Cholesterol and Why Statin Drugs are Harmful

Cholesterol and Why Statin Drugs are Harmful

For decades, health experts have told us to watch our cholesterol levels, lower our intake of saturated fats, and consume low-fat diets.

An estimated 102 million Americans have cholesterol levels higher than 200. More than 20 million Americans are on statin drugs to lower cholesterol.

In theory, if we were following recommendations from doctors, dietitians, fitness experts, and dutifully taking our medications, we should be see a reduction in disease.

But the fact is…

We don’t.
So, it’s important to ask…

• Does eating high cholesterol foods correlate to rising cholesterol levels?

• Do high cholesterol levels necessarily mean you are at higher risk for cardiovascular disease or heart attack?

• Is the use of statin drugs safe and useful in reducing the levels of cholesterol in the body, thus lowering our disease risk?

A recent government study shows that raising levels of HDL “good” cholesterol using a drug did not diminish the chance of heart disease.
From the NY Times:

“Patients taking the medicine along with Zocor had higher levels of H.D.L. and lower levels of triglycerides, a fat in the blood. Despite these seeming improvements, the patients fared no better and may have done slightly worse than those taking Zocor alone. That is why the entire theory behind trying to increase H.D.L. levels in patients with heart disease may need rethinking.

In 2010 the British Medical Journal published a study revealing that the use of statin drugs was connected to liver, muscle, eye, and kidney problems. The results showed increased risk of moderate or serious liver dysfunction, acute renal failure, moderate or serious myopathy and cataracts.

Dietary cholesterol levels are not related to serum cholesterol levels

According to Nora Gedgaudas, of Primal Body – Primal Mind:

“No study to date has adequately shown any significant link between dietary and serum cholesterol levels…or any significant causative link between cholesterol and actual heart disease. Other than in uncommon cases of genetically based ‘familial hypercholesterolemia’ (where natural mechanisms which regulate cholesterol production fail and the body cannot stop overproduction-even here the proof of the problematic nature of cholesterol is dubious, at best), cholesterol is perhaps only potentially deleterious in and of itself in oxidized forms, occurring as a result of food processing methods (such as in “reduced fat” milks, powdered milk/eggs) and high heat cooking/frying. Inflammatory processes can also be oxidizing of cholesterol in the body. Other than this, ALL cholesterol in the body is the same. ‘HDL’ and ‘LDL’ only reflect transport mechanisms for healthy cholesterol and are meaningless measures of coronary heart disease risk (Enig, Ravnskov).

It is also important to realize that ‘HDL’ and ‘LDL’ are NOT actual cholesterol at all, but merely the protein transport mechanism for cholesterol. Again, All cholesterol is exactly the same. LDL takes cholesterol away from the liver to the extremities and other organs for various purposes and HDL merely returns the same cholesterol to the liver where it may be recycled.”

Gedgaudas believes it is more important to find out why your cholesterol levels are up. When we have stress, infections, clogged arteries, high carbohydrate diets which cause insulin resistance and diabetes, weight issues, free radical activity, and low thyroid function, these can cause the liver to produce more cholesterol in order to deal with excess inflammation. If cholesterol levels are rising, it’s always a sign of some underlying problem, but it doesn’t mean cholesterol is causing the problem.

Doctors are missing the problem

Prescriptions for high cholesterol go hand-in-hand with recommendations for low-fat diets. This type of diet is not only tasteless and unsatisfying, it is also grossly deficient in the most nutrient-dense and health supporting foods on the planet: foods with healthy fats and cholesterol.

In the last five years, doctors have started recommending that obese children take statin drugs. Of course, there is little to no thought given to the staples of the Standard American children’s diet: highly processed, increasingly lower and lower in fat ast time goes on, high-carb, sugary foods with little to no nutritional content.

It’s a wonder doctors don’t draw the obvious conclusion that these foods might possibly be the culprit to children’s health and obesity issues. But they don’t. What’s more, they fail to give good, sound nutritional advice. The result is that some children end up on drugs because apparently providing real, healthy foods that support growth and development is not what they believe will solve the problem.

Truths about cholesterol:

• Cholesterol is vital to health. Without it, we have hormonal, brain, heart, endocrine, and nervous system issues and damage. Lack of adequate cholesterol in the body leads to blood sugar imbalance, mineral deficiencies, chronic inflammation, infertility, allergies, and asthma.

• Cholesterol is beneficial to the gastrointestinal environment and lining because it improves cell-membrane integrity and can also help reduce excessive permeability of substances through the intestinal wall and into the bloodstream.

• Every cell in our bodies is made of cholesterol. Without it they would become leaky and porous, causing a flood of cholesterol taken from other parts of the body to repair damage.

• Cholesterol is the precursor to Vitamin D, which is now known to be a hormone rather than a vitamin, and is responsible for helping to digest fats, mineral metabolism, protecting bones, strengthening the immune system

• Cholesterol is a powerful anti-oxidant which protects the body from free-radical damage and aging

• The theory of cholesterol being unhealthy was originally created by food processing industries to villanize animal fats and products, which are direct competitors to vegetable oils, and also from the pharmaceutical industry to develop a market to sell cholesterol-lowering drugs. Lipitor and other Statin drugs are enormous profit-bringers for pharmaceutical companies.

Truths about statin drugs:

• Taking them only masks the problem going on in your body (for a little while) and doesn’t get to the cause of the problem, which is usually chronic inflammation due to poor dietary habits which cause nutritional deficiencies

• They deplete your body of vital nutrients, such as C0Q10, which is essential to heart health. Cardiologist Dr. Peter Langsjoen conducted a study involving 20 patients with completely normal heart function. Six months later, after being on 20 mg daily of Lipitor (a low dose), two-thirds of the patients were found to have abnormalities in the filling phase of the heart. Langsjoen’s conclusion was that this occurred due to the depletion of CoQ10. A lack of C0Q10 causes muscle pain and weakness, due to the prevention of energy being produced in the mitrochondria in the cell.

• These medications can also cause other types of muscle weakness and pain. In Denmark, researchers who studied 500,000 residents (approximately 9 percent of the population) discovered that those taking prescription medications to lower cholesterol were more likely to develop polyneuropathy, characterized as weakness and pain or tingling in the hands or feet and difficulty walking.

• They cause a marked decrease of cholesterol-production in the brain. According to Dr. Barry Sears, this leads to a loss of memory due to diminished production of new synaptic connections and loss of memory.

• They are costly in more ways than one: for your wallet and for your health. Eating healthy foods that naturally maintain normal cholesterol levels in the body costs less.

• They causes other side-effects, one of them being liver damage. Liver damage is dangerous and can lead to other health issues that are very unpleasant, expensive, and time-consuming to treat

Would the real enemies please stand up?

• Industrial fats – industrially-produced, polyunsaturated fats: canola, soybean, cottonseed, corn, peanut, safflower, and sunflower oils, shortening, butter substitutes and spreads, and other fake butter products. Some of these oils come from living things, but they are processed and chemically-altered which transforms them into trans-fats (even though the label may specifically read “no trans fats”), deodorized, and subjected to high- heat temperatures, rendering them nutritionally bankrupt and rancid.

• Sugar - which causes metabolic syndrome and blood sugar imbalance, leading to insulin resistance and diabetes, and heart attacks. In 2009, the United States was ranked 4th in sugar consumption levels in the world.

