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Statin Drugs Cause Atherosclerosis and Heart Failure"


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OK - saw this one on Facebook - did some research - had to share.  Again - what can I say - science is finally catching up with me. :lol:   I hope no one minds, but some of the things I've been saying I've bolded.

 

OH - and if your wondering - I put a copy of the study from PubMed at the end of this too.

 

http://www.wellnessresources.com/health/articles/statin_drugs_stimulate_atherosclerosis_and_heart_failure/

 

"Statin Drugs stimulate atherosclerosis and heart failure” is the title of a research study published this past week. It has not made mainstream news at the time of this article writing, but it is of utmost importance to the health of the tens of millions taking statin drugs for cholesterol. The evidence continues to pile up and prove that statin drugs are hazardous to your heart and health.

The study, published in Expert Review of Clinical Pharmacology February 6, 2015, discusses the process of how statin drugs cause the demise of heart health, worsen atherosclerosis and induce heart failure. The study’s authors are located in Japan at the Nagoya City University. If and when this news reaches the American public, the tens of millions of patients on statin drugs with worsening heart disease and heart failure should be flooding their physician’s office and the drug companies’ door with phone calls demanding explanations and reprimand. So far that has not happened.

Vitamin K2

The study presented insightful information describing the physiological mechanisms on how statin drugs cause coronary artery calcification or stiffening of blood vessels perpetuating the atherosclerosis. The plaque build-up occurs because statin drugs inhibit vitamin K2 function in the body. Vitamin K2 protects arteries from calcification. Without proper levels and function of vitamin K2, plaque levels worsen because of negative interaction with the Gla-protein and the inhibition of vitamin K2. This was previously described in a large study in 2012 with the same conclusion – statin use causes increased presence of coronary plaques. They did not identify the link with vitamin K2. The tool that cardiologists use to prevent atherosclerosis actually worsens it.

Mitochondria Damage

The second finding of the study is of little surprise. It shows that statin drugs are toxic to the mitochondria, or the energy producers in cells. Mitochondrial damage in the heart is a downward slope to cardiomyopathy or heart failure. This is a dangerous, although often subtle, effect. Statins impair the heart muscle mitochondria function, severely disrupt ATP production, and alter intracellular signaling proteins. This impairment leads to muscle cell dysfunction and eventually apoptosis or muscle cell death. This is like pouring concrete into the cellular engines of energy production and heart muscle contraction. Statins are notorious for depleting coenzyme Q10 out of the heart muscle and the body. This profoundly interferes with mitochondria function. Statins also interfere with the protein called heme A. Heme A is a component of hemoglobin that helps bind onto oxygen and carry iron to the muscle cells in the heart. Without the ability to transport iron and oxygen to the heart cells, energy production is further compromised. Iron deficits in the heart myoglobin may occur and possibly contribute further to heart failure.

Coenzyme Q10

Statin drugs interfere with coenzyme Q10. This has been documented repeatedly in medical literature with strong evidence. In fact, a black box warning for statin drugs or HMG CoQ reductase inhibitors was proposed to the FDA. The proposed black box warning was:

 

“HMG CoA reductase inhibitors block the endogenous biosynthesis of an essential co- factor, coenzyme Ql0, required for energy production. A deficiency of coenzyme Q10 is associated with impairment of myocardial function, with liver dysfunction and with myopathies (including cardiomyopathy and congestive heart failure). All patients taking HMG CoA reductase inhibitors should therefore be advised to take 100 to 200 mg per day of supplemental coenzyme Q10.”

 

The FDA blocked the attempt of putting a black box warning on statin drugs in 2014. How egregious is that?

Selenium

Another factor discussed in the initial study was the interference of the production of selenium containing proteins. Statin drugs inhibit the biosynthesis of these selenoproteins. One of the most important selenoproteins in the body is a compound called glutathione peroxidase. Its job is to protect the organism, especially muscle tissue, from oxidative damage coming from hydrogen and lipid peroxides. Lack of the glutathione peroxidase enzyme promotes high levels of free radical activity and tissue damage. Blocking the selenoprotein enzyme glutathione peroxidase is akin to pouring gasoline on the fire of inflammation and free radicals, which damages muscle tissue. In fact, the scientists described this blocking of the selenoproteins reminiscent of selenium deficiency induced heart failure, known as Keshan’s disease first identified in the 1930s. Scientists have strongly recommended that individuals suffering from non-ischemic heart failure have their selenium levels tested. This is a blood test that is readily available. Get an RBC selenium level checked at your next appointment. Certainly our selenium depleted foods and soils are not helping this situation when combined with drug-nutrient induced deficits.

