Saturday, January 5, 2013
Friday, January 4, 2013
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:
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.
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Read the complete article here.
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.
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Read the complete article here.
Thursday, January 3, 2013
Cholesterol is Not the Cause of Heart Disease - Raine Saunders
Dr. Sinatra & Others Speaking Out – Cholesterol is Not the Cause of Heart Disease
Why? These doctors want their patients to get out of the perpetual cycle of sickness and into prevention and wellness. And, they want the public to know the truth about what really causes heart disease…and it’s definitely not what you would think.
How did this myth begin?
Since the earlier part of the 20th century, doctors have been rallying around the idea that cholesterol causes heart disease.In 1913, Russian researcher Nikolaj Nikolajewitsch fed cholesterol to rabbits and made the conclusion that their cholesterol levels went up (with no acknowledgement whatsoever that cholesterol is not a normal part of a rabbit’s diet).
And the idea that plaque deposits collecting in the blood vessels due to diet was born.
At the same time, companies like Proctor & Gamble were busy creating products that would replace animal fats as a way to increase profits. Read the full story of how this famous company single-handedly turned an engineered substance into a food that was introduced to kitchens in the early 1900s through clever campaigns and to this day is still found in a large percentage of processed foods on the market, and which has been heralded as a “heart-healthy” alternative to real, wholesome animal fats.
The Framington Heart Study which began in 1948 and is ongoing looked at a link between the consumption of saturated fat and cholesterol levels. A survey was taken in Framingham, MA where 6,000 people answered questions about diet and lifestyle. Researchers observed that individuals with weight problems and had abnormally high blood cholesterol levels were slightly more at risk to develop heart disease.
But actually, not all individuals in this study had high cholesterol levels. And yet, just those few who did were the ones which caused the skewed results of the study to be widely publicized. What was not revealed about those who were at higher risk was that many of these people also had sedentary lifestyles, consumed a high carbohydrate diet, smoked, and also had high cholesterol. What is not commonly told is that the more cholesterol and saturated fat people consume, this actually lowers their cholesterol levels.
The work of Dr. Ancel Keys is often cited as proof that cholesterol is harmful to heart health. In 1953, he published a well-known study which became the basis of support for the Cholesterol Theory. His Seven Countries Study made a connection between heart disease and dietary fat. What is not acknowledged is that any study he looked at which didn’t go along with his hypothesis – especially those consuming low-fat diets and which also had a strong connection to mortality from cardiovascular disease – was excluded from the final results! It’s also important to know that his full study included data from 22 countries – also excluded because it didn’t fit with what he wanted.
The result was that the health communities rallied around this false study and started campaigning to remove all animal fats from the population’s diet: red meat, eggs, butter and other dairy, and anything that was perceived as “artery clogging”. It is this and the Framington Heart studies which have been largely responsible for starting and perpetuating the lie that cholesterol causes heart disease.
Dr. Stephen Sinatra
In the book, The Great Cholesterol Myth, cowritten with Johnny Bowden, Ph.D, the failed theory that cholesterol is the cause of heart disease is debunked. They explain why saturated fat is good for your health and why it “helps to raise beneficial HDL cholesterol, improving your triglyceride/HDL ratio—a key marker of cardiovascular health.”He says to eat beef – and to make sure it’s grassfed beef, butter, nuts, and eggs. These foods are not only okay for us to eat, but vital to health! He also whole-heartedly agrees that vegetable oil is to be avoided – which is damaged during high heat processes in both manufacturing and in cooking. These oils are almost always from GMO sources, and are too high in Omega 6s – which cause excess inflammation in the body and is found in too high amounts in the Standard American diet. He also agrees that we should definitely be using extra virgin olive oil and coconut oil in our diets.
Although I am not a fan of Dr. Oz, he did a recent interview with Dr. Sinatra and Johnny Bowden that you should watch:
Part I and
Part II
Dr. Dwight Lundell
A heart surgeon with 25 years experience, Dr. Dwight Lundell, M.D. has brought the truth to light by admitting that for years he towed the party line in treating heart disease as a condition that was caused by elevated blood cholesterol due to dietary intake of saturated fat. He also reveals that anyone who went against using prescription medication for treating this issue was considered insubordinate and to do so could “possibly result in malpractice.”Dr. Lundell also founded the Healthy Humans Foundation to help people break out of the cycle of reactive medicine which treats disease with drugs and surgery, to forward the principles of truly healthy diets and real prevention of chronic disease.
