What Tells the Liver to Produce Bad LP(a) Cholesterol?
As we said before, cholesterol is a nutrient the body need very much. However, cholesterol is not water soluble so it has to be carried to the body’s cells by fats called lipoproteins. Since lipoproteins carry the cholesterol, the combination is just called “cholesterol”. The main types that make up a total cholesterol count include:
Low-density lipoprotein, or LDL – This is known as “bad” cholesterol. They carry the cholesterol from your liver around your blood stream.
High-density lipoprotein, or HDL– is known as “good” cholesterol. HDL carries the excess LDL cholesterol back to the liver to be eliminated, slowing plaque buildup.
Triglycerides– are a form of fat made in the body. People with high triglycerides often have high LDL (bad) level and a low HDL (good) level.
Lipoprotein (a), or Lp(a) cholesterol– Lp(a) is a genetic variation cousin of LDL (bad) cholesterol. It is the baddest of the sticky bad boys concerning plaque.
Your body is interested in survival and will do whatever else it can to save you’re (its) life! When the body has trouble repairing damaged coronary arteries, it goes to emergency measures.
The primary way this happens is that there are white blood cells specifically designed to attach to rough surfaces (tears). This helps heal things like cuts. We need these white blood cells!
However, in the arteries, they are only meant to be a last ditch emergency aid. If the body senses that these artery lesions are not being healed properly it sends a signal to the liver to produce more LDL cholesterol – especially a very sticky cousin of LDL cholesterol called Lp(a).
LDL and Lp(a) Cholesterol
With LDL cholesterol, a problem arises when free radicals oxidize the LDLs. Then they are more apt to attach to the white blood cells and be deposited as plaque in the artery walls.
The Lp(a) cholesterol is a much bigger problem because they are even stickier than LDLs. Lp(a) cholesterol sticks to the white blood cells like Velcro! They can even stick directly to the tears and attract other Lp(a) molecules, along with calcium. Lp(a) is so special that we will talk more about it in a moment.
These forms catch on and build up the blood vessel patch we call plaque. If there are a lot of tiny abrasions in the arterial lining, there will be a lot of plaque buildup along the walls of the artery. Plaque is simply your body’s attempt to place a patch over the damaged portions of the arteries in order to prevent them from bleeding. If vitamin C and other nutritional supplies remain scarce, a progressive accumulation of plaque deposits on the interior lining of your coronary arteries is the result.
Don’t be too hard on your body because this plaque keeps your arteries from internal bleeding! Better alive with plaque than dead from internal bleeding! However…
We would like to prevent more plaque from forming,
and remove some of the plaque that has formed!
These deposits develop over time as a reaction to lesions inside the arteries. However, we need to take a special look at the nastiest culprit in this plaque problem. Being aware of it will help you to better understand our counter-measures for healing the arteries.
Lp(a) – The Major Key to Plaque Building
Researchers with the famous Framingham Heart Study identified a relative of LDL cholesterol. It is a fat molecule called lipoprotein (a) or Lp(a). Lp(a) is a powerful and under-appreciated cause of heart disease. While LDL cholesterol is hyped as the “bad” cholesterol, Lp(a) is much worse! It can lead to heart attacks early in life, sometimes in your 40s or 50s. Lp (a) is not only a direct cause of plaque growth and plaque rupture (heart attack), but it also magnifies the dangers of LDL cholesterol.
Lp(a) molecules attach themselves to LDL cholesterol and other fat molecules. It oxidizes the LDL cholesterol which leads to free radical production and further damage.
It also has very strong adhesive properties (did we mention it is very sticky). It particularly likes to stick to lesions in the arterial wall – either to the white blood cells or just directly to the tears in the lining of the artery.
The 1985 Nobel Prize in Medicine was awarded to Michael S. Brown and Joseph L. Goldstein. They found that, when a lesion occurs in a blood vessel, certain “Lysine Binding Sites” are exposed to the blood. Remember, lysine is what holds the collagen fibers together. This is what the artery is looking for to heal it.
However, without collagen around to heal the tear, the body sends signals to the liver to produce Lp(a) and more cholesterol. Brown and Goldstein also discovered that it is Lp(a) that will initially bind to the damaged blood vessel – not the usually blamed LDL cholesterol.
