality was essentially the same for both groups.)

Disappointing Results

In 1984, the disappointing results were tabulated. Cholesterol levels in the treatment group had decreased by no more than 7 percent. Cholestyramine and the low cholesterol, low saturated fat diet had failed to lower cholesterol enough to prove that lowering cholesterol would reduce the risk of heart disease and extend the lives in the treatment group.

The difference in nonfatal heart attacks was not statistically significant. In the treatment group, 130 participants (6.8 percent) had a heart attack versus 158 in the placebo group (8.3 percent). After 7 years, the fraction of the treatment group that had benefited was less than 2 percent.

                                       Nonfatal heart attacks               Fatal heart attacks/coronary deaths
1,900 Control Group:         158 or 8.3 percent                               38 or 2.0 percent
1,906 Treatment Group:     130 or 6.8 percent                              30 or 1.6 percent

The difference in fatal heart attacks was not significant either. In the treatment group, 30 participants (1.6 percent) suffered a fatal heart attack compared to 38 in the placebo group (2.0 percent) Again – after 7 years of taking an unpleasant drug (and following a low fat diet), the fraction of the treatment group that benefited was less than 1 percent.

However, by applying relative risk statistics (a percentage of a percentage), the CPPT researchers improved their results. They took the number of people who presumably didn’t have a heart attack because of taking the drug (28) and looked at it as a percentage of the people who did have heart attacks (158) but didn’t take the drug:

The less than 2 percent absolute difference in nonfatal heart attacks rose to a reported 19 percent reduction in risk of a heart attack!

 

In similar statistical fashion, the researchers announced a 24 percent reduction in the risk of dying from a heart attack. The 8 men or 1.6 percent out of 1,900 who presumably did not have a fatal heart attack because they took the drug became the same 24 percent who reduced their risk of mortality compared to those in the control group who did die (38) but did not take the drug.

Additional study design changes

To prop up their victory, the CPPT researchers decided to exclude  “uncertain” nonfatal heart attacks from the treatment group while including  “uncertain” fatal heart attacks in the placebo group. Also, using the original 99 percent standard, the small favorable trend in either group could only be explained by chance (as defined by the researchers themselves at the start of the trial.)
By applying the less stringent 95 percent standard and by combining the two groups into one (nonfatal and fatal heart attacks), the CPPT researchers improved their results – declared victory – while the press responded with unbridled enthusiasm.

In 1984, the press and medical journals portrayed CPPT as the long sought proof that animal fats were the cause of heart disease. It was widely reported that for the first time:

“It had been proven that lowering cholesterol would reduce the mortality from heart disease and lower the risk of having a heart attack.”

 

Much of what we hear today about diet and heart disease can be traced back to this notorious failed study. When other scientists voiced their objections to the trial’s design changes, the CPPT directors simply denied that they had ever embraced the original more stringent standards.

In January 1984, the Journal of the American Medical Association (JAMA) dutifully reported:

“The trial’s implications…could and should be extended to other age groups and women, and to others with more modest elevations of cholesterol levels. The benefits that could be expected from cholestyramine treatment are considerable.”

 

George Mann, M.D., professor in medicine and biochemistry at Vanderbilt University, severely criticized the CPPT directors and the trial’s unsupportable results:

“The managers at the National Institutes of Health have used Madison Avenue hype to sell this failed trial in the way the media people sell an underarm deodorant…”

 

 Giving cholestyramine for over seven years to 1,906 middle age men – many with a genetic predisposition to atherosclerosis – had only saved the lives of eight but the Heart Institute was now recommending that cholesterol-lowering drug treatment be extended to patient groups that had not been part of the trial.

Even without the solid evidence they sought, the medical elite in the American Heart Association and the National Institute of Health decided to push ahead with cholesterol-lowering drugs and the still unproven low cholesterol, low saturated fat diet:

 “Now we have proved that it is worthwhile to lower blood cholesterol; no more trials are necessary. Now is the time for treatment.”

 

 The long War on Cholesterol had begun
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Read the complete article here.

BMJ exposes ways we have been misled over the ‘benefits’ of statins - Briffa

BMJ articles exposes the ways we have been misled over the ‘benefits’ of statins

By Dr John Briffa on 1 November 2013   

 

The ‘Cochrane Collaboration’ is an international collective of researchers whose self-proclaimed role is to provide accurate and robust assessments of health interventions. The group specialises in ‘meta-analyses’: the grouping together of several similar studies on interventions including drug therapies.
In 2011, Cochrane researchers assessed the evidence relating to statin use in individuals at low risk of cardiovascular disease (defined as a less than 20 per cent risk over 10 years), and concluded that there was limited evidence of overall benefit [1]. I appeared on Channel 4 news to discuss this publication and the issues surrounding it, and you can see the discussion here.

