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Showing posts with label coenzyme-q10. Show all posts
Showing posts with label coenzyme-q10. Show all posts

Tuesday, June 18, 2013

Are statins and omega-3s incompatible? - Davis

Are statins and omega-3s incompatible?
Posted on June 18, 2013 by Dr. Davis

French researcher, Dr. Michel de Lorgeril, has been in the forefront of thinking and research into nutritional issues, including the Mediterranean Diet, the French Paradox, and the role of fat intake in cardiovascular health. In a recent review entitled Recent findings on the health effects of omega-3 fatty acids and statins, and their interactions: do statins inhibit omega-3?, he explores the question of whether statin drugs are, in effect, incompatible with omega-3 fatty acids.

Dr. Lorgeril makes several arguments:

1) Earlier studies, such as GISSI-Prevenzione, demonstrated reduction in cardiovascular events with omega-3 fatty acid supplementation, consistent with the biological and physiological benefits observed in animals, experimental preparations, and epidemiologic observations in free-living populations.

 2) More recent studies (and meta-analyses) examining the effects of omega-3 fatty acids have failed to demonstrate cardiovascular benefit showing, at most, non-significant trends towards benefit.

He points out that the more recent studies were conducted post-GISSI and after agencies like the American Heart Association’s advised people to consume more fish, which prompted broad increases in omega-3 intake. The populations studied therefore had increased intake of omega-3 fatty acids at the start of the studies, verified by higher levels of omega-3 RBC levels in participants.

In addition, he raises the provocative idea that the benefits of omega-3 fatty acids appear to be confined to those not taking statin agents, as suggested, for instance, in the Alpha Omega Trial. He speculates that the potential for statins to ablate the benefits of omega-3s (and vice versa) might be based on several phenomena:

 –Statins increase arachidonic acid content of cell membranes, a potentially inflammatory omega-6 fatty acid that competes with omega-3 fatty acids. (Insulin provocation and greater linoleic acid/omega-6 oils do likewise.)

–Statins induce impaired mitochondrial function, while omega-3s improve mitochondrial function. (Impaired mitochondrial function is evidenced, for instance, by reduced coenzyme Q10 levels, with partial relief from muscle weakness and discomfort by supplementing coenzyme Q10.)

–Statins commonly provoke muscle weakness and discomfort which can, in turn, lead to reduced levels of physical activity and increased resistance to insulin. (Thus the recently reported increases in diabetes with statin drug use.)

Are the physiologic effects of omega-3 fatty acids, present and necessary for health, at odds with the non-physiologic effects of statin drugs?

I fear we don’t have sufficient data to come to firm conclusions yet, but my perception is that the case against statins is building. Yes, they have benefits in specific subsets of people (none in others), but the notion that everybody needs a statin drug is, I believe, not only dead wrong, but may have effects that are distinctly negative. And I believe that the arguments in favor of omega-3 fatty acid supplementation, EPA and DHA (and perhaps DPA), make better sense.

 - See more at: http://blog.trackyourplaque.com/2013/06/are-statins-and-omega-3s-incompatible.html

Friday, June 15, 2012

Statins can drain the life out of us - Briffa



Statin drugs reduce cholesterol by inhibiting the an enzyme in the liver (HMG-CoA reductase) which plays a role in the production of cholesterol in the liver. Unfortunately, this enzyme also plays a part in the production of a substance known as Coenzyme Q10, which itself is important for energy production within the body’s cells. Statins therefore have the ability to drain the life out of people. Any doctor who sees patients and actually listens to them will know this from experience, and now someone’s actually gone and shown it with a scientific study [1].

The study was published on-line in the Archives of Internal Medicine. A group of individuals were randomised to take one of two statins (simvastatin at 20 mg per day or pravastatin at 40 mg per day) or placebo for six months. Participants were rated at regular intervals through the study for their perceived fatigue on exertion, general fatigue and energy levels.

One thing worth highlighting here is that the study was only 6 months in duration. This is relevant because it’s not uncommon for the adverse side-effects of statins to come on many months or even years after the treatment is started.

Overall, statins did indeed appear to cause a significant change in energy and worsen fatigue on exertion. Women were more affected than men.

