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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

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