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Interesting Information: Misunderstandings About “Good” and “Bad” Cholesteral

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Interesting Information:  March 21, 2014

Misunderstandings About “Good” and “Bad” Cholesterol

Within the past week, two family members have had questions about “good” and “bad” cholesterol and WHAT causes heart disease.  One has been on a statin for three years now–much to my horror as you will see why if you keep reading–to lower LDL cholesterol.  The other thought saturated fats led to the plaques that can block arteries and that the plaque was formed from the “bad” LDL cholesterol which must be lowered for health.  The latter understanding is both incomplete and flawed in that saturated fats are not the culprit and undamaged LDL cholesterol is not even…cholesterol…so lowering what is called LDL cholesterol is not going to work and is going to make you sick as you will not be getting the nutrients you need.  In addition, Seneff explains in detail how statins destroy your muscles, including your heart muscle.

I’ve written about Stephanie Seneff’s article “Cholesterol:  The Essential Molecule–And the Adverse Effects and Overuse of Statins” in Mainely Tipping Points 37, available on this blog.  This comprehensive article appeared in Well Being Journal, Nov/Dec, and is not free.   Seneff, based at MIT, is doing some amazing bench science research at the cellular level, and I like her work a lot.  Her web site lists her credentials, papers, talks, etc., if you want to take a look:  http://people.csail.mit.edu/seneff/.  Or just google her name.  Much of her work is free to you, so you can find parts of the information in the above article scattered across her papers or in shortened forms.  In addition, the Joseph Mercola web site has a nice video of an interview with Seneff about statins:  http://articles.mercola.com/sites/articles/archive/2012/02/11/dr-stephanie-seneff-interview-on-statins.aspx.  (There are other interviews on Mercola with Seneff as well as her main concern is the lack of cholesterol sulfate in our bodies today. Or, sulfur, which used to come from the soil, but which, thanks to commercial farming, is no longer available in the soil in the quantities we need.)

ANYWAY, Seneff’s explanation of HDL (called the “good” cholesterol) and LDL (the “bad” cholesterol) calls into question these simplistic and erroneous labels.  These terms were coined to sell you–and your doctors–the notion that you need to take a statin to lower your LDL cholesterol.  I’ve read Seneff’s explanation from other researchers, but her explanations in this article are very comprehensive and are easy to understand.  

Seneff’s conclusion about statins is also easy to understand:

I have been driven by the need to understand how a drug that interferes with the synthesis of cholesterol, a nutrient that is essential to human life, could possibly have a positive impact on health.  I have finally been rewarded with an explanation for an apparent positive benefit of statins that I can believe, but one that soundly refutes the idea that statins are protective.  I will, in fact, make the bold claim that nobody qualifies for statin therapy, and that statin drugs can best be described as toxins (13).

So, here’s Seneff’s discussion of LDL, HDL, and Fructose:

We have been trained by our physicians to worry about elevated serum levels of low density lipoprotein (LDL), with respect to heart disease.  LDL is not a type of cholesterol, but rather can be viewed as a container that transports fats, cholesterol, vitamin D, and fat-soluble anti-oxidants to all the tissues of the body.  Because they are not water-soluble, these nutrients must be packaged up and transported inside LDL particles in the blood stream.  If you interfere with the production of LDL, you will reduce the bioavailability of all these nutrients to your body’s cells.

The outer shell of an LDL particle is made up mainly of lipoproteins and cholesterol.  The lipoproteins contain proteins on the outside of the shell and lipids (fats) in the interior layer.  If the outer shell is deficient in cholesterol, the fats in the lipoproteins become more vulnerable to attack by oxygen, every present in the blood stream.  LDL particles also contain a special protein called “apoB” that enables LDL to deliver its goods to cells in need.  ApoB is vulnerable to attack by glucose and other blood sugars, especially fructose.  Diabetes results in an increased concentration of sugar in the blood, which further compromises the LDL particles by gumming up apoB.  Oxidized and glycated LDL particles [glycation is when a sugar molecule combines with a protein or fat molecule, degrading it] become less efficient in delivering their contents to the cells.  Thus they stick around longer in the blood stream, and the measured serum LDL level goes up.