Earlier this year, the same Cochrane group updated their data and concluded that overall risk of death and cardiovascular events (e.g. heart attack or stroke) were reduced by statins in low risk individuals, without increasing the risk of adverse events (including muscle, liver and kidney damage) [2]. It seems the Cochrane reviewers had had quite some change of heart. A paper published in the BMJ on 22 October questions the evidence on which this U-turn appears to have been made [3].

The authors of the BMJ piece note that although the 2013 meta-analysis included four additional trials, these trials did not substantially change the findings. The change in advice was actually based on another meta-analysis, published in 2012, conducted by a group known as the Cholesterol Treatment Trialists’ (CTT) collaboration [4].

Among other things, the CTT authors concluded that, in low risk individuals, for each 1.0 mmol/l (39 mg/dl) reduction in LDL-cholesterol, statins reduce overall risk of death and heart attack by about 9 per cent and 20 per cent respectively. The conclusion was that statins have significant benefits in low risk individuals that greatly exceeded known risks of treatment.

However, the CTT authors took the odd step of calculating the benefits of statins according to a theoretical reduction in LDL-cholesterol levels. A much more realistic appraisal would be simply to calculate if, compared to placebo, statins actually reduce the risk of health outcomes.
The BMJ authors use the data from the CTT meta-analysis and found that risk of death was not reduced by statins at all. So, the CTT authors had used had extrapolated the data in a way that showed a benefit that actually does not exist in reality.

And what of the claim that statins reduce the risk of cardiovascular events such as heart attack or stroke? The data shows that about 150 low-risk individuals would need to be treated for five years to prevent one such event (i.e. only about one in 750 individuals will benefit per year).

They also draw our attention to the impact of statin treatment on ‘serious adverse events’. This outcome can be improved by statins as a result of, say, a reduced number of heart attacks, but worsened through side effects such as muscle or liver damage. The BMJ authors note that the CTT review did not consider serious adverse events (a major omission). Without knowing more about this, though, we simply cannot make a judgement regarding the overall effect of statins, and whether the net effect is beneficial or not. Interestingly, of three major trials that were included in the CTT review that assessed overall serious adverse effects, none found overall benefits from statin treatment.
So, while the CTT authors seem to have over-hyped the benefits of statins, they seem at the same time to have been quite keen to steer clear of talk of their very real risks and the absence of evidence foroverall benefit.

The BMJ authors draw our attention to the fact that every single trial included in the CTT was industry funded. Such trials are well known to report results more favourably and perhaps downplay risks than independently funded research. The BMJ authors cite specific ways in which the adverse effects of drugs seen in clinical trials can be ‘minimised’. These include:

• The exclusion of individuals from trials with known health issues likely to be exacerbated by statins or signal susceptibility to statin side effects (such as liver, kidney and muscle disease).
• The use of a ‘run-in’ period before the study starts which detects and then excludes individuals who do not tolerate statins.
• The possibility that individuals ‘drop out’ from the study because of side effects, meaning that the incidence of some side effects can be ‘lost’ from the data.
• Failure of the study investigators to assess and monitor adverse events such as muscle damage and changes in brain function.
• Failure to properly ascertain or report adverse events.

It is noted that the Cochrane authors admit the reporting of adverse effects in studies is generally poor, but also state that it’s unlikely statins have major life-threatening hazards. The authors of the BMJ piece are not convinced, though, writing: “[The] large discrepancies between the frequency of adverse events reported in commercially funded randomised controlled trials included in the CTT meta-analysesand non-commercially funded studies show that determination of harms cannot be left to industry alone.”

The BMJ piece is accompanied by an editorial from the journal’s editor, Fiona Godlee [5]. Her comment on this issue starts:

None of this does much to bolster confidence in the published literature.

Godlee goes on to write:

Nor am I reassured by discussions at two recent meetings co-hosted by the European Federation of Pharmaceutical Industry Associations (EFPIA). Drug company AbbVie is suing the European Medicines Agency to stop summary reports of its clinical trials becoming publicly available. AbbVie’s lawyer made clear that the company considers even the data on adverse events to be commercially confidential. Despite industry’s claims to be in favour of greater transparency, EFPIA and its American counterpart PhRMA are supporting Abbvie. The BMJ and BMA have joined forces to intervene on behalf of the EMA.

