The Cause of Heart Disease? NOT Dietary Cholesterol, Goverment finally admits

For 40 years Americans have been eating fewer eggs, butter and red meat with saturated fat and cholesterol because US government policy makers told us not to.  We were told that dietary saturated fat and cholesterol were bad for our health and caused heart disease.  Manufactured foods such as margarine, egg substitutes, and low fat products laden with sugar or high fructose corn syrup to make them palatable were touted as the healthy way to go.

 

I have been advising my patients for most of my practice to stay away from the manufactured foods and eat whole foods, including eggs, red meat and butter.  And now, the US government finally agrees with me.

 

In February 2015 the 572-page Scientific Report of the 2015 Dietary Guidelines Advisory Committee was released.  Buried on page 91 it states, "...available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum (blood) cholesterol....Cholesterol is not a nutrient of concern for overconsumption."

 

When the original recommendations were made in the 1960s and 1970s, the government policy relied on a kind of science called epidemiological or observational studies.  In these studies researchers follow large groups of people over many years.  However, these studies are limited in that they can only show an association between two things, and not that one causes the other.  Therefore a hypothesis can be formed from these studies, but it takes more rigorous studies to prove them.

There are still dietary guidelines in the current report that I don't agree with.  They continue to recommend reducing saturated fats, to the point of recommending that even lean meat be removed from the list of healthy foods, even though several recent meta-analyses have shown that there are no studies that prove that saturated fats cause heart disease.

And they continue to recommend limiting salt intake, even though in 2013 an authoritative study by the Institute of Medicine contradicted that recommendation.

While there may be a general correlation between high serum levels of cholesterol and heart disease, it is only oxidized cholesterol that leads to atherosclerotic plaque (hardening of the arteries).  High levels of non-oxidized serum cholesterol are actually protective and essential to life and all cells.  Studies of the elderly show that those with low cholesterol levels have higher death rates than those with high cholesterol levels.

 

We should be focusing on what oxidizes the cholesterol.  Inflammation in the arteries causes oxidation of cholesterol, platelet aggregation and atherosclerotic plaque formation.  Rather than focusing so much on the cholesterol levels, in our office we test Lp-PLA2 levels, a marker for inflammation and plaque in the arteries, and Cardiac C-reactive Protein, a marker for inflammation in the body.

 

What causes inflammation in the arteries?  The two most common causes are high blood glucose and insulin levels and high Homocysteine levels.  Anything else that causes inflammation in the body, such as autoimmune diseases, chronic infections, etc. can also increase inflammation in the arteries.

 

The increase of consumption of low fat, high simple carbohydrate diets high in sugar and processed grains has caused an explosion of pre-diabetes and diabetes.  The insulin levels rise to try and lower the blood glucose levels and try to drive glucose into the cells.  The cells start to become resistant to the high levels of insulin, and blood glucose levels rise. 

 

When blood glucose rises, it attaches to the proteins in a process called "glycosylation," which damages the protein and cells.  The amount of glycosylation in the body is measured by the Hemoglobin A1C.  If that level is elevated, is shows that damage is already being done in the body and in the arteries, even though it may not yet be considered full-blown diabetes.

 

When insulin levels rise, blood pressure rises, triglycerides and sometimes cholesterol increases, and it causes inflammation in the body and in the arteries.

 

Therefore, the recommendations by the government and the American Heart Association to cut down on dietary fat and cholesterol may have even worsened our health.  By cutting out meat and eggs, we have eaten more grains, pasta, sugar, high fructose corn syrup and polyunsaturated fats.  Over the past 50 years, Americans have cut saturated fat intake by 25% and increased carbohydrates by more than 30%.  However, well done studies are showing that a diet high in sugar, refined grains and polyunsaturated fats increases the risk of obesity, diabetes and heart disease much more than a diet high in natural fats and cholesterol.

 

Homocysteine is a non-protein amino acid, important in the synthesis of methionine and cysteine.  High Homocysteine levels can cause endothelial (cells that line the inner arteries) cell injury, causing inflammation and atherosclerotic plaques.