Worse than that, once LDL particles have finally delivered their contents, they become small dense LDL particles, remnants that would ordinarily be returned to the liver to be broken down and recycled.  But the attached sugars [through glycation] interfere with this process as well, so the task of breaking them down is assumed instead by macrophages in the artery wall and else where in the body, through a unique scavenger operation.  The macrophages are especially skilled to extract cholesterol from damaged LDL particles and insert it into HDL particles.  Small dense LDL particles become trapped in the artery wall so that the macrophages can salvage and recycle their contents, and this is the basic source of atherosclerosis.  HDL particles are the so-called good cholesterol, and the amount of cholesterol in HDL particles is the lipid metric with the strongest correlation with heart disease, where less cholesterol is associated with increased risk.  So the macrophages in the plaque are actually performing a very useful role in increasing the amount of HDL cholesterol and reducing the amount of small dense LDL.

The LDL particles are produced by the liver, which synthesizes cholesterol to insert into their shells, as well as into their contents.  The liver is also responsible for breaking down fructose and converting it into fat (Collison et al., 2009).  Fructose is ten times more active than glucose at glycating proteins, and is therefore very dangerous in the blood serum (Seneff et al., 2011).  When you eat a lot of fructose (such as the high fructose corn syrup present in lost of processed foods and carbonated beverages), the liver is burdened with getting the fructose out of the blood and converting it to fat, and it therefore can not keep up with cholesterol supply.  As I said before, the fats can not be safely transported if there is not enough cholesterol.  The liver has to ship out all that fat produced from the fructose, so it produces low quality LDL particles, containing insufficient protective cholesterol .  So you end up with a really bad situation where the LDL particles are especially vulnerable to attack, and attacking sugars are readily available to do their damage (15-16).

SO THE REAL CULPRIT IN HEART DISEASE IS TOO MUCH SUGAR, ESPECIALLY FRUCTOSE SUGARS.

What to eat:

Cut way back on fructose–found in processed foods and in FRUITS.  Grains also turn into sugars in the body.  Really, if it’s in a box, a can, or a package in the grocery store–or in the middle aisles–don’t eat it.

Spend time outdoors and let the sun shine on your skin as that produces useable cholesterol sulfate.  Strenuous exercise helps clear your body of excess sugars.

Eat foods that are good sources of lactate:  sour cream and cultured products like yogurt and kefir, preferably made from raw milk.

Eat foods rich in cholesterol sulfate:  GOOD eggs (NOT the ones from vegetarian chickens), liver, oysters, onions, garlic, cabbage family, GOOD meats–in other words, clean, nutrient-dense whole foods.

Written by louisaenright

March 21, 2014 at 12:23 pm

Interesting Information: New Breakthrough: Roundup DOES Harm Humans

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Interesting Information:  January 21, 2013

New Breakthrough:  Roundup® DOES Harm Humans

 

Roundup®, which is mostly the chemical glyphosate, is “the most popular herbicide used on the planet,” according to Stephanie Seneff, PhD, in “Roundup®:  The `Nontoxic’ Chemical that May Be Destroying our Health,” Wise Traditions, Fall 2013, 30-38.

Roundup® is produced by Monsanto (it went off patent in 2000), and Monsanto has claimed that Roundup® is nontoxic for humans–even though glyphosate is “an established endocrine disruptor.”

Yet, there are many real-world examples of people sickened in all kinds of ways by exposure to Roundup.   But up to now, that I know of, there’s not be an explanation for HOW glyphosate affects humans that can stand up to industry’s insistence on using it.

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The “nontoxic for humans” argument is that glyphosate kills weeds by “interfering with what is called the shikimate pathway–which is “essential in plants for the synthesis of a class of amino acids called the `aromatics.’ ”

The shikimate pathway is “nonexistent in any mammalian cell.”

BUT, BUT, BUT…AND HERE’S THE BREAKTHROUGH–“all of the microbes that take up residence in our digestive tract do have this shikimate pathway, and exposure to glyphosate…will cause them serious stress as a consequence.”

And, hopefully, each of you has become aware of the rapidly increasing knowledge of how important these gut “flora and fauna” are to human health.  And, how, if the opportunistic microbes get out of balance in our systems (sugar), they can be a real wrecking crew to your health.  This knowledge is the basis of Natasha Campbell-McBride’s work with the GAPS (Gut and Psychology Syndrome).