• Lack of nutrient-dense foods – modern diets are largely represented by nutritionally-deficient and heavily processed convenience foods which do not support the health of the human body. They cause build up in our arteries, liver damage, diabetes, premature aging, and cardiovascular disease.

• Stress - periods of stress deplete nutrients in the body causing inflammation, which triggers disease.

Watch this informative video by Dr. Mark Hyman about cholesterol:

How to keep inflammation and cholesterol levels normal in your body

Real, traditional fats from healthy animals and birds on pasture actually make us healthier because they are easy to digest and are some of the most nutrient-dense foods available. Looking back over the historical past, the human diet has always contained large amounts of fat and cholesterol.

Dr. Weston A. Price, author of Nutrition and Physical Degeneration, analyzed foods consumed by traditional, primitive peoples all over the world. In these populations, health was robust and disease nearly non-existent. He discovered that their diets allowed for at least four times the calcium and other minerals, and at least 10 times the fat-soluble vitamins and amino acids as the modern diet which were obtained from animal foods such as eggs, fish, shellfish, animal fats like butter, lard, and tallow, and organ meats. All these foods were high in cholesterol and fat.

If you want to maintain good health:

• Eat real, grass-fed butter

• Eat olive and coconut oil

• Eat grass-fed meats, poultry and pasture-raised eggs from reputable, local sources that raise their products sustainable

• Eat safe-sourced seafood

• Take cod liver oil

• Eat organic fruits and vegetables

• If you do eat grains, eat them sparingly and prepare them properly through soaking, sprouting, or fermenting. Eat grains with healthy fats such as milk, cream, butter, cheese, and other healthy foods containing fats such as olive oil, coconut oil, lard, tallow, bone marrow, and grass-fed meats and poultry.

• Avoid sugar – that means any refined carbohydrates – crackers, breads, rice cakes, cereals, pretzels, chips, bagels, pasta, desserts, sugary beverages (including juice and power “electrolyte” drinks).

• Avoid processed foods and drinks, and especially those with artificial sweeteners or high-fructose corn syrup

• Avoid unhealthy vegetable oils such as canola, soy, cottonseed, or safflower. These oils are too high in Omega 6s (which cause inflammation, cancer, and heart disease), are highly-processed at high temperatures making them rancid, and many of these oils are also likely to be genetically-modified as well, which has its own set of health risks.

• Lower stress levels with moderate and enjoyable exercise and relaxation strategies. Stress can severely deplete nutrients in the body, leading to heart disease.

For more information:
Importance of Dietary Fats
Cholesterol and Health – Chris Masterjohn
The Benefits of High Cholesterol – Weston A. Price Foundation
Dangers of Statin Drugs: What You Haven’t Been Told About Popular Cholesterol-Lowering Drugs – WAP Foundation
The Oiling of America – Sally Fallon and Dr. Mary G. Enig, PhD
I have high cholesterol, and I don’t care – The Healthy Skeptic
Medication Sense – Dr. Jay S. Cohen
Suggested reading:
Fat and Cholesterol are Good for You by Uffe Ravnskov, MD, PhD
The Cholesterol Delusion by Ernest N. Curtis, M.D.

This post is part of Sarah The Healthy Home Economist’s Monday Mania.
=====================================================================
Read the complete article here.

Myositis from Statin and PPI Drugs - Dach

A Neurosurgeon with a Painful Arm, Myositis from Statin and PPI Drugs by Jeffrey Dach MD

Sam, a 67 year old retired neurosurgeon came to see me because of pain and weakness in his right arm over the past 6 months. The pain and weakness is chronic and so severe, that he has given up Golf, his favorite pastime. His medical history is unremarkable except for his medications which includes a statin drug to lower cholesterol, simvastatin, which he has been taking for three years, and Prilosec a proton pump inhibitor (PPI) acid blocking drug for the past year for symptoms of heart burn.
Upon examination, there is diffuse tenderness of the muscles of the right shoulder and arm, as well as generalized muscle wasting.

Lab studies revealed extensive vitamin and mineral deficiencies suggesting malabsorption, B12 was low at 337 . There was a very low cholesterol level of 146.

My diagnosis was drug induced myositis from the combination of statin drug and proton pump inhibitor acid blocking drug. I advised the retired Neurosurgeon to stop these drugs and to take vitamin and mineral supplements to allow the muscles to heal.

Sam’s cardiologist and gasteroenterologist disagreed with my assessment and objected to the idea of stopping the drugs. They told Sam that these were “lifesaving drugs”. and were unlikely to be related to the muscle problems, and to continue them. In addition, Sam didn’t need any vitamins, as he was getting all his vitamins from his diet. Sam relayed this information to me on the phone. He thanked me for seeing him, but he would follow the advice of his other doctors, the cardiologist and the gasteroenterologist who he had known for years and trusted them.

Six months later, Sam’s wife called me to ask if there was anything I could do for Sam. He was still taking the statin anti-cholesterol drugs and the acid blocking drug ( PPI), and Sam’s conditionn had deteriorated to the point he was now in a wheel chair in a nursing home with early dementia.

Myopathy and Myositis are well known adverse effects of statin drugs which lower cholesterol. They also lower CoQ-10 levels and serve as mitochondrial toxins causing myopthy and dementia. The PPI drugs are also known to cause myopathy, thought to be caused by protein, mineral and vitmain malabsorption from lack of stomach acid.(1-9)



