Key Elements in the Theory of Atherosclerosis
Expect some surprises:
- Cholesterol does NOT cause heart disease.
- The first detectable signs of occluding arteries are NOT fatty streaks.
- Bypass surgery does NOT extend lives
- Polyunsaturated oils may actually do MORE harm than good (eg: Canola, Sunflower, Soybean, Corn). The main difference between polyunsaturated fat and monounsaturated fat (like olive oil) is the structure which is unstable and wreaks havoc on the cells in your body; it contributes to oxidation and free radical damage in the body, which is linked to heart disease, cancer, Alzheimer's disease, autoimmune diseases and premature aging. The instability of polyunsaturated fats is especially volatile during any kind of processing. Even small amounts of light, moisture, air or heat damage polyunsaturated fat. Plus too much omega-6 fatty acids can also interfere with the use of the very important omega-3 fatty acids in the body.
- Yes, BUTTER is good for you. In the past few decades, butter has been blamed for everything from obesity to heart disease. But recently, it has been making a comeback as a “health food.” (More: http://authoritynutrition.com/7-reasons-why-butter-is-good-for-you/)
About Cholesterol :
Cholesterol also serves as an antioxidant of last resort – when the body lacks sufficient dietary antioxidants (e.g. vitamin C, vitamin E, selenium) to counter the free radicals that damage arterial walls. In this role, cholesterol covers over patches of arterial damage and gives up electrons (i.e. becomes oxidized) in order to neutralize free radicals and prevent further damage to the arteries. In the process, this cholesterol becomes oxidized.
High
blood cholesterol levels (hypercholesterolemia) usually have little or
nothing to do with the amount of cholesterol eaten. Cholesterol is a
VITAL bodily substance. It is a constituent of bile; it helps to convert
sunlight into vitamin D; it is used to produce sex hormones; and it is
needed by every cell in the body to keep membranes waterproof and to
assist in the transmission
of nerve impulses. The brain requires large amounts of cholesterol !
Cholesterol is so important that the less of it we eat, the more of it
our bodies produce. On an omnivorous diet, from 70 to 80% of the
cholesterol in the body is endogenous (made within the body) and does
not come from diet. Since cholesterol is found only in foods of animal
origin, on a vegan (total vegetarian) diet, 100% of the cholesterol in
the body is endogenous.
Cholesterol also serves as an antioxidant of last resort – when the body lacks sufficient dietary antioxidants (e.g. vitamin C, vitamin E, selenium) to counter the free radicals that damage arterial walls. In this role, cholesterol covers over patches of arterial damage and gives up electrons (i.e. becomes oxidized) in order to neutralize free radicals and prevent further damage to the arteries. In the process, this cholesterol becomes oxidized.
The other dietary/lifestyle factors that contribute to elevated cholesterol levels include: (a) not drinking enough water, (b) excess sugar intake, (c) insufficient dietary fiber, and (d) lack of exercise. High cholesterol readings can also be an overlooked symptom of low thyroid function.
Cholesterol-lowering prescription drugs are potentially lethal. They reduce cholesterol everywhere in the body, including in the brain - where cholesterol acts as an insulator to prevent water from entering nerve cells and shorting out electrical circuits.
Cholesterol-lowering prescription drugs are potentially lethal. They reduce cholesterol everywhere in the body, including in the brain - where cholesterol acts as an insulator to prevent water from entering nerve cells and shorting out electrical circuits.
Key Elements in the Theory of Atherosclerosis
- Free Radicals and Homocysteine* create tiny tears in the lining of artery walls
- Excess blood sugar accelerates this arterial damage
- the body patches arterial tears with fibrin (a clotting protein) and scarring
- Dead macrophages (immune cells) become trapped in the patches and scar tissue
- The macrophages swell up to become foam cells
- Through time, more and more substances become attracted to and trapped in the arterial patches - including collagen, fats, minerals (especially calcium), foreign proteins, heavy metals, phospholipids, mucopolysaccharides, muscle tissue, cellular debris, triglycerides, and cholesterol.
- The parts of the arterial tree most vulnerable to the accumulation of plaque are the coronary arteries, the carotid arteries, and the femoral arteries
- Plaque that is allowed to proliferate out of control will eventually cause a heart attack, a stroke, or gangrene.
-Antioxidants protect the arteries from damaging effects of oxygen free radicals. (an atioxidant is a molecule that can absorb a renegade electron without becoming a free radical itself). Dietary antioxidants include: vitamin C, vitamin E, and selenium.
- Vitamin C and B-vitamins encourage the body to make coenzyme Q10, an internally generated antioxidant
- Selenium, zinc and manganese facilitate the body's production of the free radical scavengers
- Vitamins B6, B12 and folic acid eliminate the homocysteine* hazard
- Vitamin C in large amounts encourages the arteries to produce LPL (Lipoprotein lipase), an enzyme that emulsifies and disposes of fats that have accumulated in artery walls
- Certain high potency nutrients act as chelating agents to remove minerals and heavy metals from arterial plaque - including vitamin C, L-cysteine, DL-methionine, and thiamine
- Magnesium dissolves calcium deposits in arterial plaque
- Magnesium also prevents arterial spasms, some of which can be fatal
- Large amounts of vitamin E encourage the body to develop collateral circulation, in effect creating self-generated bypasses
- Choline emulsifies fats, keeping them from sticking together and thereby improving the flow characteristics of the blood
- Vitamin E prevents blood platelets (also called "thrombocytes", are a component of blood whose function (along with the coagulation factors) is to stop bleeding by clumping and clogging blood vessel injuries) from sticking together, thus reducing their tendency to contribute to excessive coagulation in arterial patches
- Monounsaturated oils (e.g. olive, avocado, almond) have protective effect on arterial cell membranes
* Homocysteine is an amino acid and breakdown product of protein metabolism that, when present in high concentrations, has been linked to an increased risk of heart attacks and strokes. Elevated homocysteine levels are thought to contribute to plaque formation by damaging arterial walls. High levels may also act on blood platelets and increase the risks of clot formation; however, whether high levels of homocysteine actually cause cardiovascular disease has yet to be agreed upon. In addition, some evidence suggests that people with elevated homocysteine levels have twice the normal risk of developing Alzheimer's disease.