Studies have shown that glyphosate disrupts the gut bacteria in chickens, cows, and pigs, causing inflammation in the gut along with an overgrowth of pathogenic forms and concurrent loss of beneficial bacteria.  It is now becoming apparent that our gut bacteria, which outnumber our own cells by a factor of ten to one, play many important roles in supplying nutrients and protecting us from toxins.  There’s also an intricate connection between the gut and the brain, such that an unhealthy digestive system translates into pathologies in the brain.

AND we are NOT healthy in America–likely at least in part because we–unlike western Europe–are awash with chemicals like glyphosate.

Despite spending nearly two and a half times as much on health care as our peer nations, the U.S. lags behind many of these other nations in basic metrics like infant mortality and life expectancy.  The most recent figures for infant mortality place the U.S. at number forty-six, behind Cuba and Guam.  Clearly we are doing something wrong, and our wholesale embrace of GMOs is an obvious candidate.

Autism used to be rare, affecting one in ten thousand children.  The latest numbers put out by the CDC in March 2013, show one in fifty.  This is an alarming number, and, what is even more alarming is how quickly the number has been rising in recent years.

Ninety percent of the GMO crops (GMO corn, soy, cotton, sugar beets, and canola) are engineered to be “Roundup Ready,” which means that they can be sprayed with Roundup and they will happily soak it up into their tissues.  The practice of “desiccating”crops like wheat and sugar cane just before the harvest by spraying them with Roundup is also becoming more and more popular as a way to reduce the amount of vegetation that needs to be cleared in preparation for planting next year’s crop.  These two changes in agricultural practices almost certainly mean that Roundup is entering our food supply in record amounts.

Here’s more on the mechanics of why the shikimate pathway in our gut microbes affect us, but it’s not the whole description Seneff discusses as it is complex and too long to synthesize here:

Plants and microbes use the shikimate pathway to produce the aromatic amino acids, tryptophan, tyrosine and phenylalanine.  Because they don’t have this pathway, mammals can’t produce these essential nutrients, and therefore we depend on plants and microbes to provide them for us.  So it is logical that glyphosate, by interfering with this pathway, would lead to a deficiency in these nutrients.  Tryptophan is the sole precursor to serotonin, and serotonin deficiency is implicated in a litany of diseases and conditions that are prevalent today, including autism, obesity, Alzheimer’s disease, depression, suicide, and homicidal behavior.  Serotonin is an appetite suppressant so it’s hard not to overeat when it is in short supply.

Autism is associated with two comorbidities that may yield hints as to its underlying etiology:  disrupted gut bacteria and impaired sulfur metabolism.  A characteristic feature of children with autism is an overgrowth of pathogenic bacteria in the gut, which can lead to neurological defects arising from exposure of the brain to toxins produced by these bacteria.

Two pathogens exist in our gut, and they can play a beneficial role if kept under control by other microbes:  Clostridia difficile and Pseudomonas aeruginosa.  (Both are “causing a major crisis in hospitals in the U.S. and elsewhere due to their increased prevalence and multiple antibiotic resistance.)  Pseudomonas aeruginosa can metabolize glyphosate.  BUT, formaldehyde, “a known carcinogen and neurotoxin,” is the by-product.  Clostridia diff. is a yeast pathogen that thrives on sugar.  It can punch holes in your gut that let food particles escape into the bloodstream which, in turn, cause all sorts of food allergies and autoimmune problems.  BUT, in terms of autism, Seneff has a long, involved explanation of how this pathogen is connected to sulfate transport and autism.

So, what can you do?

Eat organic foods.  Refuse to buy industrially grown, poisoned, monocrop, and/or GMO foods.  Insist on labeling of GMO foods.  And tell people who question WHY, what’s at stake.

And you can also tell them that chronic illnesses are incredibly, incredibly expensive.

Dr. Seneff works at the intersection of technology and biology.  She is a Senior Research Scientist at MITs Computer Science and Artificial Intelligence Laboratory.  She has a Bachelor’s degree from MIT in biology with a minor in food and nutrition, and her PhD from MIT is in computer science.  She has done groundbreaking work with the importance of sulfur in foods humans eat–and sulfur has seriously diminished with industrially grown produce.