Links and References
Myopathy caused by proton pump inhibitors and statins
1) http://www.ncbi.nlm.nih.gov/pubmed/16758264
Eur J Clin Pharmacol. 2006 Jun;62(6):473-9. Epub 2006 Apr 22.
Myopathy including polymyositis: a likely class adverse effect of proton pump inhibitors? Clark DW, Strandell J.Department of Pharmacology and Toxicology, School of Medical Sciences, University of Otago, PO Box 913, Dunedin, New Zealand.
Polymyositis occurring in patients treated with omeprazole has been signalled as a possible adverse drug reaction (ADR) by the New Zealand Intensive Medicines Monitoring Programme (IMMP) and the WHO Collaborating Centre for International Drug Monitoring: the Uppsala Monitoring Centre (UMC). Polymyositis and other myopathies have also been reported in post-marketing data and in the medical literature in association with proton pump inhibitor (PPI) use. We wished to follow-up these signals and investigate the evidence of causality for the association of polymyositis and other myopathy with PPI use.
METHODS: Spontaneously reported ADRs from national monitoring centres are sent to the WHO ADR database (VigiBase). VigiBase was searched for case reports of the PPIs, omeprazole, pantoprazole, lansoprazole, esomeprazole and rabeprazole, with terms indicative of myopathy, and further information was elicited from the national centres to help establish causality. Literature sources were reviewed for the occurrence of the above terms in combination with PPIs.
RESULTS: In total, there were 292 reports of various myopathies with PPIs, excluding 868 cases of ‘myalgia’. In this analysis, 69 patients recovered when the drug was withdrawn and, in 15 patients, the reaction re-occurred when the drug was reinstated. In one-third of the 292 cases, the PPI was the single administered drug, and the PPI was the single suspected drug by the reporter in 57% of reports where concomitant medication was used. In this analysis, three index cases are documented. One involves the same patient taking three different PPIs (lansoprazole, esomeprazole and rabeprazole) at different time periods, with myalgia and muscle weakness occurring with all three drugs. In the two other index cases, myopathies with esomeprazole and omeprazole were reported with positive rechallenge, and causality was assessed as ‘possible’ and ‘certain’ by the reporting centres. In 27 cases myositis or polymyositis was reported. Other myopathies were reported, including 35 cases with rhabdomyolysis. In 9 of these cases, the PPI was withdrawn and the reaction abated. The PPI was reinstated in one patient, but the reaction did not re-occur. Time to onset was given in 17 of the rhabdomyolysis cases, rhabdomyolysis occurred with the first week in 9 cases, and in 3 cases the reaction occurred between 14 days to 3 months of treatment. In 12 of these patients, an HMG-CoA reductase inhibitor (statin) was taken concomitantly.
CONCLUSION: Case reports from the WHO ADR database, including index cases involving four out of five PPIs, along with evidence of a possible mechanism, provide compelling evidence that there is a causal association between members of the PPI drug class and myopathy including polymyositis. Evidence was also obtained to support the view that PPI use may be associated with occurrence of other myopathies, including the serious reaction rhabdomyolysis.
statin induced myopathy
2) http://www.ncbi.nlm.nih.gov/pubmed/12672737
JAMA. 2003 Apr 2;289(13):1681-90.
Statin-associated myopathy. Thompson PD, Clarkson P, Karas RH.Preventive Cardiology and Cardiovascular Research, Division of Cardiology, Hartford Hospital, Hartford, Conn 06102, USA.
Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are associated with skeletal muscle complaints, including clinically important myositis and rhabdomyolysis, mild serum creatine kinase (CK) elevations, myalgia with and without elevated CK levels, muscle weakness, muscle cramps, and persistent myalgia and CK elevations after statin withdrawal. We performed a literature review to provide a clinical summary of statin-associated myopathy and discuss possible mediating mechanisms. We also update the US Food and Drug Administration (FDA) reports on statin-associated rhabdomyolysis. Articles on statin myopathy were identified via a PubMed search through November 2002 and articles on statin clinical trials, case series, and review articles were identified via a PubMed search through January 2003. Adverse event reports of statin-associated rhabdomyolysis were also collected from the FDA MEDWATCH database. The literature review found that reports of muscle problems during statin clinical trials are extremely rare. The FDA MEDWATCH Reporting System lists 3339 cases of statin-associated rhabdomyolysis reported between January 1, 1990, and March 31, 2002. Cerivastatin was the most commonly implicated statin. Few data are available regarding the frequency of less-serious events such as muscle pain and weakness, which may affect 1% to 5% of patients. The risk of rhabdomyolysis and other adverse effects with statin use can be exacerbated by several factors, including compromised hepatic and renal function, hypothyroidism, diabetes, and concomitant medications. Medications such as the fibrate gemfibrozil alter statin metabolism and increase statin plasma concentration. How statins injure skeletal muscle is not clear, although recent evidence suggests that statins reduce the production of small regulatory proteins that are important for myocyte maintenance.
===================
3) http://www.ncbi.nlm.nih.gov/pubmed/22560377
Eur J Intern Med. 2012 Jun;23(4):317-24.
Statin induced myotoxicity. Sathasivam S. The Walton Centre NHS Foundation Trust, Lower Lane, Liverpool L9 7LJ, United Kingdom.
Statins are an effective treatment for the prevention of cardiovascular diseases and used extensively worldwide. However, myotoxicity induced by statins is a common adverse event and a major barrier to maximising cardiovascular risk reduction. The clinical spectrum of statin induced myotoxicity includes asymptomatic rise in creatine kinase concentration, myalgia, myositis and rhabdomyolysis. In certain cases, the cessation of statin therapy does not result in the resolution of muscular symptoms or the normalization of creatine kinase, raising the possibility of necrotizing autoimmune myopathy. There is increasing understanding and recognition of the pathophysiology and risk factors of statin induced myotoxicity. Careful history and physical examination in conjunction with selected investigations such as creatine kinase measurement, electromyography and muscle biopsy in appropriate clinical scenario help diagnose the condition. The management of statin induced myotoxicity involves statin cessation, the use of alternative lipid lowering agents or treatment regimes, and in the case of necrotizing autoimmune myopathy, immunosuppression.
4) http://www.ncbi.nlm.nih.gov/pubmed/22154355
Atherosclerosis. 2012 May;222(1):15-21.
Statins as a possible cause of inflammatory and necrotizing myopathies. Padala S, Thompson PD.
Department of Internal Medicine, University of Connecticut, Farmington, CT 06030, USA.
Hydroxy-methyl-glutaryl Co-A reductase (HMGCR) inhibitors or statins are a well recognized cause of a variety of skeletal myopathic effects which generally resolve on stopping the medication. Recent reports, however, suggest that statins are associated with a unique autoimmune myopathy wherein symptoms persist or even progress after statin discontinuation and require immunosuppressive therapy. We performed a systematic review to examine the association of statins with inflammatory (dermatomyositis/polymyositis) and necrotizing myopathies.
METHODS: We searched PubMed, Ovid and Scopus for English language articles addressing statin associated inflammatory and necrotizing myopathies. Given the paucity of cases, we extended the search to include articles in all languages.
RESULTS: The search yielded 14 articles reporting a possible association of statins with inflammatory myopathies describing 10 cases of polymyositis and 14 cases of dermatomyositis, and 4 articles reporting a possible association of statins with necrotizing myopathies describing 63 cases. One study identified a unique antibody directed against HMGCR in patients with necrotizing myopathy. Systemic immunosuppressive therapy was required in majority of these cases for resolution of symptoms.
CONCLUSION: Statins have recently been associated with a variety of inflammatory myopathies including polymyositis, dermatomyositis, and a necrotizing myopathy. The association of statins with necrotizing myopathy is strengthened by the discovery that the serum of some of these patients contains an anti-HMGCR antibody. This suggests that statins can cause or unmask an immune mediated myopathy.
5) http://www.if-pan.krakow.pl/pjp/pdf/2011/4_859.pdf
Pharmacol Rep. 2011;63(4):859-66.
Statin-induced myopathies. Tomaszewski M, Stępień KM, Tomaszewska J, Czuczwar SJ.
Source Department of Cardiology, Medical University of Lublin, Jaczewskiego 8, PL 20-954 Lublin, Poland.
Statins are considered to be safe, well tolerated and the most efficient drugs for the treatment of hypercholesterolemia, one of the main risk factor for atherosclerosis, and therefore they are frequently prescribed medications. The most severe adverse effect of statins is myotoxicity, in the form of myopathy, myalgia, myositis or rhabdomyolysis. Clinical trials commonly define statin toxicity as myalgia or muscle weakness with creatine kinase (CK) levels greater than 10 times the normal upper limit. Rhabdomyolysis is the most severe adverse effect of statins, which may result in acute renal failure, disseminated intravascular coagulation and death. The exact pathophysiology of statin-induced myopathy is not fully known. Multiple pathophysiological mechanisms may contribute to statin myotoxicity. This review focuses on a number of them. The prevention of statin-related myopathy involves using the lowest statin dose required to achieve therapeutic goals and avoiding polytherapy with drugs known to increase systemic exposure and myopathy risk. Currently, the only effective treatment of statin-induced myopathy is the discontinuation of statin use in patients affected by muscle aches, pains and elevated CK levels.
Free full text
6) http://www.ncbi.nlm.nih.gov/pubmed/20688875
Phys Ther. 2010 Oct;90(10):1530-42.
Effects of statins on skeletal muscle: a perspective for physical therapists.Di Stasi SL, MacLeod TD, Winters JD, Binder-Macleod SA.SourceUniversity of Delaware, Newark, Delaware, USA.
Hyperlipidemia, also known as high blood cholesterol, is a cardiovascular health risk that affects more than one third of adults in the United States. Statins are commonly prescribed and successful lipid-lowering medications that reduce the risks associated with cardiovascular disease. The side effects most commonly associated with statin use involve muscle cramping, soreness, fatigue, weakness, and, in rare cases, rapid muscle breakdown that can lead to death. Often, these side effects can become apparent during or after strenuous bouts of exercise. Although the mechanisms by which statins affect muscle performance are not entirely understood, recent research has identified some common causative factors. As musculoskeletal and exercise specialists, physical therapists have a unique opportunity to identify adverse effects related to statin use. The purposes of this perspective article are: (1) to review the metabolism and mechanisms of actions of statins, (2) to discuss the effects of statins on skeletal muscle function, (3) to detail the clinical presentation of statin-induced myopathies, (4) to outline the testing used to diagnose statin-induced myopathies, and (5) to introduce a role for the physical therapist for the screening and detection of suspected statin-induced skeletal muscle myopathy.
7) http://www.ccjm.org/content/78/6/393.long
Statin myopathy: A common dilemma not reflected in clinical trials Cleveland Clinic Journal of Medicine June 2011 vol. 78 6 393-403 GENARO FERNANDEZ, MD ERICA S. SPATZ, MD CHARLES JABLECKI, MD Department of Neurosciences, University of California San Diego, La Jolla PAUL S. PHILLIPS, MD⇓ Director, Interventional Cardiology, Department of Cardiology, Scripps Mercy Hospital, San Diego, CA
myopathy and muscle pain while on the combined treatment of atorvastatin plus ezetimibe.
8) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2538990/
Can J Cardiol. 2006 February; 22(2): 141–144.
Ezetimibe-associated myopathy in monotherapy and in combination with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor Chantale Simard, B Pharm, PhD, and Paul Poirier, MD PhD FRCPC FACC
Centre de recherche, Hôpital Laval; Faculté de Pharmacie, Université Laval, Sainte-Foy, Québec
Correspondence: Dr Chantale Simard, Centre de recherche, Hôpital Laval, 2725 chemin Sainte-Foy, Sainte-Foy, Québec
9) http://www.ncbi.nlm.nih.gov/pubmed/17768174Ann Rheum Dis. 2008 May;67(5):614-9.
Increased exposure to statins in patients developing chronic muscle diseases: a 2-year retrospective study.Sailler L, Pereira C, Bagheri A, Uro-Coste E, Roussel B, Adoue D, Fournie B, Laroche M, Zabraniecki L, Cintas P, Arlet P, Lapeyre-Mestre M, Montastruc JL.Unit of Pharmacoepidemiology, EA 3696, Clinical Pharmacology Department, Paul Sabatier University, 37 Allées Jules Guesdes, 31000 Toulouse, France.

