Statins in the Drinking Water? - Packer

Statins in the Drinking Water?

by Milton Packer, MedPage Today

"Universal treatment for people at minimal risk means that a physician would need to treat more than 100 patients for 10 years to obtain an extra year of good health in one person. This marginal improvement does not meet most current standards for cost-effectiveness. The benefit is so small that it disappears if quality of life were even slightly diminished by the need to remember to take the drug daily."

.

.

.

.

"Treating every middle-aged person with a statin is the polar opposite of precision medicine.

Confused? You should not be. It is medicine that has gone insane."

Read the complete article here.

It’s official, statins do not have any side effects - Kendrick

It’s official, statins do not have any side effects

"The reality is, that unless you have had a previous heart attack, statins have no effect on overall mortality. To put that another way, they don’t save lives. They don’t even prevent heart attacks or strokes in women with no previous history of heart disease.

The statistic you really want to know about statins is the following. If you have had a heart attack, or stroke, and take a statin for five years, you will increase your life expectancy by 4.2 days. Balance that against a twenty per cent chance of having side effects, some of which are very unpleasant and long-lasting, and you can see why I am not a fan of statins."
.
.
.
"A number of things were found. The most important of which, is just how many people stopped taking their statins after one year. A pretty staggering 75%. Why did they stop?

‘More than six in ten respondents (62%) said they discontinued their statin due to side effects, with the secondary factor (17%) being medication cost. Only 12% of respondents cited lack of efficacy in cholesterol management as a reason for stopping their medication. On average, respondents who experienced side effects due to their statin stopped after trying two different statins.

Three out of ten respondents experienced side effects of muscle pain and/or weakness, and 34% stopped taking their statin because of these side effects without consulting with their doctor.'

Read the complete article by Dr Kendrick here.

Congenital abnormalities in baby born to mother using lovastatin

Thursday, 10 March 2016

Congenital abnormalities in baby born to mother using lovastatin

This study was published in the Lancet 1992 Jun 6;339(8806):1416-7

Study title and authors:
Congenital abnormalities (VATER) in baby born to mother using lovastatin.

Ghidini A, Sicherer S, Willner J.

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/1350826

This paper reports the case of an infant born with many malformations after the mother used a statin during pregnancy.

(i) A woman was treated for five weeks with lovastatin, starting approximately six weeks from her last menstrual period.
(ii) The statin was discontinued when her pregnancy was diagnosed at 11 weeks' gestation.
(iii) A female infant was delivered by cesarean section at 39 weeks' gestation. The infant had a constellation of malformations termed the VATER association (vertebral anomalies, anus not developed properly, an abnormal connection between the oesophagus and the trachea with part of the oesophagus missing, and kidney, forearm and wrist abnormalities).
(iv) Her anomalies included a deformed chest, spinal deformity, absent left thumb, foreshortened left forearm, shortened left elbow, fusion of the ribs on the left, anomalies in the spine, deformed left forearm, and a narrow lower oesophagus.

The Lancet published a meta-analysis of 27 statin trials

Data, Drugs, and Deception: a True Story

 

Wednesday, May 23, 2012

      

Last week The Lancet published a meta-analysis of 27 statin trials, an attempt to determine whether patients with no history of heart problems benefit from the drugs—true story. The topic is controversial, and no less than six conflicting meta-analyses have been performed—also a true story. But last week’s study claims to show, once and for all, that for these very low risk patients, statins save lives—true story.

Actual true story: the conclusions of this study are neither novel nor valid.

The Lancet meta-analysis, authored by the Cholesterol Treatment Trialists group, examines individual patient data from 27 statin studies. Their findings disagree with an analysis published in 2010 in the Archives of Internal Medicine, and with analyses from two equally respected publications, the Therapeutics Letter and the Cochrane Collaboration.* Despite this history of dueling data the authors of last week’s meta-analysis, in a remarkable break from scientific decorum, conclude their report with a directive for the writers of statin guidelines: the drugs should be broadly recommended based on the new analysis.

As an editorialist points out, if implemented, the CTT group recommendations in the United States would lead to 64 million people, more than half of the population over the age of 35, being started on statin therapy—true story.

Where is the magic, you ask, in this latest effort? What is different? In some ways, nothing. Indeed just a year and a half earlier The Lancet published a meta-analysis of 26 of the same 27 studies, with the same results, by the same authors (true story, and an odd choice on the part of the journal). So the findings aren’t new. They are, however, at odds with other meta-analyses. Why? It is the way they calculated their numbers. This meta-analysis, like the earlier one from the same group, reports outcomes per-cholesterol-reduction. The unit they use is a “1 mmol/L reduction in low density lipoprotein (LDL)”, in common U.S. terms, a roughly 40-point drop in LDL.

That’s the magic: each of the benefits reported in the paper refers to patients with a 40-point cholesterol drop. Voilá. One can immediately see why these numbers would look different than numbers from reviews that asked a more basic question: did people who took statins die less often than people taking a placebo? (The only important question.) Instead, they shifted the data so that their numbers corresponded precisely to patients whose cholesterol responded perfectly.
Patients whose cholesterol drops 40 points are different than others, and not just because their body had an ideal response to the drug. They may also be taking the drug more regularly, and more motivated. Or they may be exercising more, or eating right, and more health conscious than other patients. So it should be no surprise that this analysis comes up with different numbers than a simple comparison of statins versus placebo pills. Ultimately, then, this new information tells us little or nothing about the benefits someone might expect if they take a statin. Instead it tells us the average benefits among those who had a 40-point drop in LDL.

But LDL drop cannot be predicted. Some won’t drop at all, some will drop just a bit, and some may drop more. Therefore the numbers here tell an interesting story about certain patients who took statins, but they have no relevance to patients and doctors considering statins. And yet, the latter group is the target of the study's concusions.