Other Side Effects

Expand this picture further. We have skeletal muscle, cardiac muscle, and smooth muscle. The side effects of statin drugs are often discussed as skeletal muscle weakness and pain and in recent years the increased development of heart failure (cardiac muscle failure). This is most often in the context of high dose statins. There are, however, other side effects that may be linked with statin drugs and how they affect mitochondria. Common side effects with the drug simvastatin include headaches and constipation. One doesn’t normally think of headaches and constipation concerns linked with mitochondria, but they can be. Both the nervous system and smooth muscles have high levels of mitochondria. Bowel motility is dependent upon smooth muscle function and nervous system activity. When there is a disruption in the health of mitochondria in the body, one of the symptoms may be constipation.

 

This is the same with migraines. Some types of headaches, i.e. some subtypes of migraines are related with mitochondria dysfunction. Joint pain and tendon problems may also be related. Don’t forget the brain and side effects of being forgetful or depressed. Our brain desperately needs healthy mitochondria to function effectively. It is common to dismiss these symptoms, attributing them to poor diet, stress, or aging. Yet, how many statin users have the common symptoms of constipation, headaches, joint pain, and feel a little less energetic, forgetful, and weaker than they did a few years ago and chalk it up to aging. Often they go to their physician and because they do not have outright symptoms of rhabdomyolysis and liver failure from the statin drug, it is chalked up to stress and getting older. The traditional medical and research communities are heavily debating these side effects and are not owning up to the real damage caused by statins. Many are looking for more ways to prescribe statins other than for cholesterol problems.

 

The question remains:  how many people are going to suffer further heart disease with sky-rocketing rates of heart failure and subsequent loss of function and life linked with statin induced side effects? How many burgeoning statin drug class action law suits will it take to stop the pharmaceutical industry from this massive debacle and cover-up resulting in human tragedy? One is too many. It is time for the medical and pharmaceutical industry to acknowledge the truth and look at real solutions for heart disease.

Proactive Steps

If you are on statin drugs for any reason, make sure that you are taking at least 200 mg of coenzyme Q10 per day. Higher amounts, up to 600 - 800 mg, may be used for serious fatigue, mitochondrial injury, and cardiomyopathy disorders. The form of coenzyme Q10 plays a substantial role in how well coenzyme Q10 is absorbed, gets into the blood stream, and where it is used in the cell. Wellness Resources recommends the use of water and fat soluble coenzyme Q10 in either ubiquinone or ubiquinol forms.

 

Supporting selenium levels is also of primary concern. Brazil nuts, some seafood, mushrooms, asparagus, poultry and beef may provide good dietary sources of selenium or consider nutritional supplementation for standardized activated forms of selenium, like seleno-methionine.

 

Vitamin K2 must be present in adequate amounts to offset the drug-nutrient interaction. It is found in fermented foods and limited quantities in animal products. It is also produced by healthy gut bacteria and available in supplemental form.

Protecting the mitochondria from further oxidative damage should also be a priority. This is irrespective of statin drug use. Antioxidant rich, deep colored fruits and vegetables help protect the mitochondria from oxidative stress. Nutrients described above and others such as resveratrol, carnitine, bacopa monniera, curcumin, all B vitamins, vitamin C, vitamin E, K1, NAC, and lipoic acid are just some of the nutrients essential for protecting the heart from ischemic/heart attack damage, heart failure, and mitochondria injury.

 

Interestingly, in the last ten years melatonin has been found to protect the heart after heart attack injury in animal studies. Melatonin stopped heart cells from dying and protected the structural integrity of the mitochondria in heart cells and avoided marked worsening of heart damage. This too can be added to the arsenal of support for protecting the heart.

