Cholesterol is contained in the membrane of every cell in the body, as well as in blood plasma. It is critical to building and maintaining cell membranes, metabolizing fat-soluble vitamins, producing bile to help digest fat, and synthesizing many hormones, including sex hormones.
The notion that consuming foods high in cholesterol will promote heart disease is a grossly inaccurate sound bite that disregards the critical role of cholesterol in metabolism and the manufacture of steroid hormones. Cutting back on dietary cholesterol will result in the liver producing more cholesterol. In fact, virtually all the cells in the body can manufacture the cholesterol they need because the protein molecules in the cell will direct the production of more cholesterol if insufficient levels are detected in the cell. Cholesterol-lowering statin drugs override this elegant balancing process at the cellular level. They effectively lower cholesterol levels in the body, but with negative side effects. Moderating dietary cholesterol in an effort to regulate blood cholesterol is not only a fruitless effort but can also unnecessarily restrict your intake of highly nutritious foods.
There are several varieties of lipoproteins, all with different transporting functions. In order of size, from largest to smallest. VLDLs, LDLs, HDLs (very low-density, low-density, and high density lipoproteins). These lipoproteins carries a certain percentage of cholesterol, triglycerides, and other minor fats.
HDLs
HDLs take oxidized cholesterol from the bloodstream back to the liver for excretion or recycling into useful service. About 30 percent of the total cholesterol in a healthy body is composed of HDL. HDLs are known as the “good cholesterol” or “nature’s garbage trucks” for their ability to cleanse the arteries and bloodstream of oxidized cholesterol. High levels of HDL help reduce the risk of heart disease.
VLDLs
These cholesterol complexes are manufactured in the liver to transport triglyceride and cholesterol to target fat or muscle cells. Initially, VLDLs are composed of about 80 percent triglyceride. Shrink substantial in size and transform into either large, fluffy LDLs or small, dense LDLs.
Large, Fluffy, LDL
Also known as buoyant LDL, this type of cholesterol is formed from VLDL when blood levels of triglycerides and insulin are low. These molecules are generally harmless, even at high concentrations. However, in the presence of other risk factors (high insulin-producing diet, systemic inflammation, abdominal obesity, family history, smoking, etc.) even fluffy, large LDL can make a contribution to heart disease if the particle count is high enough and it’s not cleared from the blood quickly enough. With other risk factors and adverse lifestyle practices present, large, fluffy LDL can circulate in the blood for too long and become oxidized. Since HDL is so critical to clearing oxidized cholesterol from the bloodstream. Another risk factor is poor thyroid function, which down-regulates LDL receptors and causes LDL to circulate for longer periods in the bloodstream with insufficient antioxidant protection.
Small, Dense LDL
VLDL converts to small, dense LDL when triglyceride and insulin levels are elevated in the bloodstream. Small and dense, they can become lodged onto the endothelial cell layer (ECL)-the cells that line the walls of your arteries. It’s possible that small, dense LDL are already partially oxidized, and then becoming further oxidized when they attach to the ECL.
Hence, it’s noteworthy that high-carbohydrate eating patterns are not the only pathway to the accumulation of dangerous small, dense LDL. The thyroid problems trigger an elevation in small, dense LDL because LDL is being cleared from the blood slower than usual. Often this unique population of thyroid sufferers can tweak their eating habits, and regain optimal thyroid function and clearance of oxidized cholesterol.
Understanding the difference between LDL particles makes it apparent how misleading a total LDL cholesterol value can be in evaluating heart disease risk. The total LDL reading on a blood test indicates the mass, or total amount, of cholesterol carried by your LDL particles, but it does not reveal what size the particles are. A total LDL cholesterol reading of 100 could be comprised of many small, dense particles, and fewer large, fluffy particles (which are lighter and less apt to lodge into tight spaces between the endothelial cells that line the walls of your arteries). Hence, heart attacks can and do occur in individuals who have a relatively low total, and seemingly safe, LDL reading. This can be the case if a high percentage of the total LDL is small, dense LDL, and if systemic inflammation and oxidative damage are present due to adverse diet and lifestyle practices.