True story: in prior meta-analyses that found no mortality benefit the investigators simply looked at studies of patients without heart disease and compared mortality between the statin groups and the placebo groups. No machinations, no acrobatics, no per-unit-cholesterol. They took a Joe Friday approach (just the facts, ma’am), and found no mortality benefit.

Perhaps never has a statistical deception been so cleverly buried, in plain sight. The study answers this question: how much did the people who responded well to the drug benefit? This is, by definition, a circular and retrospective question: revisiting old data and re-tailoring the question to arrive at a conclusion. And to be fair they may have answered an interesting, and in some ways contributory, question. However the authors’ conclusions imply that they answered a different, much bigger question. And that is not a true story.

Guideline writers, doctors, patients, journalists, and policy makers will all have to pay close attention to avoid the trappings of deceptive data, dressed up as a true story.

*The Cochrane Collaboration analysis reports an overall mortality benefit with statins (RR=0.86), however their summary suggests that statins should be used for primary prevention “with caution.” In particular on p.12, after a discussion of the biases in many of the trials that led to their numerical finding, they clearly state that using statins for patients with anything less than a 2% per year risk of coronary events “is not supported by existing evidence.” This cutoff encompasses virtually all people that would be considered candidates for primary prevention.
=============================================================================================

Read the complete article here.

CTT the house of statin secrets - Burne

SOS: Sanity over Statins – CTT the house of statin secrets

by Jerome Burne

Should a professional body, however eminent, be allowed to keep information about the safety of products they are supplying to public hidden so no one else can run tests on them?

That is the question raised by HealthInsightUK’s finding that a large and respected organisation whose job it is to analyses the findings of statin trials – The Cholesterol Treatment Trialists’ (CTT) Collaboration in Oxford – has an agreement to keep secret much of the information contained in its huge database which holds results from 27 trials of these drugs, nearly each of which was run by a drug company.

Questions about the secrecy of the CTT have been put in the spotlight following the recent recommendation by NICE to change the guidelines on statins. If the proposals are accepted, millions more healthy people in the UK who have no sign of heart disease will be prescribed these drugs. A key part of the evidence supporting this proposal was a study by CTT published in the Lancet in 2012.

HealthInsightUK has also established that the CTT do not hold data on the side-effects of statins. A spokesman confirmed that they base their estimate of risk on the published results of trials conducted by the drug companies. He dismissed claims that side-effects such as muscle pain and depression were wide spread, saying they were only “hypotheses”.

Denied access to data

This could explain why the CTT has regularly reported a much lower rate of side-effects than trials run by independent researchers. Knowing the true rate of side-effects is particularly important with statins because many patients have to take them for one to benefit. If the estimate of side effects is too low the benefits may not outweigh the risks.

Concern about the secrecy surrounding CTT’s data is not new. Dr Jim Wright editor of the highly respected and independent journal Canadian Therapeutics Initiative which analyses drug studies has described how several years ago he had tried and failed to get access to statin data held by CTT.
“They had agreed someone from my team could have access to their data, although the researcher would have to go to Oxford to see it. However after travelling 6000 miles, they were told that the data was not available.”

This is just an anecdote but many others have since reported the same thing. The latest concern about access to CTT data was triggered last year when the Cochrane Collaboration – famed for its rigorous assessment of the benefit of drugs and other treatments – produced a report saying that statins should be more widely used on people without heart disease. The report was heavily based on the CTT Lancet study. Was it actually possible to check their findings?

Everyone wanted the data

A number of senior researchers approached by HealthInsight have supported Dr Wright’s claim that the data held by CTT hasn’t been available. Professor Rita Redberg cardiologist and editor of the journal JAMA Internal Medicine, has stated in an email that: “CTT will not make their data available to any colleagues and other researchers who wish to study risks and benefits of statins. The CTT data is not accessible publicly.”

“I have not requested access to the CTT data,’ says Dr David H. Newman, Director of Clinical Research, Mount Sinai School of Medicine, New York.

‘However, I’m not aware of anyone who has gained access to these data, which speaks volumes since everyone has wanted it. For the science to be considered even potentially credible, another independent group will have to replicate their analysis.”

Professor Harriet Rosenberg of the Health and Society Program at York University in Toronto commented that: “many scholars have asked the CTT for data without success” in a formal reply to the Cochrane review last year.

The response by the CTT when such individual claims are made is to say that anyone with a well formulated proposal can get access to their data. But emails seen byHeathinsightUK throw doubt on that. They were exchanged between one of CTT’s top researchers Professor Colin Baigent and an Australian TV journalist researching a story about statins.
===============================================================
Read the complete article here.

BMJ editor casts doubt on veracity of statin trials funded by the statin makers - Godlee

Statins for all over 50? No

Fiona Godlee, editor, BMJ

BMJ 2013; 347 doi: http://dx.doi.org/10.1136/bmj.f6412 (Published 23 October 2013)                                         Cite this as: BMJ 2013;347:f6412    

 

Should you prescribe statins to everyone over the age of 50, even those at low cardiovascular risk? A new Cochrane review seems to suggest that you should. An article in this week BMJ cries caution (doi:10.1136/bmj.f6123).

Current guidance from the UK’s National Institute for Health and Care Excellence (NICE) and the American Heart Association recommends statins only when the 10 year risk of cardiovascular disease is 20% or greater. But since these guidelines were written, a large meta-analysis of individual patient data reached a different conclusion. Published in the Lancet in 2012, the Cholesterol Treatment Trialists (CTT) Collaboration meta-analysis found that statins significantly reduced major cardiovascular events and all cause mortality in people at low risk, a benefit which, the paper said, “greatly exceeds any known hazards of statin therapy.”