Listen to Dr. Lundell’s interview on Jimmy Moore’s site Livin La Vida Low-Carb. Also read The Cure for Heart Disease by Dr. Lundell.
Still not convinced that saturated fats are good for our health?
Answer this important question:Why are disease rates so high – obesity, heart disease, stroke, diabetes, high blood pressure, and related conditions of Metabolic Disorder? If saturated fat is the enemy and we are told to avoid it, wouldn’t that correspond to a decrease – rather than an increase in these health conditions? This is because the Standard American Diet is replete in processed foods including a lot of sugar and refined carbs, very few real, whole foods that are from healthy, organic, and sustainable sources which have good bacteria, enzymes, minerals, and vitamins.
Sugar is one of the biggest enemies of heart disease, found in various studies and health professionals which reveal the connection between regular consumption of refined sugar and health problems:
The profound research of Dr. Weston A. Price – a dentist and nutritionist who traveled all over the world to 14 different countries for a decade of time during the 1930s, discovered something similar: that all healthy populations were eating diets of indigenous, local foods – including almost TEN times the amount of fat-soluble vitamins from animal and bird foods. These foods were not treated with chemicals, pesticides, antibiotics, hormones, or GMOs. These groups of people were healthy, robust, and free of physical and mental disease.
In contrast, those civilizations that did experience chronic disease were those who had introduced the following substances into their diets: vegetable oils, white flour, and white sugar.
Read Dr. Price’s groundbreaking book (available in its entirety online), Nutrition and Physical Degeneration for more information.
More information:
What’s the real scoop on red meat and mortality rates?
The importance of dietary fats
The grassfed meat challenge: busting myths about meat
Wednesday, January 2, 2013
Total cholesterol doesn’t matter...Cohen
Dear Pharmacist,
I saw Dr. Oz interview a doctor on television about cholesterol. The guest said your total cholesterol doesn’t matter and I read that in your book 6 years ago. Suzy, I take a statin, and do a “Lipid Profile” annually. Is this okay? –M.D., Austin, Texas
Answer: No, it’s not okay, and I’m about to shock everyone, unless you’ve read my books, then this will be review.
Recently I wrote a column about LDL and that we should not necessarily strive to lower it. We need to know the type and number of LDL particles. For example, Lipoprotein A or “Lp(a)” and another called apolipoprotein B or “Apo B” are two subtypes of LDL particles. These particular scores directly affect your cardiovascular risk. Do you have those numbers on your lab test? I bet you don’t.
In my first book, The 24-Hour Pharmacist from 2007 and many syndicated columns I’ve explained that statins are not very effective in reducing LDL particle number or Apo B and usually do not increase the size of your LDL particles, that’s why I don’t encourage them.
It’s confusing for consumers (and physicians who unwittingly accept drug propaganda) because studies conclude statins reduce total LDL. And yes, they do reduce “total” LDL, they are also excellent anti-inflammatories so they are not completely without merit. But I’m bent on you reducing Lp(a) and Apo B, the dangerous subtypes of LDL known to raise risk for heart attack and stroke. One day I’ll tell you which vitamin reduces those bad boys, since drugs can’t, but now, back to this testing dilemma.
I’ll never submit myself for a routine “Lipid Profile” because it would waste my money. Half the people who have heart attacks have normal total cholesterol. If your results shows a low LDL (considered the bad particle), then you may assume you’re okay but you see, a low total LDL score doesn’t say much. Your triglycerides might be through the roof! You may have a huge concentration of dangerous Lp(a) and Apo B, subtypes of LDL that are never measured in that basic lipid profile.
Likewise, you may be happy with your high HDL cholesterol score, (HDL is considered a good cholesterol), but what if you have the wrong kind of HDL particles? Yeah, some HDL is bad, you didn’t know that?! You’re still at very high risk. These basic “Lipid Profiles” don’t provide the crucial details. It’s like a car mechanic who you hire to fix your engine, but you only let him look at the hood of your car, he can’t open the hood to see inside!
The better tests, sometimes covered by insurance measure particle size, type and sometimes the actual number of LDL and HDL particles. I urge you to ask your physician to order tests from Berkeley HeartLab, a leader in this field. There’s also another one called the “VAP Test” by Atherotec Diagnostics and finally, the “NMR Lipoprofile” by LipoScience.
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Read the complete atricle here.