 

The link of melatonin and its ability to protect the heart and mitochondria leads into another tangent – the thought of sleep deprivation, sleep hygiene, and light exposure in the body and its effect on the body. With heart disease, heart failure and mitochondrial disorders at epidemic levels, it makes one question the age of electricity, sleep deprivation, and compromised melatonin production as causing a fundamental shift in the health of our heart and mitochondria. If scientists ever tackle this issue, it will be an astronomical feat for any conclusion to occur but it is an interesting thought. (Can't help but break in here - since I know of a company that HAS addressed this....but I digress...)Until then, find ways to improve your melatonin status and improve sleep to see how you and your heart feel.

 

The researchers from the headline study said “Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.” They were polite in their request and recommendations, but what about you? Are you going to follow the mainstream herd mentality, or are you going to look at the physiology and stand up for your health? Talk to your cardiologists and see if they understand these principles of physiology. If they did, they should be the first to stop prescribing these dangerous meds. Take charge of your health today!

 

http://www.ncbi.nlm.nih.gov/pubmed/25655639

 

 

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Good post, TD (as always). Yep, people are waking to to this total scam. So many of my patients know about this joke of a theory and are in complete agreement.

 

Hey Eage Eye, my best recommendation is to NOT WORRY about the cholesterol levels. I think most people have better things to be concerned with and cholesterol ISNT one of them. 

If I get a patient with "high" cholesterol levels, I will consider the thyroid and diet. A diet high in good fats (animal and fruit fats sources) and NO GRAINS will drop it IF IF IF it is suppose to be lower. Triglycerides is a far better indicator of cardio health. That should be below 100. If it is high, diet and EXERCISE are the answer. Sorry, no drugs (RX or natural) to sell. Exercise, done properly, will have a profound effect on this. Consider going ketogenic as much as possible. Less than 80 grams of carbs per day, deplete the liver stores of glycogen (about 120 gms) and life gets good. Again, NO GRAINS as a source of carbs. Veggies and some fruit is great. Hope this helps. Cheers and to your health......

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Good post, TD (as always). Yep, people are waking to to this total scam. So many of my patients know about this joke of a theory and are in complete agreement.

 

Hey Eage Eye, my best recommendation is to NOT WORRY about the cholesterol levels. I think most people have better things to be concerned with and cholesterol ISNT one of them. 

If I get a patient with "high" cholesterol levels, I will consider the thyroid and diet. A diet high in good fats (animal and fruit fats sources) and NO GRAINS will drop it IF IF IF it is suppose to be lower. Triglycerides is a far better indicator of cardio health. That should be below 100. If it is high, diet and EXERCISE are the answer. Sorry, no drugs (RX or natural) to sell. Exercise, done properly, will have a profound effect on this. Consider going ketogenic as much as possible. Less than 80 grams of carbs per day, deplete the liver stores of glycogen (about 120 gms) and life gets good. Again, NO GRAINS as a source of carbs. Veggies and some fruit is great. Hope this helps. Cheers and to your health......

 

 

Bingo!!!!!!   That's what I did. I am off my diabetic meds and feel great,

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I would like to pass on a little more information from a great site - http://www.diagnosisdiet.com/food/cholesterol/

 

Underlining inside the article is mine. Just adding a little more emphasis. (Anything underlined inside parenthisis I've added.)

 

What causes high cholesterol?

Why would the body make more cholesterol than it needs?

 

Now here’s the problem: when people eat too many sugars and starches, especially refined and high glycemic index foods, blood insulin levels can spike. When insulin spikes, it turns on HMG –CoA reductase, which tells all of the body’s cells to make more cholesterol, even if they don’t need any more. This is probably the most important reason why some people have too much cholesterol in their bloodstream. Sugars and starches can raise insulin levels, which fools the body into thinking it should grow when it doesn’t need to. This is how low glycemic index diets and low-carbohydrate diets normalize cholesterol patterns—these diets reduce insulin levels, which in turn lower HMG-CoA reductase activity.