As John Abramson and colleagues explain, it’s this meta-analysis that led the Cochrane reviewers to embrace the idea that statins should be used far more widely, even perhaps to everyone over 50, as a Lancet editorial suggested at the time.

But Abramson and colleagues’ detailed critique of the CTT meta-analysis should give us pause. Their own analysis of the data finds no evidence of a reduction in all cause mortality or in the total number of serious events. They also highlight the failure of the trials included in the CTT analysis to adequately report important harms of statin treatment, including myopathy and diabetes. They conclude that broadening the use of statins to low risk individuals “will unnecessarily increase the incidence of adverse events without providing overall health benefits.”

There is a concern underlying their critique that will be familiar to BMJ readers. It is that all of the trials included in the CTT meta-analysis were funded by the manufacturer of the statin being studied. They list the various ways in which these trials might have exaggerated the benefits of statins and minimised the harms, and they summarise what low risk patients need to know. Top of the list is the benefit of lifestyle change, something that the dominance of industry sponsored clinical trials too often obscures.

None of this does much to bolster confidence in the published literature. 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 (doi:10.1136/bmj.f1636). 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 (doi:10.1136/bmj.f4728).

As for a way forward, I can’t improve on the list of solutions proposed by Richard Lehman when emailing out his journal review blog this week (http://bit.ly/HcKvjy): “All phase 3 trials to be designed and conducted independently of manufacturers, using the best available comparator. Research priorities to be determined by patients (James Lind Alliance). Value-based pricing. All data available from all trials, with meta-data: IPD [individual patient data] level for qualified independent centres. Big increase in comparative effectiveness research, much more research into non-pharmacological treatments.”

Notes

Cite this as: BMJ 2013;347:f6412

Footnotes

• Follow BMJ Editor Fiona Godlee on Twitter @fgodlee and the BMJ @bmj_latest

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

Emphasis added.

Read the complete article here.

Saturated fat is not the major issue - Malhotra

Saturated fat is not the major issue

BMJ 2013; 347 doi: http://dx.doi.org/10.1136/bmj.f6340 (Published 22 October 2013)

Cite this as: BMJ 2013;347:f6340

Let’s bust the myth of its role in heart disease

 

Scientists universally accept that trans fats—found in many fast foods, bakery products, and margarines—increase the risk of cardiovascular disease through inflammatory processes.1 But “saturated fat” is another story. The mantra that saturated fat must be removed to reduce the risk of cardiovascular disease has dominated dietary advice and guidelines for almost four decades.

Yet scientific evidence shows that this advice has, paradoxically, increased our cardiovascular risks. Furthermore, the government’s obsession with levels of total cholesterol, which has led to the overmedication of millions of people with statins, has diverted our attention from the more egregious risk factor of atherogenic dyslipidaemia.

Saturated fat has been demonised ever since Ancel Keys’s landmark “seven countries” study in 1970.2 This concluded that a correlation existed between the incidence of coronary heart disease and total cholesterol concentrations, which then correlated with the proportion of energy provided by saturated fat. But correlation is not causation. Nevertheless, we were advised to cut fat intake to 30% of total energy and saturated fat to 10%.”3 The aspect of dietary saturated fat that is believed to have the greatest influence on cardiovascular risk is elevated concentrations of low density lipoprotein (LDL) cholesterol. Yet the reduction in LDL cholesterol from reducing saturated fat intake seems to be specific to large, buoyant (type A) LDL particles, when in fact it is the small, dense (type B) particles (responsive to carbohydrate intake) that are implicated in cardiovascular disease.4

Indeed, recent prospective cohort studies have not supported any significant association between saturated fat intake and cardiovascular risk.5 Instead, saturated fat has been found to be protective. The source of the saturated fat may be important. Dairy foods are exemplary providers of vitamins A and D. As well as a link between vitamin D deficiency and a significantly increased risk of cardiovascular mortality, calcium and phosphorus found commonly in dairy foods may have antihypertensive effects that may contribute to inverse associations with cardiovascular risk.6 7 8

One study showed that higher concentrations of plasma trans-palmitoleic acid, a fatty acid mainly found in dairy foods, was associated with higher concentrations of high density lipoprotein, lower concentrations of triglycerides and C reactive protein, reduced insulin resistance, and a lower incidence of diabetes in adults.9 Red meat is another major source of saturated fat. Consumption of processed meats, but not red meat, has been associated with coronary heart disease and diabetes mellitus, which may be explained by nitrates and sodium as preservatives.10

The notoriety of fat is based on its higher energy content per gram in comparison with protein and carbohydrate. However, work by the biochemist Richard Feinman and nuclear physicist Eugene Fine on thermodynamics and the metabolic advantage of different diet compositions showed that the body did not metabolise different macronutrients in the same way.11 Kekwick and Pawan carried out one of the earliest obesity experiments, published in the Lancet in 1956.12 They compared groups consuming diets of 90% fat, 90% protein, and 90% carbohydrate and showed that the greatest weight loss was in the fat consuming group. The authors concluded that the “composition of the diet appeared to outweigh in importance the intake of calories.”

The “calorie is not a calorie” theory has been further substantiated by a recent JAMA study showing that a “low fat” diet resulted in the greatest decrease in energy expenditure, an unhealthy lipid pattern, and increased insulin resistance in comparison with a low carbohydrate and low glycaemic index diet.13 In the past 30 years in the United States the proportion of energy from consumed fat has fallen from 40% to 30% (although absolute fat consumption has remained the same), yet obesity has rocketed.

One reason: when you take the fat out, the food tastes worse. The food industry compensated by replacing saturated fat with added sugar. The scientific evidence is mounting that sugar is a possible independent risk factor for the metabolic syndrome (the cluster of hypertension, dysglycaemia, raised triglycerides, low HDL cholesterol, and increased waist circumference).