If I were to summarise, I’d say that, at best, there seems to be a degree of complacency regarding the veracity of statin data on the part of both the CTT and the Cochrane researchers. There is a sense that they are happy to present the ‘positive’ findings in the best possible light, and at the same time seem relaxed about the clear gaps we have in our knowledge about potential harms. The fact that statins appear to have no overall benefit in those at low risk of cardiovascular disease should not go unacknowledged, either.

Worse still, we have evidence that drug trials can be designed, conducted and reported in ways that obscure the truth. And sometimes, even when we have data that can help us make informed decisions about the appropriateness of a treatment, some drug companies will fight tooth and nail to prevent that data seeing the light of day.

This sort of subterfuge may be good for sales and share price, but it is almost certainly bad for our collective health. On this point, the BMJ authors state than instead of doctors following guidelines and prescribing statins for individuals at low risk of cardiovascular disease, they should explain the magnitude of benefits and uncertainties regarding harm. In addition, they might also discuss the fact that the vast majority of cardiovascular disease risk is linked with lifestyle factors such as smoking, diet and physical activity. Fiona Godlee backs this approach, but states that the benefits of lifestyle change are: “something that the dominance of industry sponsored clinical trials too often obscures.”
Personally, I am delighted that the misdeeds of drug companies and some researchers can now be exposed in this way, and in a high-profile medical journal at that. In the past, I think there was much more opportunity for the industry and its hired hands to mislead us. Greater transparency means that the industry as a whole is getting more of what I believe it deserves: our contempt.
References:
1. Taylor F, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev 2011;1:CD004816.
Medline
2. Taylor F, et al. Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev2013;1:CD004816.
3. Abramson JD, et al. Should people at low risk of cardiovascular disease take a statin?
BMJ 2013;347:f6123
4. Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. The Lancet 2012;380(9841):581–90.
5. Godlee F. Statins for all over 50? No BMJ 2013;347:f6412.
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Read the complete article here.

The topic covered in this podcast concerns the use of the B vitamin , Niacin, when taking a statin. Is this a beneficial combination, or does it lead to an increased risk of stroke? We invite you to listen in with Lindsay and Dr. Blanchet.

http://tuesdaytalkshow.podomatic.com/entry/2013-09-19T12_12_40-07_00

Thyroid Pills & Heart Disease - Dach

Thyroid Pills Prevent Heart Attacks by Jeffrey Dach MD

Thyroid Pills Prevent Heart Attacks by Jeffrey Dach MD

The Low Thyroid Condition and Heart Disease

In 1976 Broda Barnes was the first to connect low thyroid function with heart attacks and heart disease.  His book is called, Hypothyroidism The Unsuspected Illness by Broda Barnes, Click Here to read my Book Review..

Above Left Image: Photo of WP Thyroid Pills Bottle courtesy of RLC labs Natural thyroid pills

Discovering the Connection
How did Broda Barnes discover the connection between low thyroid and heart disease?  Barnes took summer vacations in Graz Austria every year to study the autopsy files.  Graz had a high prevalence of thyroid disorders, and anyone in Graz who died over the past 100 years required an autopsy to determine cause of death, as mandated by the authorities.  This rather large amount of autopsy data showed that low thyroid patients survived the usual childhood infectious diseases thanks to the invention of antibiotics, and years later develop heart disease.  Barnes also found that thyroid treatment was protective in preventing heart attacks, based on his own clinical experience.  Likewise for diabetes, Dr. Barnes found that adding thyroid medication was beneficial at preventing the onset of vascular disease in diabetics.  Again, blood tests are usually normal.
New research like the Hunt Study confirms that Broda Barnes was right all along, creating a paradigm shift in thyroid treatment, and constituting a frontal assault on the Institution of Medicine’s thyroid dogma.

The Hunt Study - Thyroid Function and  Heart Disease
 
TSH is short for thyroid stimulating hormone, made by the pituitary gland.  TSH actually stimulates the thyroid gland to make more thyroid hormone, and can therefore be used as a barometer of thyroid function.  If thyroid function is low, the pituitary sends out more TSH to stimulate the thyroid to make more thyroid hormone.  
Mainstream Medicine regards the TSH as the single most important test for determining thyroid function. High TSH means low thyroid function, and a Low TSH means normal or high thyroid function.