Case reports have suggested that lipid-lowering drugs (LLDs), especially statins, could induce or reveal chronic muscle diseases. We conducted a study to evaluate the association between chronic muscle diseases and prior exposure to LLDs.METHOD:This was a retrospective study of chronic primary muscle disease cases newly diagnosed at the Toulouse University Hospitals between January 2003 and December 2004 among patients living in the Midi-Pyrénées area, France. All patients remained symptomatic for more than 1 year after drug withdrawal, or required drugs for inflammatory myopathy. Data on the patient’s exposure to LLDs and to other drugs were compared with that of matched controls (5/1) selected through the Midi-Pyrénées Health Insurance System database.RESULTS:A total of 37 patients were included in the study. Of those, 21 (56.8%) suffered from dermatomyositis (DM) or polymyositis (PM), 12 (32.4%) from genetic myopathy, and 4 (10.8%) from an unclassified disease. The prevalence of exposure to statins was 40.5% in patients and 20% in controls (odds ratio (OR) 2.73, 95% confidence interval (CI) 1.21-6.14; p<0 .01="" strong="">There was a significant positive interaction between statins and proton pump inhibitors exposure (weighted OR 3.3, 95% CI 1.37-7.54; p = 0.02).

Statin exposure rate was 47.6% among patients with DM/PM (OR 3.86, 95% CI 1.30-11.57; p<0 .01="" and="" between="" border="0" controls="" difference="" exposure="" fibrates.conclusion="" for="" img="" no="" patients="" src="http://jeffreydach.com/emoticons/tongue.png" there="" to="" was="">atients who developed chronic muscle diseases after the age of 50, including DM/PM, had a higher than expected frequency of prior exposure to statins. Further studies are needed to confirm this association and the role of proton pump inhibitors.

warmest regards,

Jeffrey Dach MD

Offices of Willow Grove

7450 Griffin Road, Suite 190

Davie, Fl 33314

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

Read the complete article here.

Could statins be adding to the epidemic of heart failure? - Briffa

Could statins be adding to the epidemic of ‘heart failure’?

Jan, Fri 4th, 2013 By : Dr John Briffa

 

Statins are drugs that reduce cholesterol by inhibiting an enzyme in the liver known as ‘HMG-CoA reductase’ which ‘drives’ cholesterol production (most of the cholesterol in the bloodstream is made in the liver and does not come directly from the diet). But HMG-CoA reductase also facilitates the production of a substance known as ‘coenzyme Q10’ which itself participates in the production of what is known as ‘adenosine triphosphate’ (ATP) – the most basic unit of energy ‘fuel’ in the body. The major biochemical process which involves CoQ10 that drives ATP and energy production in the body is known as ‘oxidative phosphorylation’.

Now that we have the potted biochemistry lesson over, we can see that statins have the potential, by lowering CoQ10 levels, to put a break on oxidative phosphorylation and ATP production in the muscles. The end result may be fatigue? Muscle pain is another potential consequence.

In a study published this week in the Journal of the American College of Cardiology (JACC), Danish researchers measured CoQ10 levels in individuals taking simvastatin (a commonly-prescribed statin), and compared them with those not taking statins [1]. The levels in those taking the statin were significantly lower.

Now, studies such as this one are what is termed ‘epidemiological’ in nature, which means it looks at associations between things, but cannot prove that one thing is causing another. However, of relevance here is other evidence which finds that giving statins to people does indeed have the capacity to lower levels of CoQ10 in the body [2].

What was also interesting about the JACC study is that it found that those treated with statins had lower levels of oxidative phosphorylation than those not taking them. They also had reduced ‘insulin sensitivity’. This is relevant for a number of reasons, including the fact that insulin facilitates the uptake of nutrients such as glucose into the cells. Lowered insulin sensitivity can therefore ‘starve’ the cells of essential nutrients. Reduced insulin sensitivity is also the underlying fault in type 2 diabetes. It is perhaps worth bearing in mind that statin use has been proven to increase the risk of type 2 diabetes.