Particle Size
Particle size is a critically important distinction to understand when it comes to LDL cholesterol and disease risk. LDL-C is the term for total amount of cholesterol someone is carrying, while LDL-P is the number of LDL particles in the blood. Think of it like cars on a freeway: LDL-C represents the total number of passengers on the road (total inside all the vehicles), while LDL-P represents the number of vehicles on the road.
Obsessing over a single blood reading for total LDL value is and ineffective way to evaluate heart disease risk.
All else being equal, it’s a numbers game: the more vehicles there are, the more likely it is for some to crash and cause damage. For that reason, it’s much more useful to measure the number of LDL particles someone has. This is especially important for people eating paleo or Primal diets high in natural saturated fats, which might increase the total amount of cholesterol in the bloodstream, but typically in the form of large, fluffy LDL (buses). 75 percent of patients hospitalized for a heart attack had an LDL of less than 130mg/dl, and that half of the victims had an LDL under 100, widely considered “ideal.”
Heart Disease Catalysts
There are assorted contributing factors to the severity of the oxidation and inflammation condition in the bloodstream that allow the heart disease process to occur.
Hyperinsulinemia - A dietary pattern of excess carbohydrate intake results ini chronically elevated insulin levels, promotes systemic inflammation in the body.
High Triglycerides - Chronically elevated insulin levels prevent triglyceride from being mobilized into free fatty acids for use as energy. Elevated levels of triglyceride in the bloodstream drive VLDL conversion into small, dense LDL instead of large, fluffy LDL.
Excess Cortisol - This stress hormone promotes inflammation as a component of the fight-or-flight response in the body. Chronically elevated cortisol levels produced by poor eating habits, chronic exercise habits, insufficient sleep, and other forms of life stress that overstimulate the fight-or-flight response can result in chronic, or systemic, inflammation.
Insufficient HDL - Insufficient levels of HDL due to poor diet and exercise habits, and even the use of statins (which lower HDL as well as LDL), can significantly increase heart disease risk.
Poor Diet - Besides excess carb intake and insulin production, other elements of the Standard American Diet can elevate disease risk, among them: excess consumption of PUFA oils; any consumption of chemically altered trans or partially hydrogenated fats.
Blood Testing
Triglycerides-to-HDL Ratio - Important blood metric to assess heart disease risk is not total LDL but the triglyceride-to-HDL ratio. A ratio of 3.5:1 or below is desirable, while a ratio of 1:1 is considered superior.
Blood Pressure - Hypertension puts excessive stress on the cardiovascular system and increases disease risk. High blood pressure is a reliable indicator of unhealthy dietary, exercise, and lifestyle habits. Experts agree that a safe blood pressure threshold is a systolic/diastolic reading of 120/80 or lower (for each value).
VItamin D - This essential nutrient supports healthy cell division and thus cancer prevention. Optimal blood value range of 70-100 ng/mL. There is believed to be some variation in optimal vitamin D levels based on ethnicity, with those of non-White ancestry able to thrive in lower ranges than light-skinned folks.
Fasting Blood Insulin -ideally under 10
HbA1C (5.6 or less)
Triglycerides - Under 150 mg/dL is essential to reduce disease risk, while under 100 is optimal. A reading over 150 suggests an excess of oxidized LDL and thus elevated disease risk.
High Sensitivity C-reactive Protein (hs-CRP) - Under normal circumstances or over the long-term, ideal CRP levels are well under 1 mg/L.
Coronary Calcium - Measures calcium buildup in the arteries via CT scan, a strong indicator of atherosclerosis.
Statins-
The health movement asserts that a blanket strategy of reducing total cholesterol levels through potent statin medication is problematic for several reasons.
(Take this pill, lower your LDL, and you’ll be good) For example, even relatively low levels of small, dense LDL can still be problematic when other risk factors are present, such as insufficient HDL levels and high-stress, pro-inflammatory lifestyle practices.