In previous generations cardiovascular disease existed largely in isolation. Now two thirds of people admitted to hospital with a diagnosis of acute myocardial infarction really have metabolic syndrome—but 75% of these patients have completely normal total cholesterol concentrations.14 Maybe this is because total cholesterol isn’t really the problem?

The Framingham heart study sanctified total cholesterol as a risk factor for coronary artery disease, making statins the second most prescribed drug in the US and driving a multibillion dollar global industry. In the United Kingdom eight million people take statins regularly, up from five million 10 years ago. With 60 million statin prescriptions a year, it is difficult to demonstrate any additional effect of statins on reduced cardiovascular mortality over the effects of the decline in smoking prevalence and primary angioplasty.15

Despite the common belief that high cholesterol is a significant risk factor for coronary artery disease, several independent population studies in healthy adults have shown that low total cholesterol is associated with cardiovascular and non-cardiac mortality, indicating that high total cholesterol is not a risk factor in a healthy population.16 17 18

A recent “real world” study of 150 000 patients who were taking statins showed “unacceptable” side effects—including myalgia, gastrointestinal upset, sleep and memory disturbance, and erectile dysfunction—in 20% of participants, resulting in discontinuation of the drug.19 This is massively at odds with the major statin trials that report significant side effects of myopathy or muscle pain in only one in 10 000.

A meta-analysis of predominantly industry sponsored data reported that in a low risk group of people aged 60-70 years taking statins the number needed to treat (NNT) to prevent one cardiovascular event in one year was 345.20 The strongest evidence base for statins is in secondary prevention, where all patients after a myocardial infarction are prescribed maximum dose treatment irrespective of total cholesterol, because of statins’ anti-inflammatory or pleiotropic (coronary plaque stabilising) effects. In this group the NNT is 83 for mortality over five years. This doesn’t mean that each patient benefits a little but rather that 82 will receive no prognostic benefit.21 The fact that no other cholesterol lowering drug has shown a benefit in terms of mortality supports the hypothesis that the benefits of statins are independent of their effects on cholesterol.

Adopting a Mediterranean diet after a heart attack is almost three times as powerful in reducing mortality as taking a statin. The recently published PREDIMED randomised controlled trial was stopped early after it showed that in high risk people the Mediterranean diet achieved a 30% improvement over a “low fat” diet in terms of cardiovascular events.22

Pharmacotherapy can assuage the symptoms but can’t alter the pathophysiology. Doctors need to embrace prevention as well as treatment. The greatest improvements in morbidity and mortality have been due not to personal responsibility but rather to public health. It is time to bust the myth of the role of saturated fat in heart disease and wind back the harms of dietary advice that has contributed to obesity.

Notes

Cite this as: BMJ 2013;347:f6340

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

Read also - Top heart doctor: Unprocessed fatty foods may actually be good for you

Watch this excellent video on saturated fat and heart disease. http://www.abc.net.au/catalyst/stories/3876219.htm
Here are some quotes from the video:

Dr Johnny Bowden
"Sugar is far more damaging to the heart than fat ever was, and we're beginning to see this now. So, this focus on cholesterol has been incredibly destructive because we haven't looked at these real promoters of heart disease - inflammation, oxidative damage, sugar in the diet, and number one with a bullet - stress."

Dr Johnny Bowden
"Margarine is the perfect example of the stupidest nutritional swap-out in history. We had this trans fat-laden crappy manufactured product that we were eating because we were so phobic about saturated fat and cholesterol."
Dr Stephen Sinatra
"To switch to polyunsaturated fats with the vegetable oils, that's horrific advice. The polyunsaturated fats, the vegetable oils, these omega-6 oils, are inflammatory because they're very prone to oxidation."

Dr Stephen Sinatra
"It took decades to really entrench this myth. It's probably going to take a few more decades to get us out of this myth. But to vilify saturated fats I think is one of the worst things the medical profession has done."
Dr Ernest Curtis
"I'd love to see the medical establishment saying, 'Whoops, we were wrong'. That's not going to happen. Frankly, that generation is going to have to die off, and perhaps the generation coming up can do better."

Lancet retracts Jikei Heart Study - Steve Stiles

 Lancet retracts Jikei Heart Study as scandal cuts swath across journals

         London, UK - The editors of the Lancet have formally retracted its publication of the Jikei Heart Study [1], the latest and perhaps climactic chapter in a scandal involving researchers in Japan that already had driven the European Heart Journal to pull the Kyoto Heart Study from the record earlier this year [2].

The broader story about apparent improprieties in the conduct of the trials [3,4], both of which were on the angiotensin-receptor blocker valsartan (Diovan, Novartis) in Japanese hypertension patients and which share some investigators, also includes allegations of fraud involving five papers in Circulation and other American Heart Association journals that were coauthored by Kyoto senior author Dr Hiroaki Matsubara (Kyoto Prefectural University School of Medicine, Japan).
 
The Lancet retraction was initially covered by Retraction Watch [5], which along with Cardiobrief and other blog sites has been closely tracking the larger story cutting across different journals.

Sources

1. The Lancet editors. Retraction—Valsartan in a Japanese population with hypertension and other cardiovascular disease (Jikei Heart Study): A randomised, open-label, blinded endpoint morbidity-mortality study. Lancet 2013; DOI:10.1016/S0140-6736(13)61847-4. Available here.
2. Retraction of: Effects of valsartan on morbidity and mortality in uncontrolled hypertensive patients with high cardiovascular risks: KYOTO HEART Study. Eur Heart J 2013; 34:1023.
3. Mochizuki S, Dahlof B, Shimizu M, et al. Valsartan in a Japanese population with hypertension and other cardiovascular disease (Jikei Heart Study): A randomised, open-label, blinded endpoint morbidity-mortality study. Lancet 2007; 369: 1431-1439.
4. Sawada T, Yamada H, Dahlof B, Matsubara H. Effects of valsartan on morbidity and mortality in uncontrolled hypertensive patients with high cardiovascular risks: Kyoto Heart Study. Eur Heart J 2009; 30: 2461-2469.
5. Retraction Watch. Lancet retracts Jikei Heart Study of valsartan following investigation. Available here.