Another thing worth bearing in mind here, I think, is the fact that the heart is a muscle, and depleting it of CoQ10 may be hazardous for cardiac health. Specifically, it may weaken the heart and lead to what is known as ‘heart failure’ (also known as ‘congestive cardiac failure’). I think the ‘benefits’ of statins are vastly overstated, generally speaking. However, if someone is to take statins, I think it’s a reasonable safeguard to take CoQ10 on a daily basis. 100 mg a day is a decent dose, I think, though higher doses are likely to better when symptoms of statin toxicity are present.

In researching this article, I came across an interesting review of the evidence for statin-inducted CoQ10 depletion in both humans and animals [3]. Here’s what the authors of this review have to say in their concluding remarks:

Statin-induced CoQ10 deficiency is completely preventable with supplemental CoQ10 with no adverse impact on the cholesterol lowering or anti-inflammatory properties of the statin drugs. We are currently in the midst of a congestive heart failure epidemic in the United States, the cause or causes of which are unclear. As physicians, it is our duty to be absolutely certain that we are not inadvertently doing harm to our patients by creating a wide-spread deficiency of a nutrient critically important for normal heart function.

References:
1. Larsen S, et al. Simvastatin Effects on Skeletal Muscle – Relation to Decreased Mitochondrial Function and Glucose Intolerance. J Am Coll Cardiol. 2013;61(1):44-53
2. Passi S, et al. Statins lower plasma and lymphocyte ubiquinol/ubiquinone without affecting other antioxidants and PUFA. Biofactors 2003;18(1-4):113-24.
3. Langsjoen PH, et al. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors 2003;18(1-4):101-11.
=========================================================================================================
Read the complete article here.

Statin Anti-Cholesterol Drugs Revisited - DACH

Statin Anti-Cholesterol Drugs Revisited By Jeffrey Dach (about the author)     (Page 1 of 7 pages) Life Arts 11/4/2012

This article takes a critical look at statin anti-cholesterol drugs, and asks the hard questions. Do statin drugs work? Who do they work for? Who do they harm? Who should be taking them, and who should not be taking them? Examples of Statin Drugs are Lipitor, Zocor, Simvastatin, Pravachol, Crestor, Mevacor, etc. These drugs reduce the production of cholesterol by the liver by inhibiting an enzyme called HMG-CoA. Due to a belief that cholesterol causes coronary artery disease, statin drug reduction of cholesterol is a mainstream medical treatment intended to prevent heart disease. Do statin drugs prevent coronary artery disease, heart attacks and mortality from heart disease? This article will answer that question.

Anti-Inflammatory Effect

After many decades of study and clinical trials, it has become clear that the benefit of statin drugs (if there is any) is probably not due to reduction in cholesterol, rather it is due to an anti-inflammatory effect of the drug.(link)

Reducing CoQ-10

Coincidentally, statin drugs inhibit the production of an important mitochondrial cofactor called Co-Q10, accounting for adverse effects as mitochondrial toxins. In addition, a low serum cholesterol level is a health risk for many reasons. Cholesterol is an important molecule in the body, and reducing cholesterol to low levels is associated with increased mortality and adverse effects on health. (27)

Asking A Few Questions

In this article we will revisit anti-cholesterol statin drugs while asking the following questions:

1) What is the efficacy for statin drugs in primary prevention of heart disease (in normal healthy people)?

2) What is the efficacy of statin drugs in secondary prevention (patients with known underlying heart disease)?

3) Which subgroups benefit from statin drugs, and which subgroups of the population are harmed by statin drugs?

The Elderly - Low Serum Cholesterol Predicts Increased Mortality

First, let's take a look at the medical practice of prescribing statin anti-cholesterol drugs for the elderly. Contrary to current dogma, higher cholesterol levels in the elderly are not a heath risk. Studies show that higher cholesterol in the elderly is associated with increased survival, while lower total serum cholesterol values in the elderly are a robust predictor of increased mortality. (1, 4,5)

The Prosper Study - Statins for the Elderly

When statin drugs are given to the elderly to reduce cholesterol values as was done in the PROSPER study, there was no mortality benefit for either primary or secondary prevention of heart disease. (1,6,7) True, there was a reduction in cardiac mortality of about 20% in the secondary prevention group in the Prosper study, however, this was counterbalanced by an increase in cancer mortality, yielding no over-all mortality benefit in the final analysis.

Women- No Mortality Benefit from Statins

Perhaps the best summary of the results of three decades of statin drug studies in women can be found in the Judith Walsh MD report in JAMA May 2004. (8) Again, Dr Walsh found that statin drug treatment to reduce cholesterol in women provided no mortality benefit in both primary and secondary prevention of heart disease. As we found in the PROSPER study for the elderly, statin drug use in women (with known heart disease) resulted in a reduction in mortality from heart disease, and a reduction in heart attacks in this secondary prevention group, however, this was offset by additional deaths from cancer and other mortality which yielded no over-all mortality benefit in the final analysis. (8)

MEN and Women- Primary Prevention- Dr Ray Archives of Internal Medicine

1 | 2 | 3 | 4 | 5 | 6 | 7

Jeffrey Dach MD is a physician and author of two books, Natural Medicine 101, and Bioidentical Hormones 101, both available on Amazon, or as a free e-book on his web sites. Dr. Dach is founder and chief medical officer of TrueMedMD, a clinic in (more...)

 

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

Read the complete article here.
 

Confirmed Again: Statin Drugs Accelerate Cardiovascular Disease - Mercola

Confirmed Again: Statin Drugs Accelerate Cardiovascular Disease

October 15 2012

Download Interview Transcript

Visit the Mercola Video Library

By Dr. Mercola

Statins are the world's most-prescribed class of medications. A staggering one in four Americans over the age of 45 now take cholesterol-lowering drugs such as Pravachol, Mevacor, Lipitor, Zocor, Crestor, and others. A majority of them are taking these drugs for primary prevention of heart attacks and strokes.

However, mounting research suggests this could be a critical mistake.

Most recently, two separate studies have concluded that progression of coronary artery calcification, which is the hallmark of potentially lethal heart disease, is INCREASED with statin drug use.

Statins Increase Prevalence of Coronary Calcification by More than 50 Percent!

A new study in the journal Atherosclerosis¹ shows that statin use is associated with a 52 percent increased prevalence and extent of calcified coronary plaque compared to non-users. None of the participants in the study – 6,673 in all – had any known coronary artery disease at the time of undergoing coronary CT angiography (CCTA) – a non-invasive method that allows you to see coronary atherosclerotic features, including plaque composition.

Arterial plaque is a hallmark of cardiovascular disease and increases your risk of all-cause mortality, so clearly, anything that increases calcification and stiffening of your arteries is wisely avoided. And statins seem to fall into this category.

These disturbing findings come right on the heels of another study published in the journal Diabetes Care,² which discovered that type 2 diabetics with advanced atherosclerosis who are frequent statin users have significantly higher amounts of coronary artery calcification compared to less frequent users of the drug.

Furthermore, in a subgroup of participants who initially were not receiving statins, progression of both coronary artery calcification as well as abdominal aortic artery calcification was significantly increased when they began frequent statin use.
The authors concluded that:

"More frequent statin use is associated with accelerated coronary artery calcification in T2DM patients with advanced atherosclerosis."