Four out of 10 women reported either reduction in energy or worsening of fatigue on exertion.
Two out of 10 women reported problems with both these things.
One out of 10 women reported that both of these things were ‘much worse’.

The authors remark:
Effects were seen in a generally healthy sample given modest statin doses, and both simvastatin and pravastatin contributed to the significant adverse effect of statins on energy and fatigue with exertion. Particularly for women, these unfavorable effects were not uncommon… These findings are important, given the central relevance of energy and functional status to well-being.
If you or someone you know appears to have statin-related fatigue or other symptoms (such as muscle pain), please see this blog post about how this might be reversed using supplements of Coenzyme Q10.

References:
1. Golomb BA, et al. Effects of Statins on Energy and Fatigue With Exertion: Results From a Randomized Controlled Trial. Arch Int Med epub 11 June 2012
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Read the full article here.

Tuesday, January 3, 2012

300+ Health Problems Linked To Statin Drugs



A growing body of clinical research now indicates that the cholesterol-lowering class of drugs known as statins, are associated with over 300 adverse health effects -- research boldly flying in the face of national health policy, medical insurance premium guidelines, statin drug manufacturer advertising claims, and the general sentiment of the public, with approximately 1 in every 4 adult Americans over 45 currently using these drugs to "prevent heart disease."
The Cholesterol Myth
For well over 40 years, statin drugs have successfully concretized a century old myth about the primary cause of heart disease: namely, that cholesterol "causes" plaque build up in the arteries, ultimately leading to obstruction of blood flow, and subsequent morbidity and mortality.
Indeed, the medical establishment and drug companies have been singing the praises of this "cholesterol myth," to the tune of 25 billion dollars in statin drug sales, annually.
While it is true that oxidized low-density lipoprotein is found within the atheromatous plaque that is found in damaged arteries, it is less likely a cause than an effect of heart disease. The underlying damage to the lining of the artery, which could be infectious, chemical, stress and/or nutritionally-related, comes before the immune response that results in plaque buildup there. Blaming LDL cholesterol for causing heart disease, is like blaming the scab for the injury that caused it to form, or, like blaming the band-aid for the scab it is covering -- this is, after all, the inborn and fatal flaw of allopathic medicine which focuses only on symptoms of disease, which it then -- fool-heartedly -- attempts to suppress by any chemical means necessary.
Death By Statins?
No one can deny that statins do exactly what they are designed to do: suppress cholesterol production and reduce measurable blood serum levels. The question is, rather, at what price do they accomplish this feat, and for what ultimate purpose?
With the National Cholesterol Education Program Guidelines, having been designed by "experts" on the payroll of statin drug manufacturers, requiring ultra-low levels to obtain a strictly theoretical and numerical definition of "health," statin drugs are guaranteed to receive first-line treatment status in the goal of the preventing and treating heart disease through lipid suppression.
What is at question here, is whether the unintended, adverse effects of this chemical class of drugs are less, the same or worse than the purported "cardiovascular" benefits they provide?
Fundamentally, statin drugs damage the muscles and nerves in the body -- so much so that a dose as low as 5 mg a day can kill a human. There are well over 100 studies demonstrating the myotoxic, or muscle-harming effects of these drugs, and over 80 demonstrating the nerve-damaging effects, as well. When you consider that a vast proportion of our body is comprised of muscles and coordinating nerve systems, this drug has the potential to cause damage to the entire body, and undoubtedly does so universally, differing only in the matter of degree -- the damage occurring acutely in those at the tip of the iceberg, asymptomatically in the majority of others at the base.
Moreover, statin myotoxicity is not exclusive to skeletal muscle. If you consider that the heart is also a muscle, in fact, is our most tireless muscle, an obvious red flag should go up. It is a remarkable fact that it took over 40 years before the biomedical research and publishing fields were able to produce a human study, like the one published in the Journal of Clinical Cardiology in Dec. 2009, showing that statin drugs, despite billions of advertising/marketing dollars to the contrary, actually weaken the heart muscle.
These results, while disturbing, are to be expected given the well-known problem associated with statin drug use, namely, the inhibition of the mevalonate pathway necessary to produce the heart-essential nutrient coenzyme Q10. Coenzyme Q10 deficiency itself may be a major contributing cause to heart disease. There is also research that statin drugs deplete the body of the cardioprotective minerals (and associated mineral-protein complexes) zinc and selenium. This finding may also explain why rates of heart failure may be increasing in the general population given these drugs.
While the discovery that statin drugs, instead of preventing heart disease, likely contribute to it, is surprising and counterintuitive, it should not distract from the more disturbing discovery that they contribute to over 300 disease and/or adverse health effects.
Millions of statin drugs users around the globe are risking their lives on a bad bet that taking a magic chemical pill will reduce their risk of dying of a disease that is not caused by a lack of the drug. What is more likely to happen, however, is that the quality and duration of their lives will be reduced, profoundly, along with billions of dollars of squandered cash that could have been spent on authentically medicinal and cardioprotective foods, nutrients, minerals and vitamins.
In light of these findings, a very serious question is raised: are those who are party to the manufacture, promotion, administration and/or prescribing of this chemical class of drugs, in violation of the medical ethical principle of informed consent? And is this ethical violation, insofar as it results in injury to those who have been mislead and/or coerced to take these drugs, also a legal/criminal one?