Related links

• Diovan data-manipulation scandal touches Novartis in Japan
  [Hypertension > Hypertension; Jul 19, 2013]
• AHA concerned over possible image fraud in five papers
  [heartwire > News; Mar 13, 2012]
• KYOTO and JIKEI HEART analyses show benefit of valsartan in Japanese hypertensive patients
  [Hypertension > Hypertension; Sep 01, 2010]
• Valsartan plus optimal medical therapy provides additional cardiovascular benefit in Japanese population
  [heartwire > News; Apr 26, 2007]
• KYOTO HEART study not quite sufficient to extend the role of ARBs to first-line therapy
  [Acute Coronary Syndromes > Acute coronary syndromes; Sep 01, 2009]
• Cardiovascular benefit of adding valsartan to optimal therapy in Japanese hypertensive population
  [heartwire > News; Sep 11, 2006]

Low Salt Diet Found to Increase Mortality - Dach

Low Salt Diet Found to Increase Mortality
Part 1
by Jeffrey Dach MD

Low Salt Diet Found to Increase Mortality The Low Salt Diet Revisited

A recent Lancet study on the effect of a low salt diet made headlines, finding that a low salt diet increases mortality for patients with congestive heart failure.(1-6) The study concluded there was not enough evidence to advise a low-salt diet for the rest of us. They doubted a low salt diet would benefit the population.(6) In this article we will re-examine the low salt diet, clear away the confusion, and make recommendations about salt intake, hypertension, and health.


Health Benefits of Salt

We know from many years of published studies that increasing salt intake increases blood volume and also blood pressure. Salt is essential for maintaining blood volume, blood pressure, and overall health. The salt content of blood is similar to ocean water. Both have sodium chloride, also known as salt.

Importance of Salt

One example of the importance of salt is the common practice of starting an intravenous solution of salt and water as the first line treatment for the trauma patient upon arrival to the hospital Emergency Room.

Low Salt Diet to Reduce Blood Pressure

One of the central dogmas of mainstream medicine is the “low salt diet” as a treatment for reducing blood pressure in the hypertensive patient. Indeed, popular wisdom says that the “low salt diet” is also healthy for the rest of us “normal” people who don’t have hypertension.(25) Along with the rest of my medical school class, I was indoctrinated to believe this. Is this really true? Many studies have looked at this question. They show the “low salt diet” will in fact reduce blood pressure slightly. However, this effect is minimal, and is counteracted by compensatory mechanisms that release harmful substances into the bloodstream, hormones and chemical mediators that counteract the “low salt diet”. The released chemical mediators include insulin, epinephrine, norepinephrine, renin, aldosterone, etc. These are harmful and damaging to the vascular system. (7-11)

Low Salt Diet Increases Cardiovascular Mortality

In addition, a number of studies have found that a “low salt diet” increases cardiovascular mortality. (5) A study published in the 1995 Hypertension found 4.3 times greater mortality in hypertensive men on a low salt diet.(12) They also found higher plasma renin in these men, a hormone produced by the body which causes salt and water retention by the kidney to compensate for the low salt diet.(12-15)

A 2011 JAMA provides the reasons for this increased mortality and says … (16)

The underlying mechanisms explaining the inverse association between cardiovascular mortality and 24-hour urinary sodium excretion might be that a salt intake low enough to decrease blood pressure also increases sympathetic nerve activity, decreases insulin sensitivity, activates the renin-angiotensin system, and stimulates aldosterone secretion. (16)

A 1998 JAMA report found that a low salt diet increased plasma renin 3.6-fold and aldosterone by 3.2-fold, increases that were proportional to the degree of sodium restriction. (17) The authors also reported the “low salt diet” increased other harmful substances such as noradrenaline, cholesterol, and low-density lipoprotein cholesterol (LDL). (17) A 1999 report in American Journal of Hypertension found that “moderate salt restriction aggravates both systemic and vascular insulin resistance.” (18)
==========================================================
Read the complete article here.


Low Salt Diet Part Two

In Part One, we discussed the low salt diet, and studies which show an increased mortality from a salt restricted diet. You may have been wondering about this if you saw a recent article in the New York Times by Jane Brody extolling the virtues of a low salt diet.(1) Jan Brody quotes a computer simulation model that predicted 500,000 lives saved by eliminating dietary salt in a program similar to Finland which was described in a New England Journal article.(2,3)

Gary Schwitzer does a good job on their blogs explaining where the Jane Brody article goes wrong.(4,5).

Research by Jan A. Staessen, MD, PhD, of the University of Leuven in Belgium and colleagues, raises questions regarding whether population-wide sodium restriction will actually lower cardiovascular risks. (5,6) In actually clinical studies where 24 hr sodium excretion is measured in 3681 participants and followed over 8 years, this is what they found:

In this population-based cohort, systolic blood pressure, but not diastolic pressure, changes over time aligned with change in sodium excretion, but this association did not translate into a higher risk of hypertension or CVD complications. Lower sodium excretion was associated with higher CVD mortality.(5,6)

 

This type of data seems to suggest that salt restriction has been over-hyped as an intervention, and although will help to slightly reduce blood pressure, does not reduce mortality or complications of cardiovascular disease.

I would agree with Jane Brody that hypertension, heart disease and other health problems are a direct result of diets containing large amounts of processed salt (NaCl), Trans Fats, Sugars, MSG, Aspartame, GMO corn and GMO Soy, and added wheat fillers. To focus attention on the salt content alone, while ignoring the other harmful additives may be not be a valid exercise.