Here’s her heavily researched article in total–where you can see all her citations:

Roundup: The “Nontoxic” Chemical that May Be Destroying our Health – Weston A Price Foundation.

Mainely Tipping Points 37: Statins: Profitable Toxins

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Mainely Tipping Points 37

STATINS:  PROFITABLE TOXINS

 

Stephanie Seneff is a senior research scientist in the EECS (Electrical Engineering, Computer Science) department at the Massachusetts Institute of Technology (MIT).  Her degrees–a B.S. in biology, and an M.S., E.E., and Ph.D. in EECS—were awarded by MIT.  She researches within the interdisciplinary intersections of medicine, computer science, and electrical engineering, or the highly-respected biomolecular discipline.   

Seneff’s article, “Cholesterol:  The Essential Molecule–and The Adverse Effects and Overuse of Statins” (Well Being Journal, November/December 2011, 13-24), is the most complete, chemical explanation I have read of why statins are not a solution to the prevention of heart attacks. Statins, Seneff explains, create a situation where muscles are destroyed and where, eventually, the whole body is seriously at risk. 

Once again, drug industry researchers and medical doctors only looked at one piece of an illness puzzle—prevention of heart attacks–without understanding the actual causes and without acknowledging the long-term impact of their drug (statins) solution.  (Surely they know the harm statins do and are ignoring this harm because statins are so profitable.)  After exhaustive research, Seneff says the following:  “I will…make the bold claim that nobody qualifies for statin therapy, and that statin drugs can best be described as toxins” (13).  And, “I would in fact best characterize statin therapy as a mechanism to allow you to grow old faster” (22).

In addition, the drug industry and doctors have played a game I think of as “medical math.”  Seneff notes that a meta-study reviewing seven drug trials and 42,848 patients over a three- to five-year period did show a 29 percent decreased risk of a major cardiac event.  But as heart attacks were “rare among this group, what this translates to in absolute terms is that 60 patients would need to be treated for an average of 4.3 years to protect one of them from a single heart attack.  However, essentially all of them would experience increased frailty and mental decline….” (14).       

Seneff’s article describes the chemical components within the body when cholesterol is fully present and when it has been compromised.  Her explanations are clear and fully understandable, but complicated.  If you are taking statins or are contemplating them, I urge you to read Seneff’s article.  Meanwhile, I will do my best to synthesize the high points so that you can understand why it is so dangerous to use statins to reduce cholesterol in your body. 

Furthermore, many, many studies—some of them long-term studies—clearly show that people—and especially women–with high cholesterol counts live longer than those with low cholesterol counts.  This information is readily available, and it is a mystery to me why our doctors continue to ignore it.

 Statins interfere with the synthesis of cholesterol, a nutrient, explains Seneff, that has been demonized by the drug industry and doctors, but which is essential to human health.   “Cholesterol is absolutely essential to the cell membranes of all our cells, where it protects the cell not only from ion leaks but also from oxidation damage to membrane fats” (14).  Reducing cholesterol “places a much bigger burden on the body to synthesize sufficient cholesterol to support the body’s needs, and it deprives us of several essential nutrients” (14).       

Further, Seneff notes, “there are three distinguishing factors that give animals an advantage over plants:  a nervous system, mobility, and cholesterol.”  Cholesterol, which is “absent from plants, is the key molecule that allows animals to have mobility and a nervous system” (14). In a nutshell, when statins reduce cholesterol, they force the body to jerry-rig alternative chemical systems that lead eventually to body-wide damage (20).

One mythology today is that elevated serum levels of LDL (low density lipoprotein) cholesterol is a problem.  But, Seneff explains, “LDL is not a type of cholesterol, but… [is] a container that transports fats, cholesterol, vitamin D, and fat-soluble anti-oxidants to all the tissues of the body.”  Because these nutrients are not water-soluble, they “must be packaged up and transported inside LDL particles in the blood stream.”  Thus, “if you interfere with the production of LDL you will reduce the bioavailability of all these nutrients to your body’s cells” (15).