 

High levels of Homocysteine are caused by a reduction in three simple nutrients:  Folate, B-12 and B-6.  Today most of our processed foods contain these nutrients as additives.  Red meat and whole grains have higher levels of these vitamins.  However, around 40% of the population has a genetic defect which keeps the body from creating the activated form of these vitamins which are necessary to reduce Homocysteine.  This is a mutation of the MTHFR genes (See my blog from February to find out more about this mutation).  If you have a family history of heart disease, make sure you are tested for this mutation.

 

So what is my advice on reducing heart disease?

• Check inflammatory markers Lp-PLA2 and Cardiac C-reactive protein
• Check Homocysteine levels
• Reduce oxidation of cholesterol with high levels of anti-oxidants such as those found in SpringTree SuperMulti Plus.
• Balance insulin and blood glucose with a whole foods low carbohydrate diet.  Don't forget the natural fats--they balance blood sugar and give us energy in place of the carbs.  Also consider using SpringTree Glucose Balance
• Reduce Homocysteine levels with the activated forms of B-12, folate and B-6, called methylcobalamine. 5-MTHF, and P-5-P, as found in SpringTree Methylation Factors.
• Reduce inflammation with fish oil
• Reduce inflammation with proteolytic enzymes and herbs such as turmeric, found in SpringTree's Pain and Inflammation supplement.

SpringTree Supplements can be found at www.springtreehealth.com

 

Until we meet again,

Dr. Judi

Inflammation: the Good, the Bad and the Ugly; The Cause of Most Chronic Diseases

Inflammation is very important to our bodies.  It is a protective part of our immune system to fight infection and other foreign invaders and to initiate the healing process.  Inflammatory cells aid the body's healing mechanism.  Inflammation is not the same as infection.  An infection is caused by a micro-organism. Inflammation is the body's response to fight the micro-organism.

Acute inflammation is the initial response of the body to harmful stimuli, causing and increased movement of plasma and leukocytes (especially granulocytes) from the blood to the injured tissues.  It usually appears within a few minutes or hours and ceases on the removal of the injurious stimuli.  The classic signs of acute infection are pain, heat, redness, swelling and loss of function.  Without inflammation the body would not be able to heal well.  For example, when inflammation causing heat is generalized, we experience it as a fever.  The fever is part of the body's immune response to fighting the infection.  It has been shown in studies that reducing a fever with medicine increases the length of time of an infection.  It has also been shown that taking anti-inflammatory medications continuously after an injury increases the time it takes to heal the injury.

However, when inflammation becomes chronic, it can cause damage to the body, either locally (such as in tendinitis, tendinitis, knee arthritis caused by injury, etc.) or systemically.  These can be caused by overuse (not allowing the injury to heal), using enough anti-inflammatory medication so that it cannot completely heal, genetics, chronic low grade infection, the SAD diet (Standard American Diet), dysbiosis (an alteration in intestinal bacteria), toxins such as heavy metals and environmental pollutants, improper healing from surgery, etc.  Common chronic inflammatory illnesses are:  acne, allergies, asthma, autoimmune diseases, celiac disease, chronic urinary tract infections, interstitial cystitis and prostatitis, chronic kidney disease, Crohn's disease and ulcerative colitis, osteoarthritis and rheumatoid arthritis, etc.  Inflammation of the brain and gut has been implicated in ADHD and autism, depression and other mood disorders.

In the last couple of decades, more evidence is being found through research that most of the chronic diseases leading to death are also caused by chronic inflammation, including heart disease, diabetes, Alzheimer's disease, and cancer.  For example, atherosclerosis, which causes heart attacks and heart disease, was considered to be caused by high cholesterol.  More recent studies show that inflammation is implicated in every stage of this disease.  Most scientists studying the inflammatory cause of heart disease believe the moderate success of the statin drugs in lowering cardiovascular events is more from their anti-inflammatory effect than by lowering the LDL.

Studies are also showing that inflammation plays a large role in cancer.  It is felt that inflammation can cause cell mutation leading to cancer, and inflammation has been shown to promote tumor growth and metastasis.

Once chronic inflammation has set in a cascade of problems results, making it more difficult to heal.  For example, inflammation can cause an increase in insulin, which also causes inflammation.  Elevated insulin holds onto fat in the body and causes obesity.  Fat cells also secrete inflammatory chemicals and increase inflammation in the body.  This increases insulin further and leads to insulin resistance.  This can lead to Diabetes Type 2, which increases inflammation in the macro- and micro-circulation, causing damage to the arteries.  The arterial wall damage causes a release of inflammatory cells and chemicals to repair it, which can lead to platelet aggregation and plaque deposition.  This can lead to heart and vascular disease.