The “low salt diet” for reducing blood pressure in the hypertensive patient is a central dogma of mainstream medicine. Indeed, popular wisdom says that the “low salt diet” is also healthy for the rest of us “normal” people who don’t have hypertension. Along with the rest of my medical school class, I was indoctrinated to believe this. Is this really true? Many studies have looked at this question. They show the “low salt diet” will in fact reduce blood pressure slightly. However, this effect is minimal, and is counteracted by compensatory mechanisms that release harmful substances into the bloodstream, that counteract the “low salt diet”. The released chemical mediators include insulin, epinephrine, norepinephrine, renin, aldosterone, etc. These are harmful and damaging to the vascular system.

In addition, a number of studies have found that a “low salt diet” increases cardiovascular mortality. A study published in the 1995 Hypertension found 4 times greater mortality in hypertensive men on a low salt diet.
=================================================================
Read the complete article here.

This new link added April 30, 2013: WebMD offers dangerous junk science-based dietary salt advice… This article states that "… even though one of its cited “experts” tacitly admits there is no established cause-and-effect relationship between typical/normal/current salt intake and adverse health effects."

Another article from Food Politics by Marion Nestle found here and

here: http://news.nationalpost.com/2013/09/22/little-evidence-sharp-reductions-in-salt-consumption-will-improve-health-heart-researcher-says/

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/

Why Women Should Stop Their Cholesterol Lowering Medication - Hyman

Why Women Should Stop Their Cholesterol Lowering Medication

by Dr Mark Hyman   January 19th, 2012

If you are a post-menopausal women with high cholesterol, your doctor will almost certainly recommend cholesterol lowering medication or statins. And it just might kill you. A new study in the Archives of Internal Medicine found that statins increase the risk of getting diabetes by 71 percent in post-menopausal women.

Since diabetes is a major cause of heart disease, this study calls into question current recommendations and guidelines from most professional medical associations and physicians. The recommendation for women to take statins to prevent heart attacks (called primary prevention) may do more harm than good.

Statins have been proven to prevent second heart attacks, but not first heart attacks.

Take it if you already have had one, but beware if your doctor recommends it for you if have never had a heart attack.

This current study adds to an increasing body of literature questioning the benefits of statins, while highlighting their potential risks.

New Study Shows 48 Percent Risk of Diabetes in Women Who Take Statins

This study examined the data from the large government sponsored study called the Women’s Health Initiative, the same study that disabused us of the idea that Premarin prevented heart attacks in postmenopausal women.

In fact, based on this randomized controlled trial, estrogen replacement therapy, once considered the gold standard of medical care for the prevention of heart disease, was relegated to the trash bin of history joining medicine’s many other fallen heroes including DES, Thalidomide, Vioxx, Avandia, and more.

In this new study researchers reviewed the effect of statin prescriptions in a group of 153,840 women without diabetes and with an average age of 63.2 years. About 7 percent of women reported taking statin medication between 1993 and 1996. Today there are many, many more women taking statin medications, thus many more are at risk from harm from statins.

During the 3-year period of the study, 10,242 new cases were reported – a whopping 71 percent increase in risk from women who didn’t take statins. This association stayed strong at a 48 percent increased risk of getting diabetes, even after taking into account age, race/ethnicity, and weight or body mass index. These increases in disease risk were consistent for all statins on the market.
This effect also occurred in those with and without heart disease. Surprisingly disease risk was worse in thin women. Minority women were also disproportionately affected. The risk of diabetes was 49 percent for white women, 57 percent for Hispanic women, and 78 percent for Asian women.
But in a typical “my mind’s made up, don’t confuse me with the facts” statement by the medical establishment, the researchers said we should not change our guidelines for statin use for the primary prevention of heart disease.

In a large meta-analysis published in the Lancet last year, scientists found that statins increased the risk of diabetes by 9 percent. If current guidelines were followed for those who should take statins, and people actually took them (thank God only 50 percent of prescriptions are ever filled by patients), there would be 3 million more diabetics in America. Oops.

Other studies have recently called into question the belief that high cholesterol levels increase your risk of heart disease as you get older. For those over 85 it turns out having high cholesterol will protect you from dying from a heart attack, and, in fact, from death from any cause.

Low Cholesterol May Kill You

A recent study showed that in healthy older persons, high cholesterol levels were associated with lower non-cardiovascular-related mortality. This is extremely concerning because millions of prescriptions are written every day to lower cholesterol in the older population, yet no association has been found between higher cholesterol and heart disease deaths for those aged 55 to 84; and for those over 85, the association seems to be inverse — higher cholesterol predicts lower risk of death from heart disease.

The pharmaceutical industry, medical associations, and academic researchers whose budgets are provided by grants from the pharmaceutical industry continue to preach the wonders of statins, but studies like these should have us look good and hard at our current practices. Are we doing more harm than good?

Cardiologists recommend putting statins in the water and giving them out at fast food restaurants and having them available over the counter. They believe in driving cholesterol as low as possible. Statin prescriptions are handed out with religious fervor, but do they work to prevent heart attacks and death if you haven’t had a heart attack already?

Bottom line: NO! If you want to learn why this is true, read on.

Statins Don’t Work to Prevent First Heart Attacks

Recently, the Cochrane Group did a review of all the major statin studies by an international group of independent scientists. The review failed to show benefit in using statins to prevent heart attacks and death. In addition, many other studies support this and point out the frequent and significant side effects that come with taking these drugs. (i) If scientists found that drinking two glasses of water in the morning prevented heart attacks, even if the evidence was weak, we would jump on board. Big up side, no down side.