What Did The Hunt Study Find?
The Hunt Study from the April 2008 Archives of Internal Medicine examined mortality from coronary heart disease (CHD) and TSH level.  The authors conclude,
“The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.”
Above Image: Thyroid Gland makes thyroid hormone.

The Hunt Study measured thyroid function with the TSH test in 17,000 women and 8,000 men with no known thyroid disease or heart disease. All patients had “normal TSH” levels meaning the TSH values were in the lab reference range of 0.5 to 3.5.   The women were stratified into three groups, lower TSH, intermediate and upper TSH levels, and mortality from heart disease was recorded over an 8 year observation period.

 (see chart below).
70% Increase in Heart Disease Mortality for TSH in Upper Normal Range
The Hunt study found that group with the higher TSH had a 70% increased mortality from heart disease compared to the lower TSH group.  Remember all these TSH vales were in the normal lab range. See chart below for results of the Hunt Study:

Left Image: Heart with Occluded Coronary Artery and Infarction at the apex, courtesy of wikimedia commons.

Results of the Hunt Study:

	TSH	Death from Heart Disease
Group 1	0.50-1.4	baseline risk
Group 2	1.5-2.4	40% higher than baseline
Group 3	2.5-3.5	70% higher than baseline

This Finding is Earthshaking !!

This means that merely by taking natural thyroid pills to reduce TSH to the low end of “normal” (0.5), one can reduce death from cardiovascular disease by 70 percent.  This mortality benefit is mind boggling and far exceeds any drug intervention available.

Thyroid Hormone Also Improves LDL Lipo-Proteins
Another report from the Hunt Study published in 2007 showed that LDL cholesterol was linearly associated with TSH level. (see chart below).
Below Chart showing LDL cholesterol (non-HDL) goes up as TSH goes up.  Note that TSH always remains within in the lab “normal range” (0.5-3.5).
Above chart shows linear increase in LDL cholesterol as TSH increases. Image Courtesy of Hunt Study European Journal of Endocrinology, Vol 156, Issue 2, 181-186, 2007
The Conclusion is Clear:
The best way to normalize lipoprotein profile and reduce mortality from heart disease is to reduce TSH to the lower end of the normal range with thyroid medication.  A TSH in the upper end of the normal range is associated with increased cardiovascular mortality and elevations in LDL lipo-protein measurements.  A TSH at the lower end of the normal range is associated with protection from heart disease.

Statin Drugs or Thyroid to Prevent Heart Disease in Women?

My previous article discussed the issue of statin drugs for women.  Decades of published statin drug studies show that statin drugs simply don’t work for women, and don’t reduce mortality from heart disease in women.  But on the other hand, the HUNT study shows that TSH levels in the lower normal range provide a 70% reduction in heart disease mortality for women.  This can be accomplished safely with inexpensive thyroid medication under a physician’s supervision.  So for women concerned about preventing heart disease, this is good news, pointing out a natural alternative to statin drugs that works much better.

Natural Thyroid is Better
Rather than Synthroid, we prefer to use natural thyroid which is a dessicated porcine thyroid gland from RLC Labs.  The reason for this is that we have seen better clinical results with the natural thyroid preparations compared to synthroid.
Above image: thyroid hormone Courtesy Wikimedia .
Natural Thyroid is Safer, but can Cause Adverse Effects of Palpitations
Although natural thyroid is safe, there is always the possibility of adverse effects from thyroid excess, defined as too much thyroid medication.  The first sign of thyroid excess is usually a rapid heart rate at rest or perhaps palpitations (at rest).  We spend about five minutes at the office going over this adverse effect before starting patients on thyroid medication.  Usually patients will notice the heart rate going up or the heart beat sounding louder than usual as the first sign that can be easily recognized.  Once recognized, the patient is instructed to stop the thyroid medication, and symptoms usually resolve within 6 hours (for natural thyroid).  It is perfectly safe to stop the thyroid medication at any time, as there will be no acute changes, merely a gradual reversion to the original state that existed before starting the thyroid pills.

Some patients are very sensitive to thyroid medication and will have thyroid excess symptoms such as rapid heart rate and palpitations from small amounts of thyroid medication.  These are usually the elderly with underlying heart disease and/or magnesium deficiency, and we usually avoid giving thyroid medication to these patients.  We also liberally supplement everyone with magnesium if their RBC magnesium levels are low.