Dr Harpel discovered that lysine binds to the free-floating Lp(a) in the blood. The tears in the lining of the arteries are attempting to attract lysine molecules in the collagen fibers. Instead, the Lp(a) molecules, with lysine molecules on them, attach themselves to the site of the lesion. In fact, studies show that Lp(a) sticks fast to damaged blood vessels, as we said, like velcro. In fact, analysis shows that…
The cholesterol in plaque
is mostly the Lp(a) type.
The stickiness of Lp(a) is stronger than white blood cells so other Lp(a) molecules also stick strongly to it. In addition, the protein segment of the Lp(a) molecules has residuals that encourage both LDL cholesterol and calcium to also stick to them. This pattern repeats itself and is the cause of plaque formation.
Now, this is a good thing for a short-term remedy if your body isn’t able to form collagen. Of course, if your nutritional deficiency continues, this plaque will continue to grow thicker and thicker in order to do their job of preventing your coronary arteries from springing a leak. Over time, it can become dangerous!
It is interesting that animals don’t have these sticky Lp(a) particles. This suggests that their continual production of high levels of vitamin C have made it unnecessary for them to produce Lp(a) lipoproteins. However, humans seem to need this emergency back-up plan.
Some studies have also indicated that Lp(a) can trigger blood clot formation in addition to its plaque building. Lp(a) then poses an additional risk for blood clots when plaque ruptures. When this loose plaque jams in an artery joint, Lp(a) can increase the possibility of a blood clot. This emphasizes why we say that, while oxidized LDL cholesterol is harmful, Lp(a) is far worse!
German researchers examined cardiovascular risk factors in 788 middle-aged men over ten years. The researchers found that Lp(a) levels were higher in the men who eventually suffered a major coronary event. In fact, the risk of a major coronary event nearly tripled in the men with higher levels. L. Pauling studies have found even higher rates. In fact…
A high Lp(a) carries a 3-10x greater risk
for heart disease than LDL cholesterol level.
Naturally, the focus of a lot of recent research now is how to neutralize these sticky Lp(a) agents. This would greatly reduce plaque buildup. If we can cause them to release their hold, it is even better. This means we could actually reduce plaque build-up!
Family History
People who have a family history of heart disease might also be interested in Dr Lam’s studies (some of which are included on our site). He has found that a high Lp(a) is genetically linked. Some people’s liver have a hyper-active response to the body’s signals to make Lp(a). They will be happy to know that we are going to address both reducing that signal from the body and lowering the liver’s production of Lp(a).
What we have seen so far is that there are two things that make us more prone to heart disease than animals:
1. Animals produce a large amount of their own vitamin C, which humans do not. This helps them form collagen to keep their blood vessels healthy. It would seem wise to us to increase our vitamin C intake to levels the rest of animals have.
2. Animals do not have these sticky Lp(a) particles. They just have normal fat particles. This stickiness is the second reason why human beings are much more prone to this heart disease. Again, wisdom would be to use any nutrients or supplements that would reduce this problem.
Checking for Lp(a) – (for those interested)
Do you have high levels of Lp(a)? Having a test is not really necessary since there are no negative side effects. Most people that suspect high cholesterol or plaque buildup simply enter into a nutritional program as a safe guard measure.
However, if you are concerned, have a genetic family history of heart disease, or just simply want to know, you can take a Lp(a) test. A Lp(a) test is a simple blood test and can be measured by most clinical laboratories. Just be aware that, at last notice, the test remains non-standardized. This is not a huge problem, just understand that results do vary from lab to lab. Therefore, it might be important to stick to the same laboratory when you have your Lp(a) checked. This will give some consistency to the results.
Nmol/l measurement: Ideally, the laboratory will measure Lp(a) in nmol/l. This is a measure of Lp(a) particle number and is not influenced by the variable size of Lp(a) particles.
Mg/dl measurement: If your measure is in mg/dl or mg/l—measures of weight—then it may be affected by particle size and may not accurately reflect your true risk. But even a weight measure is better than nothing if you don’t have a choice.
What’s a desirable value for Lp(a)? As with LDL cholesterol, this is the toughest question of all. However, some guidelines:
Hmol/l: 75 nmol/l or less is desirable, under 50 is preferred.
Mg/dl: 30 mg/dl or less is desirable, under 20 mg is preferred.
(It is not unusual for the Lp(a) level to be slightly elevated from its baseline level for the first few months of taking suggested supplements. This is normal as the Lp(a) is being cleared out of your arteries. A follow-up test can be done 9-12 months after starting the nutritional program.)