But this is not the case with statins. These drugs frequently cause muscle damage, muscle cramps, muscle weakness, muscle aches, exercise intolerance (ii) (even in the absence of pain and elevated CPK – a muscle enzyme), sexual dysfunction, liver and nerve damage and other problems in 10-15 percent of patients who take them. (iii) They can also cause significant cellular, muscle, and nerve injury as well as cell death in the ABSENCE of symptoms. (iv)

There is no lack of research calling into question the benefits of statins. Unfortunately, that research doesn’t get the benefit of billions of dollars of marketing and advertising that statins do. One big trial was touted as proving statins work to prevent heart attacks, but the devil is in the details.

It was the JUPITER (v) trial that showed that lowering LDL (or bad cholesterol) without a reduction in inflammation (measured by C-reactive protein) didn’t prevent heart attacks or death. (vi) Statins happen to reduce inflammation so the study has been touted as proof of the effectiveness of these medications.

Mind you it wasn’t lowering the cholesterol that helped (which is the intended purpose of statins), but the fact that they lower inflammation. What is ignored by people who use this study to “prove” that statins work is the fact that there are so many better ways to lower inflammation than taking these drugs.

Yet other studies have shown no proven benefit for statins in healthy women (vii) with high cholesterol or in anyone over 69 years old. (viii) Some studies even show that aggressive lowering of cholesterol can cause MORE heart disease. The ENHANCE trial showed that aggressive cholesterol treatment with two medications (Zocor and Zetia) lowered cholesterol much more than one drug alone, but led to more arterial plaque and no fewer heart attacks. (ix)

Other research calls into question our focus on LDL or the bad cholesterol. We focus on it because we have good drugs to lower it, but it may not be the real problem. The real problem is low HDL that is caused by insulin resistance (diabesity).

In fact studies show that if you lower the bad (LDL) cholesterol in people with low HDL (good cholesterol) that is a marker of diabesity – the continuum of obesity, prediabetes and diabetes – there’s no benefit. (x)

Most people simply ignore the fact that 50-75 percent of people who have heart attacks have normal cholesterol. (xi) The Honolulu Heart Study showed older patients with lower cholesterol have higher risks of death than those with higher cholesterol. (xii)

Some patients with multiple risk factors, or who have had previous heart attacks do benefit, but when you look closely the results are underwhelming. It’s all in how you spin the numbers. For high-risk males (those who are overweight and have high blood pressure, diabetes, and/or a family history of heart attacks) and are younger than 69 there is some evidence of benefit, but one hundred men would need to be treated to prevent just one heart attack.

That means that 99/100 men who take the drug receive no benefit. Drug ads say the risk is reduced by 33 percent. Sounds good, but that just means the risk of getting a heart attack goes down from 3 percent to 2 percent.

Despite the extensive data showing that statins are a questionable therapy at best, they are still the number one selling drug in the US. What isn’t so well known is that 75 percent of statin prescriptions are written for people who will receive no proven benefit. The cost of these prescriptions? Over $20 billion a year.

Yet somehow the 2004 National Cholesterol Education Program guidelines expanded the previous guidelines to recommend that even more people without heart disease take statins (from 13 million to 40 million) (xiii) What are we thinking?

Why would respected scientists go against the overwhelming research that statins don’t prevent heart disease in people who haven’t already had a heart attack?

You can find the answer if you follow the money. Eight of the nine experts on the panel who developed these guidelines had financial ties to the drug industry. Thirty-four other non-industry affiliated experts sent a petition to protest the recommendations to the National Institutes of Health saying the evidence was weak.

What Should Women Do?
It is time to push the sacred cow of statins overboard.
But first let me say this. If you have had a heart attack, or have heart disease, the evidence shows they do in fact help protect against a second heart attack, so keep taking them. However, you should be aware that most prescriptions for statins are given to healthy people whose cholesterol is a little high. For these folks the risk clearly outweighs the benefit.

The editorial that accompanies the recent study on women taking cholesterol-lowering medication that I opened this article with was quite clear. Dr. Kirsten Johansen from the University of California, San Francisco said that the increased risk of diabetes in women without heart disease has “important implications for the balance of risk and benefit of statins in the setting of primary prevention in which previous meta-analyses show no benefit on all-cause mortality.”

In plain English, she said that we shouldn’t be using statin drugs for women without heart disease because:

1. The evidence shows they don’t work to prevent heart attacks if you never had one.
2. They significantly increase the risk of diabetes.

Treating risk factors like high cholesterol is misguided. We must treat causes – what we eat, how much we exercise, how we handle stress, our social connections and environmental toxins are all more powerfully linked to creating health and preventing disease than any drug on the market.
Remember what you put at the end of your fork is more powerful than anything you will ever find at the bottom of a pill bottle.

My new book The Blood Sugar Solution, which comes out at the end of February, gives exact details on what you should put at the end of your fork to prevent and reverse diabesity. It provides a comprehensive solution to the health problems facing our nation today.

Now I’d like to hear from you …

What do you think of statins?

Have you taken statins? What has your experience been?

Why do you think the medical establishment prescribes drugs that research shows don’t work?
Please leave your thoughts by adding a comment below – but remember, we can’t offer personal medical advice online, so be sure to limit your comments to those about taking back our health!

To your good health,
Mark Hyman, MD

References:

---

(i) Abramson J, Wright JM. Are lipid-lowering guidelines evidence-based? Lancet. 2007 Jan 20;369(9557):168-9

(ii) Sirvent P, Mercier J, Lacampagne A. New insights into mechanisms of statin-associated myotoxicity. Curr Opin Pharmacol. 2008 Jun;8(3):333-8.

(iii) Kuncl RW. Agents and mechanisms of toxic myopathy. Curr Opin Neurol. 2009 Oct;22(5):506-15. PubMed PMID: 19680127.