 

“Statin” drugs, such as Lipitor®, which are prescribed to lower cholesterol levels, work partly by interfering with the activity of HMG-CoA reductase. If your cells happen to need more cholesterol under certain circumstances, but the statin drug is blocking this critical enzyme, your cells may not be able to make cholesterol when needed. And what’s worse is that the cholesterol synthesis pathway doesn’t just make cholesterol; branches of this same pathway are responsible for synthesizing a wide variety of other important molecules, including: Vitamin A, Vitamin E, Vitamin K, and Coenzyme Q. So, you may want to think twice before you artificially interfere with this pathway by taking a statin drug.

 

When you eat less carbohydrate, you are not artificially blocking the pathway; you are simply allowing HMG-CoA reductase to listen to other more important signals (such as cholesterol levels and growth requirements) and decide naturally when it should turn on and when it should turn off.

 

So, to recap: refined carbohydrates speed up the cholesterol assembly line and statins slow it down. Which approach would you rather take to manage your “cholesterol problem”—taking a drug that artificially slows down this assembly line, or changing your diet so that the assembly line only runs when it’s supposed to? [Hint: Dietary changes require no monthly co-pays, and have no potentially dangerous side effects.]

 

Chances are: if you have “high cholesterol” you do not have a cholesterol problem—you have a carbohydrate problem.

 

Good Cholesterol and Bad Cholesterol

 

This gets into the very complicated relationship between cholesterol blood tests and heart disease risk. This is an enormous topic that will be covered in future articles on this site, but I’ll summarize some basic points here now.

 

When you get your cholesterol levels checked, you will see numbers for HDL and LDL, as well as triglycerides.  Triglycerides are fats, so we’ll set them aside and just focus on HDL and LDL.

HDL particles collect extra cholesterol from around the body and carry it back to the liver to be eliminated from the body if we don’t need it. It is typically thought of as “good cholesterol” so higher HDL levels are considered a good sign.

 

LDL particles carry extra cholesterol made in the liver out to the rest of the cells in the body. We used to think of LDL as “bad cholesterol” so lower levels of LDL were considered a good sign.

The cholesterol inside of HDL and LDL particles is exactly the same, it’s just that, for the most part, HDL is carrying it in one direction and LDL is carrying it in the opposite direction. The reason why LDL had been dubbed “bad” and HDL has been dubbed “good” is that numerous epidemiological studies (most famously, the Framingham Heart Study) told us that high LDL levels were associated with a higher risk of heart attack, and that high HDL levels were associated with a lower risk of heart attack.

 

We used to think that HDL was good because it acted like a garbage truck, clearing evil cholesterol out of our bodies, and we used to think that LDL was bad because it burrowed its way into our coronary arteries, depositing evil cholesterol there—forming plaques and causing heart attacks.

Cholesterol, Carbohydrates and Heart Disease

 

However, this simplistic way of thinking about cholesterol and heart disease is changing before our very eyes. It turns out that it is more complicated than this. LDL, for example, exists in a variety of forms. It can be big and buoyant and “fluffy” or small and dense and oxidized (damaged). The new thinking is that small, dense, oxidized LDL may be the only type of LDL that is associated with heart disease. Therefore, instead of thinking of all LDL as “bad”, it would be more accurate to say that all LDL is not created equal—big fluffy LDL is “good” and small, dense, oxidized LDL is “bad.”

 

Unfortunately, standard blood tests can’t tell you which type of LDL you have because it lumps all types of LDL particles together.  Standard tests can only estimate how much of your cholesterol is travelling inside of LDL particles.  They can’t tell you how many LDL particles you have, how big they are, how dense they are, or how oxidized they are.  [For a detailed explanation of the complexities involved in interpreting cholesterol blood test results, I recommend Dr. Peter Attia’s blog at www.eatingacademy.com.]

 

What we do know from research studies is that people who eat a diet high in refined carbohydrates tend to have a higher number of “bad” (smaller, denser, oxidized) LDL particles. This makes sense, because we know that carbohydrates are “pro-oxidants” —meaning they can cause oxidation. (Leading to oxidative stress - a Redox issue.)