So much for statins being the answer for diabetics... Diabetes is a risk factor for cardiovascular disease, which is why many diabetics are prescribed a statin drug to reduce their risk. Alas, as these studies show, statins actually accelerate the progression of disease!

Making matters worse, statins have also been shown to significantly increase your risk of developing type 2 diabetes³ if you don't have it already. This is a risk everyone needs to be aware of. In one study, statins increased the risk of type 2 diabetics in postmenopausal women by 48 percent.⁴

Few People Really Benefit from a Statin Drug

Statins, I believe, are one of the most unnecessary drugs on the market. A small group of people with familial hypercholesterolemia, a genetic defect that causes cholesterol levels above 325-350, do seem to benefit from statins. However, in my clinical experience over more than two decades and tens of thousands of patients, I had a grand total of three patients that fell into this category as it's a relatively uncommon genetic problem.
The fact that one in four Americans over the age of 45 is now taking a statin drug as a form of "preventive medicine" does not bode well when you consider the massive increases in disease risk these drugs are now associated with. It's downright shocking that doctors are so slow to realize the potential damage inflicted on their patients for no reward at all.

The research that led to statins being heavily promoted as a form of primary prevention of heart disease and stroke was funded by AstraZeneca, the maker of Crestor. Since the release of that study in 2008, none of their claims have turned out to hold water in subsequent research. On the contrary, as the two featured studies show, they actually worsen cardiovascular disease progression.

The drugs also come with an avalanche of other potential side effects, which tend to be dose dependent.⁵ In fact, as of 2009 there were well over 900 studies proving their adverse effects, which run the gamut from muscle problems to increased cancer risk. One of the primary mechanisms of harm appears to be CoQ10 depletion. If you take statin drugs without supplementing with CoQ10 (or ideally, the reduced form, called ubiquinol, which is far more effective), your health is at serious risk.

GreenMedInfo.com has compiled over 300 documented adverse health effects associated with statins,⁶ some of the most common of which include:

Muscle problems, polyneuropathy (nerve damage in the hands and feet), and rhabdomyolysis (a serious degenerative muscle tissue condition)	Anemia
Acidosis	Sexual dysfunction
Immune depression	Cataracts
Pancreas or liver dysfunction, including a potential increase in liver enzymes	Memory loss

What You Need to Know About Cholesterol in Order to Understand the Dangers of Statins

Statin drugs work by preventing the formation of cholesterol and reduce LDL cholesterol, which is considered the "bad" cholesterol. There is no argument that these drugs can effectively lower your cholesterol levels. However, what has NOT been proven is that they significantly lower your risk of dying from heart disease. In no way, shape or form do they treat the underlying cause of your problem. They are nothing more than a toxic band-aid.

So just what makes statins so dangerous, and why are they not the answer for managing your cholesterol levels?

First you need to understand the biological workings of cholesterol. In fact, there is no such thing as "good" or "bad" cholesterol. Both HDL and LDL cholesterol perform vital functions in your body, which is why it's actually dangerous to bring your LDL levels down too low.

HDL (high density lipoprotein) and LDL (low density lipoprotein) are actually proteins that transport the cholesterol to and from your tissues. Cholesterol in turn is a precursor to your steroid hormones, bile acids, cell membrane walls and vitamin D. For example, cholesterol is essential for you to make testosterone or estrogen, cortisol, DHEA or pregnenolone, or a multitude of other steroid hormones that are necessary for health, without cholesterol. Even more importantly, your cells cannot regenerate their membranes without it.

The reason you have LDL to begin with is to transport the cholesterol to the tissues in order to make new cells and repair damaged ones. However, there are different sizes of LDL particles and it's the LDL particle size that is relevant, and statins do not modulate the size of the particles. Unfortunately, most people still don't know about that part, and very rarely, if ever, get tested for particle size. The particles are sticky, so very small LDL's can easily get stuck in different areas, and the build-up eventually causes inflammation and damage.

The only way to make sure your LDL particles are large enough to not cause damage is through your diet. In fact, it's one of the major functions of insulin.

Conveniently enough, a healthy diet is also the answer for type 2 diabetes, so by focusing on what you eat, you're treating both your diabetes and your cholesterol levels, and reducing your associated risk of heart disease. If you eat properly, which is really the only known good way to regulate LDL particle size, then it does the right thing; it takes the cholesterol to your tissues, the HDL takes it back to your liver, and no plaque is formed.

The Critical Importance of CoQ10

Again, if you're on a statin drug, you MUST take at least 100-200 mg of ubiquinol or CoQ10 per day. Ubiquinol is also beneficial for those not taking statins. If you're not on a statin drug, the amount of CoQ10 or ubiquinol you might need depends on how sick you are. The sicker you are, the more you need. As a general guideline if you're not ill, taking 50-100 mg per day would probably be sufficient. If you're over the age of 70, double that dose, or up to 200 mg per day. This is because your natural CoQ10 levels begin to drop after the age of 40, and by the age of 70, levels begin to precipitously drop.
Ideally, you'll want to split the dose up to two or three times a day, rather than taking it all at once, as this will result in higher blood levels. Other dosing guidelines include:

Hypertension 200 mg/day	World class athletes who need extra ATP turnover, 300-600 mg/day	Heart transplant or severe CHF, 300-600 mg/day in divided doses
Arrhythmia 200 mg/day	Typical athlete 100-300 mg/day	Mitral valve prolapse, a combination of 400 mg magnesium and 100-200 mg of CoQ10

How to Help Lower Your Cholesterol Naturally

There's really virtually NO reason to take statins and suffer the consequences from these ill-conceived drugs. If you truly want to normalize your cholesterol levels, following these simple lifestyle changes can help get you there:

• First, normalize your insulin levels by eliminating sugar (particularly fructose) and grains. A fasting insulin level is easy to draw and is very inexpensive. It should be below 3.
• Take a high-quality animal-based omega-3 supplement, such as krill oil.
• Eat a good portion of your food raw (ideally organic to avoid agricultural chemicals).
• Eat healthy, preferably raw, fats, such as:
  
  

  Olive oil	Coconut and coconut oil	Organic raw dairy products	Avocados
  Raw organic nuts	Seeds	Pastured eggs (raw, or lightly cooked with yolks intact)	Organic, grass-fed meats

• Regular exercise is another important tool. When you exercise you increase your circulation and the blood flow throughout your body. The components of your immune system are also better circulated, which means your immune system has a better chance of fighting an illness before it has the opportunity to spread.
• If you are a man, or a woman who is in menopause, you should check your iron levels, as elevated levels of iron can cause major oxidative damage in the blood vessels, heart and other organs. Excess iron is also one of the major contributing factors of cancer risk.
• Avoid smoking and drinking alcohol excessively.

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

Statins: why you should think twice - Jerome Burne

Great Review of $TATIN NATION by Award-Winning medical Journalist Jerome Burne:http://jeromeburne.com/2012/09/08/statins-why-you-should-think-twice/

Statins: why you should think twice

 

September 8, 2012 By Jerome Burne

 

If you’re over 45 there’s a good chance that you are taking or have at least been offered a statin drug to lower your cholesterol and so cut your risk of heart disease but is it good idea? Your doctor obviously thinks it is, but there is another side to the statin story. The link between cholesterol and heart disease is not as strong or as simple as the familiar statin story suggests.