http://www.greenmedinfo.com/blog/consumer-alert-300-health-problems-linked-statin-drugs

Saturday, September 10, 2011

Why Statins Do More Harm Than Good - Stephanie Seneff



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by Stephanie Seneff

Senior Research Scientist at MIT (Massachusetts Institute of Technology)

Americans have been well trained over the past few decades to avoid dietary fat and cholesterol and to stay out of the sun. Their conscientious implementation of this misguided advice has led to an epidemic in obesity and heart disease, along with a host of other debilitating conditions like arthritis and Alzheimer's disease.

Cholesterol is to animals as chlorophyll is to plants. Cholesterol, absent from plants, is what gives animals mobility and a nervous system. It is therefore not surprising that statin drug side effects mainly impact muscles and the nervous system.

The heart, as a muscle, is not exempt from statin toxicity. This is why the incidence of heart failure has steadily risen in step with the widespread adoption of statin therapy, now displacing cardiovascular disease as the number one killer. In this article I am going to take you on a whirlwind tour of the 60,000 foot view of my understanding of the principle causes of the current health crisis in America.
My extensive research has caused me to hypothesize a remarkable feat that the human body can perform in the presence of sunlight, which is to extract sulfur from hydrogen sulfide in the air and convert it to sulfate, taking advantage of the sun's energy to catalyze the reaction.

This process takes place in the skin upon sun exposure, and also in the endothelial cells lining blood vessels, and in the red blood cells, platelets, and mast cells in the blood. This feat is performed by a very interesting molecule called "endothelial nitric oxide synthase,'' a misnomer, since its main responsibility is to synthesize sulfate rather than nitric oxide.

The sulfate so produced plays a huge role in cardiovascular health, both by preventing blood clots and by keeping pathogenic microbes (bacteria and viruses) at bay. But it also plays another role that is just as important, which is to give cholesterol (as well as vitamin D and other sterols) a free ride through the blood stream.

Vitamin D3 (a highly touted nutrient) is synthesized in the skin from cholesterol (a highly demonized nutrient) and its chemical structure is almost identical to that of cholesterol. By attaching to cholesterol or vitamin D3, sulfate makes the molecule water soluble, and this means that it no longer has to travel packaged up inside an LDL particle. LDL, as you probably know, is the so-called "bad'' cholesterol, which will cause doctors to prescribe statins if the level is too high.

A great way to lower LDL levels is to get adequate sun exposure. It's not going to work to take a vitamin D supplement: you have to go outside and soak up the sun, because supplements are never sulfated and vitamin D is not cholesterol. Raw cow's milk is the only dietary source I know of that actually supplies sulfated vitamin D3, but even that is still not cholesterol sulfate.

Because most Americans have inadequate cholesterol in their skin and grossly inadequate amounts of sun exposure, they suffer from a huge deficiency in cholesterol and sulfate supply to the tissues. Not surprisingly, most impacted are the muscles and nervous system.

Because the heart muscle is indispensible, the body has developed a back-up strategy to give it special treatment, which is to synthesize cholesterol sulfate from LDL and homocysteine in the fatty deposits (plaque) that build up in arteries supplying the heart. The macrophages in the plaque extract cholesterol from damaged small dense LDL particles, and export it to HDL-A1. The platelets in the plaque will only accept cholesterol from HDL-A1, which they then convert to cholesterol sulfate.