The LDL package, explains Seneff, is “vulnerable to attack by glucose and other blood sugars, especially fructose.”  If “gummed up” by sugars, “the LDL particles become less efficient in delivering their contents to the cells,” they “stick around longer in the bloodstream,” and the “measured serum LDL level goes up” (15).  But, worse, after the LDL particles have delivered their contents, they “become small dense LDL particles, remnants that would ordinarily be returned to the liver to be broken down and recycled.”  However, “the attached sugars interfere with this process…so the task of breaking them down is assumed instead by macrophages in the artery wall and elsewhere in the body.”  These “small dense LDL particles become trapped in the artery wall so that the macrophages can salvage and recycle their contents, and this is the basic source of atherosclerosis” (15). 

The liver, explains Seneff, produces the LDL particles.  Statin therapy “greatly impacts the liver, resulting in a sharp reduction in the amount of cholesterol it can synthesize.”  Also, the liver breaks down fructose and converts it into fat.  So, when there is a lot of fructose in the system, the liver becomes burdened with the task of converting it to fat and cannot “keep up with the cholesterol supply.”  Both conditions mean that “fats cannot be safely transported”(16).

Additionally, as the liver is burdened with handling the fructose, “it produces low quality LDL particles” (16).  So, harmful chain reactions begin to occur, such as the following:  fructose builds up in the blood stream, which causes more damage; the skeletal muscle cells are severely affected; and the brain, which houses 25 percent of the body’s cholesterol, is impaired.  Diabetes and arthritis are also associated with statin therapy (19, 21).   

When overburdened, the liver shifts the processing of excess fructose to the muscle cells, explains Seneff.  The muscle cells themselves begin to use an alternative fuel source that requires an abundance of fructose and which allows the production of lactate, which is a high-quality fuel for the heart.  This desperate production of lactate is why statin therapy can lead to a “reduction in heart attack risk.” (17).

But, continues Seneff, “the muscle cells get wrecked in the process” (17).  In effect, the muscles “can no longer keep up with essentially running a marathon day in and day out.”  The muscles “start literally falling apart, and the debris ends up in the kidney, where it can lead to the rare disorder rhabdomyolysis, which is often fatal” (20).  The drug industry readily admits to muscle pain and weakness with statin use (17).

The dying muscles also “expose the nerves that innervate them to toxic substances, which then leads to nerve damage such as neuropathy, and ultimately amyloid lateral sclerosis (ALS), also known as Lou Gehrig’s disease, a very rare, debilitating, and ultimately fatal disease that is now on the rise due (I believe) to statin drugs” (20).

Also, as the cells struggle with ion leaks caused by insufficient cholesterol, they begin to replace a potassium/sodium system with a calcium/magnesium-based system.  The result is the “extensive calcification of artery walls, heart valves, and the heart muscle itself.”  Indeed “research has shown that statin therapy leads to increased risk of diastolic heart failure” (20). 

Seneff is very interested in the role of cholesterol sulfate.   Cholesterol sulfate is “very versatile.  It is water soluble, so it can travel freely in the blood stream, and it enters cell membranes ten times as readily as cholesterol, so it can easily resupply cholesterol to cells” (24).

Cholesterol sulfate, explains Seneff, is produced by the skin in large quantities with sun exposure.  Seneff  thinks that “the natural tan that develops upon sun exposure offers far better protection from skin cancer than the chemicals in sunscreens.”  And, Seneff thinks we should eat foods “rich in both cholesterol and sulfur”—“eggs are an optimal food, as they are well supplied with both of these nutrients” (24).     

To avoid heart disease, Seneff suggests cutting back on fructose intake, eating whole foods instead of processed foods, and eating foods which are good sources of lactate (sour cream, yogurt, and milk products in general).  (One can use goat-milk products if cow’s milk is a problem.)  Strenuous physical exercise helps “get rid of any excess fructose and glucose in the blood, with the skeletal muscles converting them to the much coveted lactate” (23) 

Seneff further advises:  “spend significant time outdoors; eat healthy cholesterol-enriched, animal-based foods like eggs, liver, and oysters; eat fermented foods like yogurt and sour cream; eat foods rich in sulfur like onions and garlic.  And, finally say `no-thank-you’ to your doctors when they recommend statin therapy” (24).