Most of us are dealing with one or more of these problems and have no idea of how to heal it.  Most doctors simply treat the symptoms rather than dealing with the root cause:  inflammation.  My next blog will look into medications generally used for the chronic inflammation that threatens our health and our lives, how well they work and if they are safe.

Until we meet again,
Dr. Judi

Are Statins Beneficial in Preventing Heart Disease?

If you are taking a statin drug to prevent heart disease even though your cholesterol levels may be normal, think again.

The following is quoted from Family Practice News, Volume 40, Issue 12, Pages 10-11 (July 2010):

Studies Dispute Statins Benefits for Prevention

The only large clinical trial to find that statins reduce mortality in patients taking them for primary prevention—a group that comprises 75% of statin users—was so seriously flawed that its conclusions were termed “clinically inconsistent” and invalid by one group of researchers and “extreme and exaggerated” by another, according to separate reports.

In the first critique of the 2008 JUPITER (Justification for the Use of Statins in Primary Prevention) trial, Dr. Michel de Lorgeril of Université Joseph Fourier and Centre National de la Recherche Scientifique, Grenoble, France, and his associates, analyzed the methods and findings of this only major study to claim that rosuvastatin produced a striking decrease in mortality in low-risk patients who have no evidence of coronary heart disease. These findings, which immediately provoked controversy, “have undoubtedly propelled many healthy persons without elevated cholesterol levels onto long-term statin treatment,” Dr. de Lorgeril and his colleagues said.

First among its major flaws, JUPITER was terminated early and apparently without proper justification according to the study's own protocol prespecifications. Early termination, a practice confined largely to industry-sponsored trials, tends to introduce biases that exaggerate the benefit and minimize the long-term harm of the treatment being assessed, according to the researchers. In this case, it also meant that the study was stopped just as mortality curves between the statin group and the control group had begun to converge, “suggesting that the borderline significant difference between groups may have disappeared” if follow-up had not been prematurely terminated, they wrote.

The main justification for terminating JUPITER was explained as an “unequivocal reduction in cardiovascular mortality” with statin therapy. Yet the JUPITER investigators did not include data on cardiovascular mortality in their published report. Readers would have to infer this result by extrapolating from data on a table. When examined closely, however, that data showed identical cardiovascular mortality between the treatment groups.

“Such a lack of effect on cardiovascular mortality [together] with a strong effect on nonfatal complications strongly suggests a bias in the data set and should have led to the continuation of the trial rather than to its premature ending,” Dr. de Lorgeril and his colleagues asserted.

Second, the ratio of fatal to nonfatal MI was so low as to be “incredible.” In particular, the case-fatality rate in the placebo group was only 8% when it would be expected to be about 50%, “a clinical inconsistency that suggests a major flaw in the study.” Moreover, the case-fatality rate with rosuvastatin was 29%, which implies that the “beneficial” drug actually tripled the case-fatality rate, they noted.

Third, JUPITER failed to explain why a strikingly high number of deaths—19 of 31 deaths in the rosuvastatin group and 25 of 37 deaths in the placebo group—were attributed to cardiovascular causes other than MI or stroke. Proponents of the JUPITER study argued after its publication that this referred to causes “such as aneurysm rupture.”

“Would this mean that in the same period of time there were 6 fatal infarctions and 25 fatal aneurysm ruptures in the placebo group? This is highly unlikely,” Dr. de Lorgeril and his associates said.

JUPITER also failed to report data on sudden cardiac deaths, which is surprising given that this is “the simplest and most reliable diagnosis in cardiology” and that it usually comprises 65%-70% of total cardiac mortality. “The way sudden cardiac death is reported—or not reported—may be a good indicator of the quality of the methods used in a trial,” they noted.

Equally important to these methodological flaws, the JUPITER trial involved several conflicts of interest.

“It was conducted by a sponsor with obvious commercial interests. Nine of 14 authors of the JUPITER article have financial ties to the sponsor. The principal investigator has a personal conflict of interest as a co-holder of the patent for the C-reactive protein test” that figured prominently in the rationale for statin therapy.