About 5 per cent of our patients initially started on thyroid will notice symptoms of thyroid excess with a rapid heart rate, and they will stop the medication for a day or two and restart at a lower dosage with no problem.  This is more common in Hashimoto’s patients whose own production of thyroid hormones may fluctuate from month to month.  Patients with magnesium deficiency or adrenal fatigue with low cortisol output on salivary testing will also tend to be more sensitive to small amounts of thyroid medication, so caution is advised in these groups as well.

Thyroid Excess Can Rarely Cause Atrial Fibrillation
Upper Image: EKG strip with Red Arrow shows atrial fibrillation, no recognizable P-wave.  Lower Image: EKG strip with normal rhythm with recognizable P wave (blue arrow). Courtesy of Wikimedia Commons.
So far, we have not had a patient go into atrial fibrillation from thyroid medication, probably because we spend so much time with each patient discussing the symptoms of thyroid excess, and the importance of stopping the thyroid medication if these symptoms are noted.

Mainstream Docs Don’t Have Time To Discuss Adverse Effects
One of the reasons the mainstream conventional docs will give only a minuscule amount of synthroid to the low thyroid patient is that they simply don’t have the time to discuss thyroid excess and can’t afford an adverse event which is more likely if the patient doesn’t have a clue about what to watch out for.  In addition, mainstream medical docs don’t recognize the syndrome of adrenal fatigue or magnesium deficiency , so they can run into problems with thyroid excess without understanding why, and this also makes them very cautious, tending to under treat.
Left Image: Doctor thinking about thyroid dosage.
In patients with underlying heart disease who are prone to cardiac arrhythmias, thyroid excess can cause atrial fibrillation with characteristic EKG appearance.  Atrial fibrillation can be a problem, because if it becomes chronic and doesn’t go away on its own, the cardiologist will try a maneuver called cardioversion, the application of an electrical shock to restart a normal cardiac rhythm.  Or, if that doesn’t work, prescribe blood thinners, all of which is not without risk.  So it is better to avoid atrial fibrillation altogether by simply stopping the thyroid pills whenever symptoms of rapid heart rate or palpitations are noted while at rest.  Exercise induced rapid heart rate, of course, doesn’t count since that is normal cardiovascular response to exercise.

How To Design A Better Hunt Study
How would I design an even better Hunt Study? That’s easy. Include another group of patients with TSH levels above and below the study group, namely, below 0.5, and above 3.5.  I would also include data on annual CAT coronary calcium scores.  I would predict that the lower TSH group (below 0.5) would have even less heart disease than the higher TSH group, and that coronary calcium score, indicating plaque burden, would go up as TSH went up.

Read More About the Hunt Study from William Davis MD and Jacob Teitelbaum MD:
Is normal TSH too high?   by William Davis MD
Low Thyroid (Even if Tests are Normal) is a Major Cause of Heart Attacks by Jacob Teitelbaum, MD.

Credit and Thanks is given to William Davis MD and Jacob Teitelbaum MD for bringing the Hunt Study to my attention.

For more information on thyroid and heart disease, read my previous articles:
Saving Time Russert and George Carlin
Healthy Men Should Not Take Statin Drugs
Heart Disease Vitamin C and Linus Pauling
Getting Off Statin Drug Stories
How to Reverse Heart Disease with the Coronary Calcium Score (part one)
Reversing Heart Disease Part Three
Cholesterol Lowering Drugs for the Elderly, Bad Idea
Cholesterol Lowering Statin Drugs for Women Just Say No

Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie Florida 33314
954-792-4663
www.jeffreydach.com
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(c) 20013 Jeffrey Dach MD All Rights Reserved, This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.
Link to this article:http://wp.me/P3gFbV-LU
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Links and References:
http://archinte.ama-assn.org/cgi/content/abstract/168/8/855
Arch Intern Med. 2008;168(8):855-860. Thyrotropin Levels and Risk of Fatal Coronary Heart Disease,
The HUNT Study
Arch Intern Med. 2008;168(8):855-860. Background  Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.
Methods  In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.
Results  During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.
Conclusions  Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.
Author Affiliations: Department of Public Health, Faculty of Medicine (Drs Åsvold and Vatten), and Human Movement Science Programme (Dr Nilsen), Norwegian University of Science and Technology, Trondheim, Norway; St Olavs Hospital, Trondheim University Hospital, Trondheim (Dr Åsvold); Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway (Dr Bjøro); and Department of Social Medicine, University of Bristol, Bristol, England (Dr Gunnell).
http://www.eje-online.org/cgi/content/full/156/2/181
European Journal of Endocrinology, Vol 156, Issue 2, 181-186, 2007  CLINICAL STUDY  The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study
Bjørn O Åsvold1,2, Lars J Vatten1, Tom I L Nilsen1 and Trine Bjøro3  1 Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, N-7489 Trondheim, Norway, 2 St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway and 3 Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway (Correspondence should be addressed to L J Vatten
Jacob Teitelbaum MD
http://www.endfatigue.com/health_articles_f-n/Heart-low_thyroid_major_cause_heart_attacks.html
Jacob Teitelbaum, MD. Low Thyroid (Even if Tests are Normal) is a Major Cause of Heart Attacks,
William Davis MD
http://heartscanblog.blogspot.com/2008/06/is-normal-tsh-too-high.html
William Davis MD, begin quote:”Is normal TSH too high? There’s no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.  But how do we distinguish “normal” thryoid function from “low” thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.  Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called “negative feedback loop:” If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.  An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)  The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid “rules.” endquote WIlliam Davis MD
International Hormone Societyhttp://www.intlhormonesociety.org/ref_cons/
Ref_cons_9_thryoid_treatment_of_clinically_hypothyroid_biochemically_hypothyroid_patients.pdf
International Hormone Society, references, clinically hypothyroid , lab euthyrroid
Other Blogs:
http://thyroid.blogspot.com/
Thyroid Blog by Dr. Richard B. Guttler M.D., F.A.C.E.
Location: Santa Monica, California, United States
http://www.stopthethyroidmadness.com/
Stop the Thyroid Madness Blog – a patient tries in vain to convince soctors to switch from Synthroid to Armour
http://thyroid.about.com/
MAry Shomon thyroid blog
Disclaimer click here: http://www.drdach.com/wst_page20.html
The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship.  Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.  Finally, the material produced by myself may be reproduced for personal use, provided that appropriate credit is given
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(c) 2007-2013 Jeffrey Dach MD All Rights reserved. This article may be copied or reproduced on the internet provided a link and credit is given.

 

Large meta-analyses of statins

The following was posted on the Track Your Plaque forum on 9/14/2013

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  Here are some highlights from here: http://chriskresser.com/the-diet-heart-myth-statins-dont-save-lives-in-people-without-heart-disease backed up by studies. 

An analysis by Dr. David Newman in 2010 which drew on large meta-analyses of statins found that among those with pre-existing heart disease that took statins for 5 years (1):

96% saw no benefit at all

1.2% (1 in 83) had their lifespan extended (were saved from a fatal heart attack)

2.6% (1 in 39) were helped by preventing a repeat heart attack

0.8% (1 in 125) were helped by preventing a stroke

0.6% (1 in 167) were harmed by developing diabetes

10% (1 in 10) were harmed by muscle damage  A heart attack or stroke can have a significant negative impact on quality of life, so any intervention that can decrease the risk of such an event should be given serious consideration. But even in the population for which statins are most effective—those with pre-existing heart disease—83 people have to be treated to extend one life, and 39 people have to be treated to prevent a repeat heart attack.

Primary prevention (those without pre-existing heart disease)Statins do reduce the risk of cardiovascular events in people without pre-existing heart disease. However, this effect is more modest than most people assume. Dr. Newman also analyzed the effect of statins given to people with no known heart disease for 5 years (5):

98% saw no benefit at all

1.6% (1 in 60) were helped by preventing a heart attack

0.4% (1 in 268) were helped by preventing a stroke

1.5% (1 in 67) were harmed by developing diabetes

10% (1 in 10) were harmed by muscle damageThese statistics present a more sobering view on the efficacy of statins in people without pre-existing heart disease. They suggest that you’d need to treat 60 people for 5 years to prevent a single heart attack, or 268 people for 5 years to prevent a single stroke. These somewhat unimpressive benefits must also be weighed against the downsides of therapy, such as side effects and cost. During that hypothetical 5 year period, 1 in 67 patients would have developed diabetes and 1 in 10 patients would have developed muscle damage (which can be permanent in some cases, as we’ll see later in this section).

To summarize:

The only population that statins extend life in are men under 80 years of age with pre-existing heart disease.