 

There is also lots of evidence telling us that refined carbohydrates can cause inflammation.  Just because doctors find cholesterol inside artery-clogging plaques does not mean that cholesterol causes plaques. It is now well established that heart disease is a disease of inflammation. It is not simply that an innocent, smooth, buoyant sphere of fat and cholesterol traveling through the bloodstream decides to somehow randomly dig its way into a healthy coronary artery. The first step in the development of a vessel-clogging plaque is inflammation within the lining of the artery itself. When doctors cut into plaques they don’t just find cholesterol—they find many signs of inflammation (such as macrophages, calcium, and T cells). Wherever there is inflammation in the body, cholesterol is rushed to the scene to repair the damage—because we need cholesterol to build healthy new cells. Jumping to the conclusion that coronary artery plaques are caused by the cholesterol found inside of them is like assuming that all car accidents are caused by the ambulances that are found on the scene.

 

The latest research suggests that diets high in refined and high glycemic index carbohydrates increase the risk of inflammation throughout the body, especially in blood vessels. Diabetes, a disease which is intimately associated with high blood sugar levels, is infamous for causing damage to blood vessels in the retina, kidneys, and tiny vessels that feed nerve endings in the feet. It is well established that people with diabetes are also at higher risk for heart disease. It should therefore not be a stretch for us to imagine that all people with high blood sugar and/or insulin levels due to diets rich in refined carbohydrates may also be at increased risk for cardiovascular disease.

 

Cardiology researchers are now turning away from the notion that saturated fat and cholesterol cause heart disease. After all, how could saturated fat and cholesterol, which we have been eating for hundreds of thousands of years, be at the root of heart disease, which is a relatively new phenomenon? Cardiologists are finding instead that refined carbohydrate (such as sugar and flour), which we have only been eating in significant quantities for about a hundred years, is the single most important dietary risk factor for heart attacks:

 

    “Strong evidence supports …associations of harmful factors, including intake of trans-fatty acids and foods with a high glycemic index or load.”

    “Insufficient evidence of association is present for intake of…saturated and polyunsaturated fatty acids; total fat,… meat; eggs; and milk.” [Mente et al 2009].

 

Sweetheart? 

 

There are several plausible mechanisms for how refined carbohydrate could increase risk for heart disease and change cholesterol profiles:

 

  •     Diets high in refined carbohydrate lower HDL levels and set the stage for high insulin levels, oxidation, and inflammation throughout the body, including in the coronary arteries. (Means this is a Redox issue also)
     
  •     High blood sugar and insulin levels turn big, fluffy, innocent LDL particles into small, dense, oxidized LDL particles, which are associated with increased risk for heart disease.
     
  •     High insulin levels turn on the cholesterol building enzyme HMG-CoA reductase, forcing the body to make more cholesterol than it needs.

It is becoming increasingly obvious that cholesterol is innocent until corrupted by refined carbohydrate.

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So, after $50,000 or so of Lipitor, we are once again informed (now that the patent has expired) that the wise men erred by confusing co-location with causation.  Or was it an error?  Hmm, how many billions of profits?  Much like the sudden epidemic of ADHD that magically occurred right after the drugs to control it got their patents.

 

But it MUST have worked, my cholesterol plunged from around 125 down to around 110.  Or maybe that happened because I switched from sugar to Splenda, skipped the fries, and got off my ass once in a while.  Well, at least I had the good sense to ignore them 40 years ago when they told me eggs and avocados would kill me. 

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No, I think you missed the point. HAVING LOW CHOLESTEROL CONFERS NO BENEFIT TO YOU. Having low cholesterol is NOT an indicator that you have less of a chance of having a heart attack or stroke. In fact, having low cholesterol means you MORE likely to die from an infection verse someone who has "high" cholesterol.

When I was an aviator in the military my cholesterol was at 220. I followed the low-fat diet ideas, exercised my a$$ off and ate mostly organic, vegetarian ways. Now, it is 160 and I am up to 70% animal/fruit fats in the diet. Why did that happen? I wish another doc could explain this to me, but NONE can. Why? Because they would have to admit their theory is UTTER and COMPLETE CRAP.

Nstoolman did it right. Cured himself (I take it he is a man. Sorry if I am wrong) of incurable diseases by proper DIET. Nothing to sell. No drugs to take. No backward BS to follow from over-educated FOOLS who just follow research journals that do hack jobs for pharmacy. To your health...Better worrying about the color of your hair then you cholesterol levels!