In addition, the monitoring board that made the decision to halt the trial early was chaired by an investigator who “has been and still is involved in many other industry-sponsored lipid-lowering trials,” Dr. de Lorgeril and colleagues said (Arch. Intern. Med. 2010;170:1,032-6).

“In conclusion, the results of the JUPITER trial are clinically inconsistent and therefore should not change medical practice or clinical guidelines.” Given that all 12 of the other large cholesterol-lowering trials conducted so far have failed to show any benefit from statins as primary prevention, it appears that “the presumed preventive effects of cholesterol-lowering drugs have been considerably exaggerated,” they said.

In the second study, Dr. Kausik K. Ray of the University of Cambridge (England) and his associates performed a meta-analysis of 11 randomized controlled trials that assessed the effects on all-cause mortality of statins versus a placebo or control therapies on all-cause mortality. They restricted their analysis to data on high-risk patients with no known cardiovascular disease and included previously unpublished data, “to provide the most robust information to date” on statins as primary prevention in this patient group.

The meta-analysis involved 65,229 men and women in predominantly Western populations, with approximately 244,000 person-years of follow-up. There were 2,793 deaths during an average of 4 years of follow-up.

All-cause mortality was not significantly different between patients taking statins and those taking placebo or control therapies. This suggests that “the all-cause mortality reduction of 20% reported in JUPITER is likely to be an extreme and exaggerated finding, as often occurs when trials are stopped early,” Dr. Ray and his colleagues said (Arch. Intern. Med. 2010;170;1024-31).

This meta-analysis shows that statin therapy as primary prevention in high-risk patients is less beneficial than is generally perceived, and it can be inferred to be even less helpful in low-risk patients.

One of Dr. de Lorgeril's associates served as an expert in litigation involving the pharmaceutical industry (not involving rosuvastatin). Dr. Ray and an associate reported financial ties to the majority of companies that market lipid-lowering agents; other associates reported ties to Pfizer Inc., Astra Zeneca, Bristol-Myers Squibb, and Merck & Co.

My Take
Both Critiques Are On-Target
These two critiques offer valuable insights and likely will reignite the long-simmering controversy over the use of statins as primary prevention of cardiovascular events.

Dr. de Lorgeril's critical analysis highlights several anomalies in the JUPITER trial data. In particular, early termination of the study allowed for inflated estimates of benefits, understated harms, allowed the findings to be published earlier (and hence used to advantage in marketing), and reduced the cost of the trial—which all significantly benefited the industry sponsor and a financially invested research team.

Tens of billions of dollars of revenue for the sponsor over the patent life of the drug were at stake in the JUPITER trial, as well as potentially millions of dollars in royalties for the principal investigator. And with three-quarters of statin users taking the drugs for primary prevention, enormous revenues are at stake.

The analysis by de Lorgeril et al. clearly demonstrates why research must be free of incentives to find a particular desired result.

Dr. Ray's report presents what is to date the cleanest and most comprehensive meta-analysis of pharmacological lipid lowering for prevention.

The results make it clear that for primary prevention in the short term, statins' benefits are very small. And in the long term, although sincere advocates on both sides will try to convince us otherwise, we really must admit that we do not know.

LEE A. GREEN, M.D., is in the department of family medicine at the University of Michigan Medical School, Ann Arbor. He reported no financial conflicts of interest. His comments appeared in an editorial (Arch. Intern. Med. 2010:170;1007-8).

From Archives of Internal Medicine

PII: S0300-7073(10)70742-8
doi:10.1016/S0300-7073(10)70742-8

Dr. Judi here: Statin medications have a lot of side effects which have an insidious onset and are hard to tell that the statin is causing them, including muscle pain and memory loss.

Other studies have shown that the best benefit from statins comes from those with high cholesterol and high cardiac c-reactive protein between the ages of 40-60. It is interesting to note that the elderly do not receive benefit from lowering their cholesterol. In fact, those with the lowest cholesterol have higher death rates than those with higher cholesterol. So when your doctor tells you that the statin drugs are the new wonder drug, look at benefits vs. the risks, do some research, and determine what is best for you.

Until we meet again,
Dr. Judi