Dangers of Statin Drugs - Seneff
Drug Side Effect Discovery from Online Patient-Submitted Reviews: Dangers of Statin Drugs
by Jingjing Liu, Alice Li and Stephanie Seneff MIT Computer Science & Artificial Intelligence Laboratory
Abstract—In recent years, consumers have become empowered to share personal experiences regarding prescription drugs via Web page discussion groups. This paper describes our recent research involving automatically identifying adverse reactions from patient-provided drug reviews on health-related web sites. We focus on the statin class of cholesterol-lowering drugs. We extract a complete set of side effect expressions from patient-submitted drug reviews, and construct a hierarchical ontology of side effects. We use log-likely ratio estimation to detect biases in word distributions when comparing reviews of statin drugs with age-matched reviews of a broad spectrum of other drugs. We find a highly significant correlation between statins and a wide range of disorders and conditions, including diabetes, amyotrophic lateral sclerosis (ALS), rhabdomyolysis, neuropathy, Parkinson’s disease, arthritis, memory loss, and heart failure. A review of the research literature on statin side effects corroborates many of our findings.
I. INTRODUCTION
The last few decades have witnessed a steady increase in drug prescriptions for the treatment of biometric markers rather than overt physiological symptoms. Today, people regularly take multiple drugs in order to normalize serum levels of biomarkers such as cholesterol or glucose, or to reduce blood pressure. All drugs have side effects, which are sometimes debilitating or even life-threatening. When a person taking multiple drugs experiences a new symptom, it is not always clear which, if any, of the drugs or drug combinations are responsible.
Increasingly, consumers are turning to the Web to seek information, and, increasingly, this information comes in the form of consumer-provided comments in discussion groups or chat rooms. User reviews of products and services have empowered consumers to obtain valuable data to guide their decision process. Recently, statistical and linguistic methods have been applied to large datasets of reviews to extract summary and/or rating information in various domains ([9] [22]).
Health care and prescription drugs are a growing topic of discussion online, not surprising given that almost half of all Americans take prescription drugs each month, costing over $200 billion in 2008 alone ([5]). Though drugs are subject to clinical trials before reaching market, these trials are often too short, and may involve too few people to give conclusive results. A large study recently conducted on the heart failure drug, nesiritude, invalidated the findings of the smaller study that had led to the drug’s approval [11]. While regulatory agencies do attempt to monitor the safety of approved medical treatments, surveillance programs such as the U.S. Food and Drug Administration’s (FDA’s) and Adverse Event Reporting System (AERS) are often difficult for patients to use.
In addition, the large language gap between medical documents and patient vocabulary can cause confusion and misunderstanding ([23]). We hope to take advantage of the vast amount of information available in patient anecdotes posted online to address the dual problems of insufficient clinical studies and mismatched terminology.
We envision a system that increases patient awareness of drug-related side effects by enabling consumers of prescription drugs to easily browse a large consolidated database of posts from health-related web sites. Beyond aggregating data from drug review and health discussion sites, we plan to support spoken queries, which would be answered via a set of succinctly summarized hits that best match the query, based on sophisticated statistical and linguistic techniques. The user could then click on any one of these displayed summaries to read the associated post.
This paper describes our preliminary efforts to detect associations between a drug class and its side effects. We use statistics and heuristic methods to build up a hierarchical ontology of side effects by aggregating patient-submitted drug reviews. We use log-likelihood ratios to extract summary information derived from biases in word and phrase distributions, and to quantify associations between drugs and symptoms. For the scope of this paper, we focus on statin drugs, which are among the most costly and commonly prescribed drugs in the United States. The methods described are applicable to all drug classes.
In the remainder of this paper, we will first review the research literature reflecting known or suspected side effects associated with statin drugs. After explaining our data collection and side-effect ontology construction, we describe our methodology and verify that many of our extracted associations align with observations from the literature.
II. BRIEF LITERATURE REVIEW
A. Side Effects of Statin drugs
Statins (Hydroxy methyl glutaryl coenzyme A reductase inhibitors) have become increasingly popular as very effective agents to normalize serum cholesterol levels. The most popular of these, atorvastatin, marketed under the trade name, Lipitor, has been the highest revenue branded pharmaceutical for the past 6 years. The official Lipitor web site lists as potential side effects mainly muscle pain and weakness and digestive problems. However, several practitioners and researchers have identified suspected side effects in other more alarming areas, such as heart failure, cognition and memory problems, and even severe
neurological diseases such as Parkinson’s disease and ALS (Lou Gehrig’s disease). [21] provides compelling arguments for the diverse side effects of statins, attributing them mainly to cholesterol depletion in cell membranes.