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Learning, Your Memory, and Cholesterol

 
July, 2005
 
by Chris Masterjohn
 
One of the many important roles cholesterol plays in the body is in our nervous system, enabling learning and memory to take place. In fact, one of the reasons that sleep is beneficial to our learning and memory is because it enables our brain to make more cholesterol!
 
While the war on cholesterol is waged full-speed ahead, and many web sites are now touting low-fat, low-cholesterol diets as "brain-healthy" due to unfortunate misinterpretations about the role of a cholesterol byproduct in Alzheimer's disease, science is continually showing that cholesterol is one of the most important parts of our brains.
 
Sleep, Memory, Learning, and Cholesterol
 
Evidence to date strongly supports the concept that sleep plays an important role in increasing performance of newly learned activities, consolidating memories, and increasing brain plasticity-- which is the ability to form new, as well as break, connections between neurons called synapses.
 
These benefits of sleep are not simply the absence of stress from sleep-deprivation, but an independent, critical role, in the actual process of learning and memory-formation.1
 
But why?
 
Exciting research was published in the pages of Neuron last year (2004),2 identified about 100 genes that increase their activity during sleep. They found about as many that increased their activity during wake, and others whose activity varied with circadian rhythm, independent of sleep or wakefulness.
 
While there are many important cellular and molecular events that happen during sleep, and we are only cracking the surface in our understanding of them, one of the things this study showed is that cholesterol synthesis increases during sleep-- which, given the research described below, undoubtedly is part of the reason sleep is beneficial to mental functioning.
 
Cholesterol is abundant in the tissue of the brain and nervous system. Myelin, which covers nerve axons to help conduct the electrical impulses that make movement, sensation, thinking, learning, and remembering possible, is over one fifth cholesterol by weight.3
 
Even though the brain only makes up 2% of the body's weight, it contains 25% of its cholesterol.4
 
One of the groups of genes that the above study found to be upregulated during sleep were genes important for the synthesis and maintenance of myelin, including myelin structural proteins and genes relating to the synthesis and transport of cholesterol.
 
But the benefits of cholesterol extend beyond both sleep and myelin. In fact, in 2001, cholesterol was found to be the most important factor in the formation of synapses, the basis of our learning and memory.
 
Memories and Learning are Directly Dependent on Cholesterol
 
In the late 1990s and early 2000s, research was pointing to an unknown compound made by glial cells that was responsible for the ability of neurons to form synapses, or connections between each other.
 
Thoughts, memories, learning, and all mental function is dependent on the formation of synapses, so the ability to form them will directly impact mental functioning and health.
 
In the absence of this-- as yet unknown-- "glial factor," neurons formed few synapses, and the synapses they formed were inefficient and poorly functioning. In the presence of glial cells, which secrete the unknown factor, neurons formed many, highly efficient synapses.
 
So what is this "glial factor"?
 
Research in 2001, by Mauch, et al., published in volume 294 of Science magazine, determined that the unknown glial factor is cholesterol, which is released by the glial cells in a carrier called "apolipoprotein E."5
 
Initially, the researchers thought that the apolipoprotein E (apoE) may have been the glial factor itself. But it turned out that when neurons were treated with apoE, the beneficial effects on synapse formation were not observed.
 
The researchers then reasoned that, since apoE fit the bill in some ways, but did not have the desired effect, some of the lipids it carried may have been the elusive glial factor.
 
As it turned out, treating the neurons with a 10 mcg/mL solution of cholesterol increased synapse formation by 12 times! Other lipids, carried by apoE, such as phosphatidylcholine and sphingomyelin, did not have a significant effect, and were even toxic to the neurons at very high doses.
 
On the other hand, when low-cholesterol glial secretions were produced by using the cholesterol-lowering drug, mevastatin, the effect of the glial secretion on synapse formation was strongly diminished. When cholesterol was added back to the low-cholesterol secretion, the positive effect on synapse formation was fully restored.
 
The authors identified cholesterol as a limiting factor of synpase formation. In other words, the need for cholesterol in the brain is large enough relative to the supply of cholesterol that the availability of cholesterol can directly limit the ability to form synapses.
 
