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"Elevated" Cholesterol May Not Be the Controlling Cause of Heart Disease

In spite of the prevailing advice that tells us to lower the amount of saturated fat in our diet in order to keep our cholesterol levels within an "optimal range," there is currently an epidemic of heart disease. Is it that people are not listening to this guidance? No! Many of us throughout the world are actually following this well-known advice, coming to shun any food that is "high-fat" or "high in cholesterol," so the problem may lie elsewhere.

Let's consider the possibility that eating foods with cholesterol does not cause heart disease and that these same foods might actually decrease your chances of getting heart disease.

First let's take a look at a few healthy roles cholesterol plays in the body:

Cholesterol is the precursor to bile acids, which are needed to digest and absorb long-chain fatty acids. Cholesterol is also recognized for its physiological importance in the skin and the intestines, where it plays an important structural role as a component
of the organ membranes.
Cells lining the digestive tract are particularly rich in cholesterol. Among its other various roles in the cell are the signaling activities that, for example, tell the gastrointestinal musculature when to contract. I don't know how many people I have seen relieved of their chronic constipation, as well as any related irritable bowel syndrome (IBS), when they finally ate enough cholesterol in their daily diet.
Cholesterol is responsible for our sex and adrenal hormones. It is also one of our primary repair mechanisms, which is why our arteries end up with patches of repairing cholesterol. Low density lipoproteins, or LDL, carries cholesterol to the cells,
which means that our LDL numbers need to be high enough.
Foods high in cholesterol help to repair the liver. As the body heals, it needs more cholesterol to repair the liver and to replace broken-down cells.
Even the Framingham Heart Study, which the pharmaceutical companies use to promote cholesterol-lowering drugs, show that the higher the cholesterol level and the more fat in the diet, the longer the study participants lived and the more optimally the participants weighed.

Second, let's look at the information that is being given to people by many medical doctors through the current pharmaceutical-influenced guidelines from the National Cholesterol Education Program.

These guidelines suggest that therapy should begin in everyone with LDL-C, or low-density-lipoprotein cholesterol, above 160 mg/dl, and should reach targets as low as 100 mg/dl for secondary prevention or in diabetics.

At this point, I ask you to think about and compare the

guidelines from the National Cholesterol Education Program with the possibility that due to the healthy role that cholesterol plays in our bodies, we might actually want "elevated" cholesterol levels.

Even while these pharmaceutical-influenced guidelines do widely discuss the use of therapeutic lifestyle changes such as diet, exercise, and the increased use of fiber and plant sterols (essential components of plant membranes that resemble the chemical structure of animal cholesterol and carry out similar cellular functions in plants and are present in small quantities in many fruits, vegetables, nuts, seeds, cereals, legumes, vegetable oils, and other plant sources), most clinicians confidently, enduringly, and with concern guide their patients toward a lifetime of a lipid-lowering pharmaceutical agent to effect LDL-C.

Unfortunately, the overwhelming emphasis on the role of saturated fats in the diet, "elevated" cholesterol levels, and the risk of coronary artery disease has distracted the medical community from fully understanding and integrating into their recommendations the other factors that may play a major role in cardio-metabolic risk reduction and must be addressed in tandem with lipoprotein markers.

The role of insulin resistance, obesity, inflammation, and glycation are just a few of the many components which need to be addressed when dealing with at-risk patients. Robust data suggests that lifestyle changes (diet, exercise, stress management, etc.) have incremental effects on each of these risk factors without the risk of side effects.

As is shared in the testimonials Colon Cancer Survivor and Back to Old Self, high blood pressure can be resolved using nutritional programs high in cholesterol such as Kristina Amelong's Ten Days to Optimal Health along with managing stress and understanding and addressing other risks factors.

Other considerations:

High blood pressure can be a sign of kidney impairment, which can be determined through a low sodium/potassium ratio. You can determine your sodium to potassium ratio through a Hair Tissue Mineral Analysis.
The toxic mineral cadmium affects blood pressure. Removal of cadmium can be safely done using a therapeutic colon cleanse program.
Biounavailable calcium and magnesium contributes to high blood pressure.
High cortisol levels can contribute to high blood pressure, which is commonly seen in Cushing's Disease. However, one does not need to present with Cushing's Disease in order to have high cortisol levels affect their blood pressure. To determine if your cortisol levels are contributing to your high blood pressure, have a Adrenal Stress Index test.

SOURCES:

1. Saturated fats: what dietary intake? J Bruce German and Cora J Dillard. American Journal of Clinical Nutrition, Vol. 80, No. 3, 550-559, September 2004.
2. Digestion and Absorption of Food Fats Mary G. Enig, PhD. Wise Traditions in Food, Farming and the Healing Arts, Summer 2004
3. Baseline characteristics of participants in the JUPITER trial, a randomized placebo-controlled primary prevention trial of statin therapy among individuals with low low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein Ridker PM, Fonseca FA, Genest J, Gotto AM, Kastelein JJ, Khurmi NS, Koenig W, Libby P, Lorenzatti AJ, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ; JUPITER Trial Study Group.
4. Saturated fat prevents coronary artery disease? An American paradox Robert H Knopp and Barbara M Retzlaff. American Journal of Clinical Nutrition, Vol. 80, No. 5, 1102-1103, November 200