Side Effects -
Statins suppress the production of cholesterol in the liver, producing lower blood values of all forms of lipoproteins, including beneficial HDL. Can interfere with healthy serotonin balance (less energy and alertness; potential mood consequences too); hampered vitamin D synthesis, disturbances in regulating blood sugar, disturbances in controlling inflammation, and disturbances in an assortment of critical hormonal processes.
Statins have been shown to cause inflammation in the liver and also have a tendency to deplete cells of critical energy-producing nutrient known as coenzyme Q-10 (CoQ10). Indicators of muscle dysfunction. Statin use comes with serious side effects and fails to address the proximate cause of heart disease: oxidation and inflammation.
Furthermore, statins do not affect triglyceride (blood fat) levels or LDL (the so-called bad cholesterol) particle size, nor do they decrease risk of death in any women, in men over 65, or in men under 65 who have not had a heart attack. That said, statins have been shown to reduce risk of heart attack in specific high-risk populations, and have been shown to generate some incidental benefits outside their intended effect of lowering total cholesterol levels. There is a blood thinning effect and a plaque stabilizing effect.
It is universally agreed that Omega-3 fats are health-promoting, due to their anti-inflammatory effect. Omega-3s, found in highest concentration in oily, coldwater fish, are lauded for enhancing cardiovascular, brain, skin, and immune function. Monounsaturated fats (found in macadamias, avocados, olives and extra-virgin olive oil) are also universally regarded as healthy as they enhance cardiovascular and immune function and help protect against heart disease.
In the absence of high carbohydrate intake and other stress factors, saturated fat is an efficient, clean burning energy source for the body. Unfortunately, conventional wisdom makes an inaccurate association between saturated fat consumption and heart disease. While saturated fat and cholesterol are indeed agents that clog your arteries and cause heart attacks and strokes, the process by which saturated fat and cholesterol turn dangerous is completely independent of their intake in the diet.
When fat is consumed in the context of a high-carbohydrate diet, the excess insulin production promotes a state of oxidation and inflammation in the bloodstream, along with high triglycerides. These are the key risk factors for atherosclerosis. The suggestion to avoid saturated fat negates the high satiety factor of saturated fat, which helps regulate appetite and total caloric intake naturally.
The Real Heart Disease Catalysts Are:
Excess insulin: Promotes inflammation, stiff arteries, sticky platelets, and oxidized small, dense LDL (from a high-carbohydrate diet).
High triglycerides: Promotes conversion of VLDL into small, dense LDL instead of large, fluff LDL, and locking into fat-storage pattern (from a high-carbohydrate diet).
Excess cortisol: Chronic stress promotes an inflammatory environment in the bloodstream and damage to the sensitive ECL (from poor diet, chronic exercise, insufficient sleep, emotional stress).
Insufficient HDL: Body is less efficient at clearing oxidized cholesterol from bloodstream (from poor diet, statin use, chronic exercise).
LDL cholesterol readings are minimally relevant to heart disease risk, and in fact many heart attack victims have LDL values considered within the “safe” range. HDL are nature’s garbage trucks, cleansing the arteries and bloodstream of potentially problematic oxidized cholesterol. More relevant blood tests to track disease risk are triglyceride-to-HDL ratio (3.5:1 or better imperative; 1:1 or better ideal); blood pressure.
Statins lower all types of cholesterol, including HDL, and deplete the critical nutrient CoQ10, which helps the mitochondria produce energy. They fail to address the true cause of heart disease and deliver disturbing side effects. Decades-long meta-studies involving hundreds of thousands of subjects are finally encouraging mainstream appreciation for the idea that dietary saturated fat and cholesterol are not the proximate causes of heart disease.
Conventional wisdom has made an inaccurate association between dietary fat and fat in the blood (triglycerides).
Failure to distinguish between health and unhealthy fats.
Excess carb intake drives excess insulin drives high triglycerides and a fat-storage pattern.
Keep Moving Forward 😊 Sarah
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