They obtain the sulfate through yet another process which requires energy and oxidizing agents, extracting the sulfur from homocysteine. With insufficient homocysteine, the sulfur will most likely be extracted from cartilage, which gets its strength from extensive disulfide bonds. This, in my view, is the main cause of arthritis -- depletion of sulfur from the cartilage in the joints. So now you have both cardiovascular disease and arthritis as a consequence of a low-fat diet and aggressive sun avoidance.

Statin drugs dramatically lower LDL levels by interfering with cholesterol synthesis, and this wreaks havoc on the liver, the main back-up supplier of cholesterol to the tissues when cholesterol intake and cholesterol sulfate production are down. With the American diet, the liver has another huge task, which is to convert fructose to fat.

The fat cannot be stored or shipped (via LDL) if there is insufficient cholesterol. As a consequence, the liver abandons this task, and the fructose builds up in the blood, causing extensive glycation damage to blood proteins. One of the impacted proteins is the apoB in LDL, which interferes with LDL's ability to deliver its goods to the tissues, including cholesterol, fats, vitamins A, D, E, and K, and antioxidants. So LDL levels fall sharply with statins, and so does the bioavailability of all these nutrients.

Muscle cells come to the rescue, heroically, by extracting excess fructose from the blood and converting it to lactate, using anaerobic metabolism. They have to switch over to anaerobic metabolism anyway, because coenzyme Q10, another casualty of statin therapy, is in low supply. Coenzyme Q10 is crucial for aerobic metabolism.

Lactate is a great fuel for the heart and liver, but the problem is that the muscle cells get wrecked in the process, due to massive overdoses of fructose, in the context of inadequate cholesterol, which would have offered some protection. This is a principle contributor to the excessive muscle pain and weakness associated with statins. Eventually, the muscles can't do it any more, and you're now on the verge towards heart failure.

People on long-term statin therapy start to notice that their hair is receding faster, they're developing cataracts, they can't hear as well as they used to, they keep forgetting things, they can't open the pickle jar any more, and perhaps they'll need rotator cuff surgery soon, as their shoulders are so sore. They think it's just because they're growing old, but these are all side effects that my research, together with my students at MIT, has uncovered, by comparing statin drug side effects with side effects associated with other drugs in age-matched reviews.

Even more alarming are the rare but debilitating and even life-threatening side effects we've detected, such as ALS and Parkinson's disease, heart and liver failure, neuropathy and severe muscle damage. A 17-year study on the elderly confirmed what I already suspected: low serum cholesterol is associated with increased frailty, accelerated mental decline, and early death. (Ref 1.)

Statins are not the answer for anyone seeking to avoid cardiovascular disease. The answer, instead, is to modify the diet to include foods that are rich in cholesterol and saturated fat, to avoid empty carbohydrates, especially high fructose corn syrup, to eat foods that are good sources of sulfur, and, most especially, to spend plenty of time outdoors in the sun.

Stephanie Seneff is a Senior Research Scientist at MIT's Computer Science and Artificial Intelligence Laboratory.
She has a Batchelor's degree from MIT in biology with a minor in food and nutrition, and a PhD in Electrical Engineering and Computer Science, also from MIT. Her website at MIT: people.csail.mit.edu/seneff
Her blog: stephanie-on-health.blogspot.com

Ref 1. http://www.ncbi.nlm.nih.gov/pubmed/21254906

September 2011
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Please visit Spacedoc.com to read this and other related and very credible articles.

Sunday, August 16, 2009

What makes statins so dangerous?

In his popular newsletter, Dr. Mercola provides this analysis of the ubiquitous, cure all statin drug and the stance by the Mayo clinic.


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 do work very well at lowering your cholesterol levels. However, was 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 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 steroid hormones. For example, you can’t 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 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 second thing you need to know is that statins work by reducing the enzyme that causes your liver to make cholesterol when it is stimulated by high insulin levels.

Again, you can achieve the same, or better, result by simply reducing your insulin levels by eliminating sugar and most grains, which is also what you need to do to successfully address type 2 diabetes.

Read the complete article here. Thank you Dr Mercols for a clear, concise explanation.