(iv) Tsivgoulis G, et. al, Presymptomatic Neuromuscular Disorders Disclosed Following Statin Treatment, Arch Intern Med. 2006;166:1519-1524

(v) Mora S, Ridker PM. Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER)–can C-reactive protein be used to target statin therapy in primary prevention? Am J Cardiol. 2006 Jan 16;97(2A):33A-41A.

(vi) Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ; JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008 Nov 20;359(21):2195-207.

(vii)Abramson J, Wright JM. Are lipid-lowering guidelines evidence-based? Lancet. 2007 Jan 20;369(9557):168-9

(viii) IBID

(ix) Brown BG, Taylor AJ Does ENHANCE Diminish Confidence in Lowering LDL or in Ezetimibe? Engl J Med 358:1504, April 3, 2008 Editorial

(x) Barter P, Gotto AM, LaRosa JC, Maroni J, Szarek M, Grundy SM, Kastelein JJ, Bittner V, Fruchart JC; Treating to New Targets Investigators. HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events. N Engl J Med. 2007 Sep 27;357(13):1301-10.

(xi) Hansson GK Inflammation, Atherosclerosis, and Coronary Artery Disease N Engl J Med 352:1685, April 21, 2005

(xii) Schatz IJ, Masaki K, Yano K, Chen R, Rodriguez BL, Curb JD. Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. Lancet. 2001 Aug 4;358(9279):351-5.

(xiii) http://www.nhlbi.nih.gov/about/ncep/index.htm

About Dr Mark Hyman

MARK HYMAN, MD is dedicated to identifying and addressing the root causes of chronic illness through a groundbreaking whole-systems medicine approach called Functional Medicine. He is a family physician, a four-time New York Times bestselling author, and an international leader in his field. Through his private practice, education efforts, writing, research, and advocacy, he empowers others to stop managing symptoms and start treating the underlying causes of illness, thereby tackling our chronic-disease epidemic. More about Dr. Hyman or on Functional Medicine. Click here to view all Press and Media Releases

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

Read the complete article here.

Scant Evidence That Salt Raises BP - Kaiser

Scant Evidence That Salt Raises BP, Review Finds

By Chris Kaiser, Cardiology Editor, MedPage Today  Published: December 04, 2012

 

The evidence for health benefits associated with salt reduction is controversial and the "concealment of scientific uncertainty" is a mistake, researchers suggested.

Controversy about what effect too much sodium intake has on the body goes back to the early part of the 20th century, according to Ronald Bayer, PhD, and colleagues from Columbia University Mailman School of Public Health in New York City.

But in the last few years, the discourse has reached a fever pitch, they wrote online in Health Affairs.

In 2011, for example, the Journal of the American Medical Association published a study by Stolarz-Skrzypek et al. that found only a weak correlation between salt and blood pressure. An editorial in the Lancet lambasted the JAMA study as "disappointingly weak" and "likely to confuse public perceptions of the importance of salt as a risk factor for high blood pressure, heart disease, and stroke."

Also in 2011, the Cochrane Review published two studies finding little or no relationship with all-cause mortality and salt reduction. The Lancet criticized both the Cochrane Library and the authors, saying, "They have seriously misled the press and thereby the public."

One of those reviews had concluded that "after more than 150 randomized controlled trials and 13 population studies without an obvious signal in favor of sodium reduction, another position could be to accept that such a signal may not exist."

Bayer and colleagues cited several studies that could not find a link between salt intake and elevated blood pressure, including a 1967 study of the Framingham cohort, and Japanese and Scottish reports in the 1980s totalling 15,000 people that concluded the association between sodium and blood pressure is "extremely weak."

The researchers noted that most of the evidence pointed to the weakest of correlations between salt and blood pressure. Yet, the cause to reduce salt was taken up by government agencies with special speed.

They cited a 2010 Institute of Medicine report called "Strategies to Reduce Sodium Intake in the United States." In the report, the IOM claimed that the "harmful relationship of salt with hypertension has been known for 40 years," which Bayer and colleagues argue is debatable -- based on the evidence.

"The [IOM] report was welcomed by the incoming president of the the American Society of Hypertension," the investigators wrote, "who warned that the 'outcomes mafia' might challenge the justification for a regulatory approach."

In 2011, the FDA also called for data and recommendations "that would help it shape regulatory policy on salt in food."

"All the while, skeptics still were asking for the evidence," Bayer and colleagues wrote.
More than 20 years prior to the IOM report, C. Everett Koop, MD, the U.S. Surgeon General, issued a report noting that government agencies were "very quick to embrace the importance of salt reduction in the 1970s and 1980s, which stood in stark contrast for the snail's pace of recommendations related to reducing blood cholesterol levels."

The authors cited many more studies finding little association between salt and blood pressure that did not eliminate the stigma attached to the mineral.

Advocates for salt reduction questioned the science behind studies that didn't conform to their opinion, and proponents partially blamed the food industry because it was in their best interest to muddy the waters and keep the debate going.

One of the interesting things about this debate, Bayer and colleagues pointed out, was that you could find respected academics on both sides.

"At the most fundamental level, we believe that it is essential to recognize the role that judgment and values must play in evidence-informed policy making," the authors concluded.

"Science must remain open, skeptical, and concerned about unmeasured confounding and selection bias in studies that accompany even the best efforts to articulate the evidence for new interventions," they added.

The investigators said that one of the reviewers of this paper had asked, "In the end, does the harm of exaggerating certainty do more harm than good? After all, it would be very hard to make any policy from a position of informed, complicated, contextualized ambivalence."

They concluded that the "concealment of scientific uncertainty is a mistake that serves neither the ends of science nor good policy. Simplistic pictures of translation from evidence to action distort our ability to understand how policy is, in fact, made and how it should be made."
==================================================================
Read the complete article here.

Another article 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/

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.

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