For instance, the UK is quite high in the international heart attack league table but on a table ranking countries average cholesterol level, it’s quite far down. If high cholesterol equalled high heart attack risk, the two should match. What’s more the number of people in the UK with high cholesterol has been falling for several decades but during that time the rate of heart attacks has been flatlining. Likewise you’d expect the two to come down together.

And there are more examples where the population-wide figures don’t match the theory. One big study found that the average cholesterol level of over 100,000 people admitted to hospital in the States with a heart attack was actually lower than the level in the general population.

High risk but low cholesterol

Or this one: your social class is one of the best predictors of your risk of a heart attack – if you’re a fairly well off ABC1 it’s much lower than if you’re a poorer C2, D or E. There are all sorts of reasons for this – diet, access to information etc – but if cholesterol was a key factor you’d expect the As to have low levels and C2s to be high. Actually it is the other way around.

These are just a few of the points made in a very watchable new video called $tatin Nation which combines interviews with a number of cholesterol sceptical doctors and researchers with clips and strong graphics. By the end, at the very least, you are going to have a lot more questions to ask your doctor.

The video come at a time when the debate over statins is hotting up. In the last couple of years several large trials have concluded that if you are healthy, but just have some risk factors – being over 55 is one – then statin benefits are vanishingly small.

Give them to everyone

But in the last few weeks, two more big studies have come out claiming that statins are safe and well-worth taking whatever your cholesterol level. Their message is that giving them to everyone over 55 would greatly cut premature heart disease deaths saving the NHS billions.

So what to do? The case for statins is available on every official website about heart disease while sceptical case is spread across dozens of sites. $tatin Nation saves you an impossible hunt by summarising the sceptical case in one place. It’s worth finding out what it is.

Here are a few more pointers from the video. You might ask: how come lots of reports say statins cut the risk of heart disease by 30%, 40% even 50%. How can that be bad? The short answer is clever marketing and a nifty way with statistics. Here’s how it works.

A couple of years ago a statin trial called Jupiter came out with a remarkable result: statins cut the chance of a heart attack by 54%. To understand why that is not exactly a lie but is astoundingly misleading, you have to look deeper into the results than the drug company’s own summary – the one used by nearly all the newspaper and media reports – which is where the 54% figure came from.

3/1000 chance

What you are interested in is the difference between those getting the drug and those getting a placebo. This shows that 0.35% of those taking statins had a heart attack compared with 0.7 of those on a placebo. In other words, out of 1000 people who had no treatment. 7 had a heart attack.

There were certainly fewer heart attacks in the statin group – only 3.5 people out of 1000 had one. Now that is a 54% improvement, so no lies are being told, but it means that a thousand people have to take statins for just three to avoid a heart attack. Taking statins does seem less appealing doesn’t it?
And then there are the side-effects such as diabetes which showed up as a risk in the Jupiter trial. The figures aren’t precise but there could be one extra case of diabetes for every 200 people on the drug.
That’s not far off the number who can expect to benefit.

But diabetes isn’t the only possibly side effect. There is a frightening section in the film where patients describe the range of nasty effects linked with statins – muscle pain is by far the most common, other include fatigue, memory loss and brain fog. A common theme is how uninterested and unhelpful doctors are when told about them.

Several of the experts estimate that between 10% and 20% of patients suffer some sort of side-effect. That’s 100 to 200 people having unpleasant or possibly disabling symptoms for every three people who avoid a heart attack.

There’s lots more in $tatin Nation, such as clear links between stress, loneliness and heart disease that has been largely side-lined by the heavy concentration on cholesterol lowering. And then there is CoQ10, an enzyme and anti-oxidant called CoQ10 that’s vital for energy production in both the muscles and in the heart. As well as cutting cholesterol production, statins also cut CoQ10 production.

Do have a look at it.
==================================================================
Read the complete article here.

There Is No Such Thing As Bad Cholesterol

Putting The Myth To Rest: There Is No Such Thing As Bad Cholesterol
Perhaps one of the biggest health myths propagated in western culture and certainly in the United States, is the correlation between elevated cholesterol and cardiovascular disease (CVD). Unfortunately, despite dozens of studies, cholesterol has not been shown to actually cause CVD. To the contrary, cholesterol is vital to our survival, and trying to artificially lower it can have detrimental effects, particularly as we age.

Cholesterol seems to be one of those things that strikes fear into the hearts of many, so to speak. We have become obsessed with eating foods low in cholesterol and fat. Ask almost anyone, and they can tell you their cholesterol levels.

What is certain is that the 'little knowledge' that the media often imparts means many folks assume cholesterol is simply a 'bad' thing. Alternately, a good number of us may have heard the terms 'good' cholesterol and 'bad' cholesterol bandied about without knowing much about what this really means. In fact it is a fairly safe bet that if you asked anyone on the street for his or her instinctive response, if asked about cholesterol, they would probably say that we simply need to 'reduce it'.

The 'noddy-science' offered by marketing men to a generally scientifically-naive public has led many people to believe that we should replace certain food choices with specially developed products that can help 'reduce cholesterol'. Naturally this comes at a price and requires those who can afford it to pay maybe four or five times what a 'typical ordinary' product might cost. But is this apparent 'blanket need' to strive towards lowering our cholesterol justified? And, indeed, is it healthy?

For anyone who has had the official diagnosis of 'high cholesterol' in their bloodstream, they may even have embarked upon a program of medicinal intervention. In fact it is quite likely that they may have joined the legions of long-term pill-poppers who are already lining the pockets of the profit-oriented pharmaceutical giants.

But let's take a moment, now, to review some of the facts and fallacies about the much-maligned substance: cholesterol.

Cholesterol is needed to make hormones. Without it we would not produce estrogen, progesterone or testosterone. It is vital for the functioning of nerve synapses and provides the structural integrity for our cell membranes. Cholesterol is used by the skin to help prevent water evaporation and to make our skin waterproof. Vitamin D is synthesized from cholesterol. And bile, used for fat digestion, consists mostly of cholesterol. The liver produces about 90 percent of the cholesterol in our bodies; only 10 percent comes from diet. If we eat too much cholesterol, the liver decreases the output of cholesterol.

Cholesterol is a naturally occurring lipid. This means it is a type of fat or oil and it is in fact an essential component in creating and sustaining the membranes of the cells of all bodily tissues. So this alone means we need cholesterol to survive! Most of the cholesterol that is found in our bodies is actually naturally manufactured within our own cells. However there is also an additional contribution that we get from external 'nutritional' sources - the foods we consume. In a typical diet providing around 400mg of cholesterol per day from food sources, about half to two-thirds of this amount is actually absorbed through the process of digestion. The body will normally secrete about a gram (1000mg) of cholesterol per day into the bile via the ducts, and approximately three-fifths of this is then re-absorbed.

Where our tissues or organs are a particularly dense complex of cells, which have closely packed cell membranes, there will naturally be higher levels of cholesterol. The key organs that need, and contain, these higher amounts of cholesterol include the liver, the brain and the spinal cord - none of which would work well if we reduced cholesterol too much!

In effect cholesterol plays an essential role in the development and maintenance of healthy cell walls. It is also a critical factor in the synthesizing of steroid hormones, which are a key factor in our natural physical development.