It is widely acknowledged that statin drugs cause muscle pain, weakness and damage ([7] [12]), likely due in part to their interference with the synthesis of the potent antioxidant Coenzyme Q10 (CoQ10) ([10]). CoQ10 plays an essential role in mitochondrial function to produce energy. Congestive heart failure is a condition in which the heart can no longer pump enough blood to the rest of the body, essentially because it is too weak. Because the heart is a muscle, it is
plausible that heart muscle weakness could arise from longterm statin usage. Indeed, atorvastatin has been shown to impair ventricular diastolic heart performance ([14]). Furthermore, CoQ10 supplementation has been shown to improve cardiac function ([13] [20]).
plausible that heart muscle weakness could arise from longterm statin usage. Indeed, atorvastatin has been shown to impair ventricular diastolic heart performance ([14]). Furthermore, CoQ10 supplementation has been shown to improve cardiac function ([13] [20]).
The research literature provides plausible biological explanations for a possible association between statin drugs and neuropathy ([15] [24]). A recent evidence-based article ([1]) found that statin drug users had a high incidence of neurological disorders, especially neuropathy, parasthesia and neuralgia, and appeared to be at higher risk to the debilitating neurological diseases, ALS and Parkinson’s disease. The evidence was based on careful manual labeling of a set of self-reported accounts from 351 patients. A mechanism for such damage could involve interference with the ability of oligodendrocytes, specialized glial cells in the nervous system, to supply sufficient cholesterol to the myelin sheath surrounding nerve axons. Genetically-engineered mice with defective oligodendrocytes exhibit visible pathologies in the myelin sheath which manifest as muscle twitches and tremors ([16]).
Cholesterol depletion in the brain would be expected to lead to pathologies in neuron signal transport, due not only to defective myelin sheath but also to interference with signal transport across synapses ([17]). Cognitive impairment, memory loss, mental confusion, and depression were significantly present in Cable’s patient population ([1]). Wagstaff et al. ([19]) conducted a survey of cognitive dysfunction from AERS data, and found evidence of both short-term memory loss and amnesia associated with statin usage. Golomb et al. ([6]) conducted a study to evaluate evidence of statin-induced cognitive, mood or behavioral
changes in patients. She concluded with a plea for studies that “more clearly establish the impact of hydrophilic and lipophilic statins on cognition, aggression, and serotonin.”
B. Relationship between Cholesterol and Health
ALS and heart failure are both conditions for which published literature suggests an increased risk associated with statin therapy ([1] [10]). Indeed, for both of these conditions, a survival benefit is associated with elevated cholesterol levels. A statistically significant inverse correlation was found in a study on mortality in heart failure. For 181 patients with heart disease and heart failure, half of those whose serum cholesterol was below 200 mg/dl were dead three years after diagnosis, whereas only 28% of the patients whose serum cholesterol was above 200 mg/dl had died. In another study on a group of 488 patients diagnosed with ALS, serum levels of triglycerides and fasting cholesterol were measured at the time of diagnosis ([2]). High values for both lipids were associated with improved survival, with a p-value <0 .05.=".05." p="p">
A very recent study on the relationship between various measures of cholesterol status and health in the elderly came up with some surprising results, strongly suggesting that elevated cholesterol is beneficial for this segment of the population [18]. A study population initially over 75 years old was followed over a 17 year period beginning in 1990. In addition to serum cholesterol, a biometric associated with the ability to synthesize cholesterol (lathosterol) and a biometric associated with the ability to absorb cholesterol through the gut (sitosterol) were measured. For all three measures of cholesterol, low values were associated with a poorer prognosis for frailty, mental decline and early death. A reduced ability to synthesize cholesterol showed the strongest correlation with poor outcome. Individuals with high measures of all three biometrics enjoyed a 4.3 year extension in life span, compared to those for whom all measures were low.
III. SIDE-EFFECT DISCOVERY
A. Data Collection
To learn the underlying associations between side effects and drug usage from patient-provided reviews, we collected drug reviews from three drug discussion forums (“AskPatient.com,” “Medications.com” and “WebDB.com”) which allow users to post reviews on specific drugs and share their experiences. Table 1 gives the statistics on the review data collection. A total of 8,515 statin reviews were collected from the three data sources. We also collected 105K drug reviews from the AskPatient.com, on drugs to treat a broad range of problems such as depression, acid reflux disease, high blood pressure, diabetes, etc. This set includes reviews for non-statin cholesterol lowering drugs.
Continue Reading the Research Study Here: http://people.csail.mit.edu/seneff/IMMM.pdf