In men under 80 without pre-existing heart disease, men over 80 with or without heart disease, and women of any age with or without heart disease, statins have not been shown to extend lifespan.

Statins do reduce the risk of cardiovascular events in all populations. A heart attack or stroke can have a significant, negative impact on quality of life—particularly in the elderly—so this benefit should not be discounted.

However, the reductions in cardiovascular events are often more modest than most assume; 60 people with high cholesterol but no heart disease would need to be treated for 5 years to prevent a single heart attack, and 268 people would need to be treated for 5 years to prevent a single stroke.

Statins have been shown to cause a number of side effects, such as muscle pain and cognitive problems, and they are probably more common than currently estimated due to under-reporting.

My intention here is not to suggest that statins have no place in the treatment of heart disease, but rather to give you the objective information you need to decide (along with your doctor) whether they are appropriate for you. The decision whether to take them should be based on whether you have pre-existing heart disease, what your overall risk of a heart attack is, how healthy your diet and lifestyle is, what other treatments you’ve already tried, and your own risk tolerance and worldview. It’s clear that statins reduce heart disease as well as the risk of death in those that have already had a heart attack, so if you’re in this group and you’ve already tried diet and lifestyle interventions without much impact on your lipid or inflammatory markers, you are more likely to benefit.
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Read the whole thing here if you are a member.

Is salt really so bad for you? - Fenster

Is salt really so bad for you?

Decades of science show NO conclusive evidence that cutting back on dietary sodium reduces cardiovascular morbidity

By Michael S. Fenster                     
                        

Enlarge

(Credit: This piece originally appeared on Pacific Standard.

 

No salt, low salt, salt free, heart-healthy salt substitution–any added salt will hurt your constitution. It reads like some bizarre, Seussian tale. Excepting that we’ve heard it not from the good Dr. Geisel but from the medical community and public health advocates everywhere. We watch as celebrity chefs take the salt elimination cooking challenge to prepare an “improved healthy” cuisine. Self-anointed “experts” cadge, coax, and cajole us to decrease our salt, or, more specifically, sodium intake. If that doesn’t work then the specter of heart attacks and strokes is unleashed upon us, along with a dash of fire and brimstone for good measure. It is, after all, clearly in our best personal and the greater public interest.
The hypothesis is sound and the supporting data is impeccable, right?

The theory goes as follows: Salt acts to make us retain fluid. When we retain more fluid it increases our blood pressure (albeit temporarily). Increased blood pressure is hypertension. Hypertension is a risk factor for cardiovascular disease like heart attacks and stroke. Heart attacks and strokes are bad. Therefore, hypertension is bad. Thus, sodium must be bad; A causes B which causes C, therefore A causes C. Get rid of A and you get rid of C—simple basic arithmetic, no? Reduce sodium intake and you will reduce blood pressure and thus reduce the incidence of stroke and heart attack. Reducing sodium intake is good—simple, effective, and undeniably the prevailing conventional wisdom these days.

Except… one thing is missing.

The conclusive data—or any data-that definitively shows that cutting back on dietary sodium reduces mortality or significantly reduces cardiovascular morbidity. For over half a century, starting in the 1960s, there has been a vehement and salty exchange just out of public earshot involving respected scientists on both sides of this line. But with the advent of an aggressive public policy to reduce dietary sodium intake for presumed public health benefit and studies emerging suggesting negative consequences of a low-sodium diet, the clamor of dissension is heating up.
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JAMA on salt HERE.
Read the complete article here.

Here is an article from The Kennebec Journal on the division regarding the salt controversy. Here are a couple of quotes:

"Four months after an Institute of Medicine report said reducing salt to the lowest recommended level doesn't improve health and may harm it, the U.S. Centers for Disease Control and Prevention said they disagree. In an article published Monday in the American Journal of Hypertension, the CDC and New York City health officials said getting Americans to eat less salt remains a key objective with the potential to save thousands of lives."

and

"Lowering sodium to the extent required to lower blood pressure has a variety of other effects," including some that boost heart attacks, strokes and death, he said. "It's just not that simple. The message from the evidence is we don't know."

Here is another article from Food Politics by Marion Nestle.
Another article on salt here.

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203

An article by Marion Nestle - http://www.foodpolitics.com/2014/08/its-salt-arguments-again-new-research-arguments-over-public-health-recommendations-and-issues-of-conflicts-of-interest/