Being a lipid, cholesterol is fat-soluble, but it is not soluble in blood. However it needs to be transported around the body to the places where it can be utilized. This is why, in order to be moved around, it must become 'associated' with certain lipoproteins which feature a water-soluble (therefore 'blood transportable') coat of proteins. There are two key types of lipoproteins that transport cholesterol around the body: low-density and high-density variants. The essential cellular function of cholesterol requires that sufficient amounts are manufactured by specialized sub-systems (or organelles) within the body's cells called the endoplasmic reticulum. Alternatively, the cholesterol we need must be derived from our diet. During the process of 'digestion and assimilation' of foods, it is the low-density lipoprotein (LDL) that carries dietary cholesterol from the liver to various parts of the body.

When there is sufficient cholesterol for cellular needs, the other key transport mechanism in this amazing 'logistics system' - high-density lipoprotein (HDL) - can take cholesterol back to the liver from where any unnecessary excess can be processed for excretion.

The 'noddy-science' of the so-called 'functional food' manufacturers would have us believe that there is such a thing as 'bad' cholesterol and 'good' cholesterol. This is, in fact, totally untrue. The cholesterol itself, whether being transported by LDL or HDL, is exactly the same. Cholesterol is simply a necessary ingredient that is required to be regularly delivered around the body for the efficient healthy development, maintenance and functioning of our cells. The difference is in the 'transporters' (the lipoproteins HDL and LDL) and both types are essential for the human body's delivery logistics to work effectively.

Problems can occur, however, when the LDL particles are both small and their carrying capacity outweighs the transportation potential of available HDL. This can lead to more cholesterol being 'delivered' around the body with lower resources for returning excess capacity to the liver.

LDL can vary in its structure and occur in particles of varying size. It is the smaller LDL particle sizes that can easily become 'trapped' in the arteries by proteoglycans, which is, itself, a kind of 'filler' found between the cells in all animal and human bodies. This can then cause the cholesterol the LDL carries to contribute to the formation of fatty deposits called 'plaques' (a process known as atherogenesis). As these deposits build up, they restrict the arteries' width and flexibility. This causes an increase in blood pressure and can also lead to other cardiovascular problems such as heart attacks or strokes.

The LDL itself is consequently sometimes referred to as 'bad cholesterol', but you can now appreciate the fact that this is simply incorrect. In fact LDL, HDL and cholesterol are all essential to our health. However, it seems that it has become common for humans to have a preponderance of 'unhealthily' small LDL particles, which can become a precursor to heart and arterial disease due to the mechanisms described. It is apparently healthier to have a smaller number of larger LDL particles carrying the same quantity of cholesterol than a large number of small LDL particles might transport, but for some reason this is less common. This is an interesting area that demands more research.

When LDL becomes retained by the glycol-proteins in the arteries it is subject to being oxidized by 'free radicals'. This is when the process can become health threatening. It has therefore been suggested that increasing the amount of antioxidants in our diet might effectively 'mop up' free radicals, and consequently reduce this harmful oxidation. Although the idea of consuming foods rich in antioxidants, or even using supplements, is now widely promoted, the scientific evidence for their efficacy still remains to be fully established.

Another point to consider is the occurrence of substances called 'very-low-density-lipids' or VLDL, also known as triglycerides. VLDL is converted to LDL in the bloodstream and therefore contributes towards increased levels of LDL and to subsequent potential cholesterol-related health problems. This is why triglycerides are usually measured when a cholesterol test of your blood is undertaken.

The production of VLDL in the liver - which amounts to a combination of cholesterol and low-density apolipoprotein - is exacerbated by the intake of fructose. Fructose is the type of sugar found in many fruits, it is also a component of sucrose and of the widely used food ingredient high-fructose corn syrup. This implies that anyone whose LDL or triglyceride levels are unduly high should cut back on those sweet sugary snacks, and even on the sweeter, fructose laden fruits; not simply reduce their intake of fatty foods!

Vitamin B3, otherwise known as niacin, on the other hand, actually lowers the amount of VLDL, and therefore also LDL. In addition, niacin helps to stimulate the production of helpful HDL, the lipoprotein that carries excess cholesterol back to the liver for excretion. However, in keeping with the best traditions of consuming 'all things in moderation', currently recommended upper limits for daily intake of niacin is 35mg, given that it can have toxic effects in larger amounts. Even so, medical professionals have been known to prescribe niacin in doses as high as 2g, up to three times a day, for treatment of those with dangerously high blood cholesterol levels. Naturally you should never self-medicate with high doses of niacin without taking appropriate medical advice.

Niacin in the diet is typically derived from high protein foods including liver and other meats, as well as significant amounts being found in certain nuts and whole grains.

However one of the fashionable types of pharmaceutical drugs of recent times, introduced to treat the apparently increasing incidence of high cholesterol levels particularly in the West, are Statins. Most likely you have a friend or relative taking these useless drugs (Lipitor, Mevecor, Crestor, etc.) to lower cholesterol. Statin medications are the number-one-selling drugs in the world. They work by interfering with the liver function and reducing the production of LDL. But Statins are a questionable innovation on at least a couple of accounts. Firstly they are not without side-effects: they can, for example, lead to the breakdown of major muscular material, which can ultimately overwhelm the kidneys and even cause acute renal failure.

Statins also appear to reduce the body's natural levels of the vitamin-like, cellular protection agent known as Co-enzyme Q10. This benzoquinone plays an important role in cellular energy release, particularly in hard worked areas like the lungs, liver and heart. CoQ10 (as it is sometimes called) has also been shown to protect the brain against neurological degeneration. But perhaps most interestingly, with respect to cholesterol, CoQ10 also acts as an antioxidant, particularly active in protecting the system against LDL oxidation and the potential problems associated with this as described above. So whilst Statins might provide a reduction in LDL per se, they might also be causing more problems in the long-term. Naturally, as with many modern drugs, they generally have to be taken for the long-term by anyone who has been prescribed them.

What is particularly disturbing about Statins is, perhaps, the fact that they may be seen as a 'quick fix' for unhealthily high LDL, and consequently cholesterol levels throughout the body. They need to be taken over a long period - which makes them very profitable for drugs manufacturers. But they may also be prescribed without the over-arching message that in order to address any cholesterol problem 'naturally', the sufferer must change their lifestyle and diet. Statins can seem an easy option but may indeed merely be the beginning of a process where the 'negative health pay-off' is simply delayed rather than actively defused! That is not to say that in extreme cases of high blood cholesterol, or hypercholesterolemia, there may not be a useful role for Statin therapy when natural strategies fail or do not prove effective, or feasible.

In truth, and in summary, cholesterol is an important and essential substance that we need for health at a cellular level. It is most likely that any imbalance in our cholesterol transport system comes down to long-term poor dietary and exercise habits. Ensuring that we consume some extra anti-oxidant foods, along with including niacin rich foods, might well be of benefit. But it is perhaps most important to recognize that deliberate and continued levels of activity and the consumption of a healthful diet is a better solution than questionable quick-fix drugs, if we ever are diagnosed with levels of cholesterol and triglycerides that might give cause for concern.

Dr. Ron Rosedale On The Facts About Cholesterol Dr. Ron Rosedale talks about common cholesterol myths, and exposes the deceptions and misconceptions that most people have been told. (Interview with Dr. Mercola).

More articles on Cholesterol

Reference Sources 114, 136, 151, 158

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

Read the full article here.