TRUTH ABOUT CHOLESTEROL
Turbulence results in creation of a blood clots that can block blood flow to the brain and heart. Because plaque contains cholesterol, it was theorized that dietary cholesterol would raise blood cholesterol which would infiltrate into the walls of the arteries and cause a blockage. The theory was falsely confirmed by a physiologist named Ancel Keys in 1956.
In 1997 Dr. Keys admitted that this cholesterol based turbulence theory was flawed. He said, “…there is no connection whatsoever between cholesterol in food and cholesterol in the blood. None. And we’ve known that all along.”
After nearly seventy years, the then current director of the 1948 Framingham Heart Study admitted that your diet has nothing to do with your cholesterol levels.
This study of 5,000 patients, done under the direction of the National Heart Institute, had concluded that cholesterol levels were related to risk for coronary artery disease
In 1976, another large study of over 4,000 patients in Tecumseh, Michigan was published showing that there is no relationship whatsoever between the amounts of saturated fat eaten (animal fat, coconut oil, palm oil) and the levels of blood cholesterol. As a side note, it is important to clarify that these studies did not address the plastic fat called transfat.
Figure 6.15 Cholesterol metabolism and statin drugs
HMG (HYDROCYMETHYLGLTARIC ACID) ENZYME PRODUCTS
Cholesterol is one of three products produced from HMG (Cholesterol, CoQ10 and Dolichol). The enzyme HMG-CoA Reductase is required to start the process of cholesterol metabolism. Statin drugs inhibit this enzyme. The above diagram illustrates the cholesterol pathway and the resulting substrates.
The cholesterol pathway process begins with the two carbon molecule, acetyl-CoA to form hydrocymethylglutaric acid (HMG). Statins are known as HMG-CoA Reductase inhibitors because they prevent the formation of HMG-CoA, and they thereby also block cholesterol production. Unfortunately, statins also interfere with the formation of important metabolic processes and can lead to numerous adverse effects.
DRUGS FOR LOWERING CHOLESTEROL MAY NOT PREVENT HEART DISEASE
Studies prove no relationship between cholesterol and coronary artery disease. According to The Center for Practice Management and Outcomes Research, current clinical evidence does not demonstrate that titrating lipid therapy to achieve proposed low LDL cholesterol levels is beneficial or safe (Hayward, Hofer, & Vijan, 2006). In addition, litigation has taken place against manufacturers of statin drugs for allegedly failing to warn doctors and patients about the increased potential risk for type 2 diabetes in women.
As VLDL chylomicrons lose triglycerides, they become smaller and smaller and are gathered up by HDL cholesterol which takes them back to the liver. Because HDL reduces the small remnants of VLDL cholesterol in the blood, HDL has been labeled as “good cholesterol”.
THE PROTECTIVE ROLE OF LDL AND VLDL CHOLESTEROL
LDL cholesterol acts like a sponge for toxins in your gut. More than half of the bacterial toxin lipopolysaccharide (LPS) is bound up in these chylomicron particles to help remove them from your body and protect you from disease. Blood serum LPS toxin is found to bind predominantly to LDL and VLDL. The binding of LPS to LDL and VLDL emphasizes their crucial role in the scavenging of LPS bacterial toxins that lead to inflammation.
ASSOCIATION IS NOT CAUSATION
The so called “bad cholesterol” has gotten a bad reputation by association with vascular calcification or hardening of the arteries. (Vreugdenhil, Snoek, van ‘t Veer, Greve, & Buurman, 2001).
Association is often confused with causation, a situation of mistaken identity in this case, often distracting medical professionals from treating the underlying causes contributing to the formation of the plaque.
Fire engines are often present at the scene of the fire, but they do not cause the fire and are there to help put it out; inflammation in your gut leads to an elevation in cholesterol as protection of the digestive tract from the inflammation.
TREAT THE WHOLE PERSON AND NOT JUST THE LAB RESULTS
Typically, statins are prescribed in cases of cardiovascular disease. The doctor measures cholesterol and gets cholesterol numbers from the lab report. The patient is given a prescription drug to decrease cholesterol if it is over 200 mg/dl. Most labs currently recommend that cholesterol levels be lower than 200 mg/dl. This practice instills a protocol for treating a number and not the individual and therefore the inflammation that is triggering elevated cholesterol remains. Inflammation can lead to an increased risk of stroke and cancer if cholesterol is not present in sufficient quantities to protect the body.
CASE STUDY: CHOLESTEROL REMOVES TOXINS Dr. Turcotte
In one case study my patient came in after having received six rounds of the antibiotic Cipro.
She developed high cholesterol a year later from gastrointestinal dysbiosis because all her good bacteria were killed off. She also consumed foods that caused inflammation in her digestive system, and her own body was making cholesterol to carry away the toxins.
Serrapeptase, an enzyme derived from silkworms, which has anti-inflammatory effects and can help prevent blood clots and can also dissolve biofilm. The natural antibiotic SuperNatent Plus was added to kill the pathological bacteria. A strong probiotic of 100 billion friendly bacterial strains was given to restore the health of the gut. Food sensitivity testing with ALCAT revealed which foods should be avoided as a source of an inflammatory response for her individual genetics.
Her cholesterol dropped down to normal, and no statin drugs were required.
SMALL DENSE CHOLESTEROL AND RISK FOR CARDIOVASCULAR DISEASE
Lp (a), LDL IV and Very Dense LDL are the small dense LDL. They are easily oxidized and are more dangerous than other types of cholesterol. Lp(a) does not respond to traditional LDL-lowering drugs.
Lifestyle modifications such as diet, weight loss, and exercise generally have little or no effect on Lp(a) levels. Compared to the well reported LDL-lowering effects of statins and bile acid sequestrants (resins), these drugs generally have little, or no effect on Lp(a) levels (McKenney et al., 2007; M. Miller, 2009). Niacin supplements has been proposed as the most effective option to treat Lp(a) elevations (McKenney et al., 2007).
STANDARD CHOLESTEROL TESTING IS OUTDATED
Current standard cholesterol testing does not provide an adequate assessment of cardiovascular risk. A true risk assessment for the development of plaque must address the size and density of the particles in the blood that make up the LDL cholesterol count. Researchers now know that plaque accumulations are related to the percentages of the small dense cholesterol that become oxidized.
ASSESSING CHOLESTEROL RISK
Plaque risk can be assessed using lab work that can identify the risk of cardiovascular disease such as the subclasses of lipids that are known and emerging risk factors for cardiovascular disease, such as LDL particle size and lipoprotein (a).
Figure 6.14 Lipoprotein sizes and density
CHOLESTEROL PARTICLE SIZE AND RISK
The pie chart below shows the risk levels associated with the cholesterol components found in plaque. Interpretation of particle size helps the doctor to individualize treatment based on the underlying cause of the problem within the lipid metabolism.
Table 6.3 Risks associated with cholesterol particle size
THE LITTLE GUYS ARE THE PROBLEM
The only lipoproteins found in plaque at biopsy are IDL, LDL-R and the Lp(a).
These need to be addressed appropriately with NiaCel (riboside nicotinamide) and lifestyle choices to reverse mitochondrial damage, address genetic mutations and correct gut imbalances. These first restorative steps should be implemented before considering the use of statins as statin drugs may not lower Lp(a) and cause potentially cause additional unwanted dangerous side effects.
The NMR LipoProfile test is a diagnostic tool used to identify and manage risk for lipid-related heart disease. The NMR LipoProfile test has proved to be a superior predictor of CHD outcomes than standard lipid tests in clinical trials. Prediction by the number of LDL particles (LDL-P) was independent of traditional lipids (www.labcorp.com).