Neurites Lose Their Way Without Cholesterol
 
"Neurites" refer to the extensions from the cell of a neuron that connect with other neurons or muscles. The type of neurite that sends impulses away from the cell is an axon, and the type of neurite that receives impulses is a dendrite.
 
Connections between neurons, called synapses, are contantly being formed and broken in our brains, where dendrites and axons meet.
 
But they can't just grow randomly. Neurites grow in response to a stimulus given by a signaling protein in the membranes of neurons.
 
These signaling proteins rely on lipid rafts, which are beds of cholesterol and phospholipids made from long-chain saturated fatty acids that secure some proteins.
 
A 2004 study found that disrupting lipid rafts by extracting some of the cholesterol from the membrane of a neuron completely destroyed the ability of neurons to find the signaling proteins attracting them!6
 
Statins Could Kill Your Memory — Eggs Could Cure It
 
We now know that the formation of synapses, or connections between neurons, is directly dependent on the availability of cholesterol.
 
The formation of these synapses are what give us the ability to remember and learn. The benefits of sleep for memory formation and learning are in part a result of increased cholesterol synthesis during sleep.
 
The implications are important and powerful. In our society's quest to lower cholesterol at all costs and without second thought, could some of the methods we use, such as taking cholesterol-lowering drugs, or eating low-fat, low-cholesterol diets, be limiting the availability of cholesterol to our nervous system?
 
The authors of the 2001 Science study described above concluded that the "results imply that genetic or age-related defects in the synthesis, transport, or uptake of cholesterol in the CNS may directly impair the development and plasticity of the synaptic circuitry."
 
But the authors left out one thing: in addition to genetic or age-related defects, there is currently a boombing industry founded upon the deliberate inhibition of the synthesis of cholesterol using pharmaceutical drugs. Some statins cross the blood-brain barrier (BBB); others may affect cholesterol levels in the brain without necessarily crossing the BBB; still, without crossing the BBB, the peripheral nervous system could likewise be damaged.
 
In fact, amnesia and cognitive dysfunction are reported as side-effects in some statin users. Dr. Duane Graveline, MD, former NASA scientist and astronaut, describes his bout of statin-induced memory loss, in which his wife caught him wandering aimlessly in his yard while he failed to recognize her.
 
In an article on the side-effects of cholesterol-lowering drugs, the Geriatric Times cites two randomized trials, several case reports, and one large case series pointing to memory loss as a result of statin drugs.
 
Conversely, dietary cholesterol can help reverse the effects of declining memory with age.
 
Mary Enig, PhD, cites a study in her book, Know Your Fats, that found that the cholesterol in eggs can help improve memory in the elderly.5
 
Remember...
 
One of the basic parts of ourselves that defines us as humans is our mind. We imagine, think, study, learn, remember, come up with new ideas, remember old faces, and form friendships and familial relationships that are based, in large part, on our memories of those people.
 
Cholesterol is a central building block of the connections within our brain that hold these memories and learning processes together. Remember that... thanks to cholesterol, you can!
 
You can share this article, or leave a comment below.
 
Read more about the author, Chris Masterjohn, PhD, here.
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Dude, Neanderthals were TOTAL bad-a$$! Killing animals with their bare-hands (and I don't mean chickens! Saber-tooth tigers and mastodons: insane, mean animals) and then wearing the skins as a fashion statement. "Clubbing" meant beating the crap outta someone and dragging the old lady back to the den for some real monkey business! hahahaha. Good for you. A title of respect and honor in my book! Cheers and keep-up the good health. In your case, eat like a Neanderthal.

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Thanks to everyone who posted. Bottom line: The Statin fraud has been known

for at least 10+ years and little was done about it because it sure was a

profitable run.

 

Thankfully more learned to question their docs and their logic,

and it is now becoming more main stream and some docs have ceased

offering this type drug to their patients because of the slow degradation

they were seeing in their health, and it is now understood "cholesterol"

is a MUST for proper health and has never been the threat it was made out

to be...the motive was always profit and the fraud is real.

 

The "solution" often made patients sick while blaming many of the symptoms

on their "high cholesterol". What we tolerate and believe from the medical communtiy is

truly amazing. Thanks TD and Doc. :)

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