FACTS:
- The true cause of atherosclerosis is whatever damages the arterial wall. The most likely suspects are free radicals, homocysteine, and diabetes.
- The first visual evidence we have of developing atherosclerosis is what mistakenly appear to be fatty streaks in the inner liner of arteries.
- Cholesterol is a slippery, waxy substance that cannot possibly adhere to a smooth, healthy arterial lining. (similarly, fats cannot stick to a healthy arterial lining).
- blood cholesterol levels are less influenced by cholesterol content of food than by stress factors. Such stress-causing factors can apparently consist of foods which contain virtually no cholesterol - like the microwaved vegetables.
- Reducing Stress Is extremely Important: (
- countries like France have both a high consumption of fat and low incidence of heart disease ! (the French paradox)
- There is just as much cholesterol circulating in your veins as in our arteries, but plaque is found only in arteries and NEVER in veins.
Oxidized Cholesterol
Inflammation
Oxidized Cholesterol
Scientists observed that NOT all cholesterol in arterial deposits is the same; some of it has become OXIDIZED. They speculated that it must be the oxidized cholesterol that causes the damage; and from this assumption followed a number of dietary precautions, such as cooking eggs over low heat so as not to damage their cholesterol content. The oxidized cholesterol theory has 2 flaws:
1) the oxidized cholesterol is one of the last ingredients laid down in the arterial plaque, not the first
2) it is more likely that this cholesterol became oxidized after it accumulated in the plaque. An outer layer of cholesterol may have sacrificed itself in order to protect deeper layers and the artery itself from damaging effects of oxygen free radicals. From this perspective, cholesterol could be considered an antioxidant of last resort.
Inflammation
Inflammation is a nonspecific immune response that occurs in reaction to any type of bodily injury. C-reactive Protein (CPR) is a protein found in the blood, the levels of which rise in response to inflammation and are associated with atherosclerosis, diabetes, autoimmune disorders and sport injuries. In other words, atherosclerosis raises CPR levels, but not all elevated CPR levels are triggered by atherosclerosis.
Arterial inflammation usually increases CPR levels before any significant blockage shows up on ultra sound tests. This does not mean that inflammation causes atherosclerosis, however. Jumping to this kind of erroneous conclusion is known in logic as the post hoc proper hoc fallacy - meaning that just because one event precedes another does not prove that the former caused the latter. In scientific terms, this is the error of assuming that correlation is cause.
Inflammation is an effect, not a cause. Inflammation does not cause atherosclerosis any more than inflammation causes arthritis or sports injuries. In all cases, inflammation is a response to damage of some kind. We need to find out what is causing the damage. With respect to atherosclerosis, the most causative agents are: FREE RADICALS, HOMOCYSTEINE and ELEVATED BLOOD GLUCOSE (as in diabetes).
Vitamin C
Here is a remarkable fact: animals which produce ascorbate in the livers do NOT develop atherosclerosis. If you wish to induce atherosclerosis in animals for research purposes, you have to use monkeys or guinea pigs. The ability to produce vitamin C internally prevents an animal's arteries from plugging up. This is due to at least 3 biochemical mechanisms:
1) vitamin C is required for the production of Lipoprotein Lipase (LPL), an arterial cleansing enzyme
2) vitamin C is required for the production of coenzyme Q10, an antioxidant that protects arteries from damaging oxygen free radicals
3) vitamin C itself is a powerful antioxidant.
If the human liver were capable of producing vitamin C in the same way that animals' livers do, it would probably produce a range of 2gr to 10gr per day, when converted for equivalent body weight, the higher amounts being required during times of stress.
The implication is that by taking suitably high amounts of vitamin C throughout our entire lives, we may be able to prevent atherosclerosis. It is unlikely, however, that vitamin C supplementation alone would be capable of removing arterial plaque that has been accumulating over years.
Lipoprotein Lipase
Cholesterol, triglycerides and phospholipids are LIPOPROTEINS, the molecules of which consist of fats chemically linked to proteins. Lipoproteins are classified as very low-density (VLDL), low-density (LDL), intermediate density (IDL), and high density (HDL). It is thought that individuals with high blood levels of HDL are less predisposed to coronary heart disease than those with high blood levels of VLDL or LDL. This is because the lower density lipoproteins are puffer and tend to more easily block openings in the tiny capilaries or in the arteries that have become narrowed by pre-existing plaque. The body's natural way of reducing excess lipoproteins is to make Lipoprotein Lipase (LPL).
Lipoprotein Lipase (LPL) is a water soluble, fat splitting enzyme (an emulsifier) that hydrolyze triglycerides in lipoproteins, such as those foundin very low density lipoproteins (VLDL) in the blood, into free fatty acids and one monoacylglycerol molecule. It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and free fatty acids. LPL is attached to the surface of some cells that line the capillaries and arteries, and is also distributed in adipose, heart and skeletal muscle tissue, as well as in lactating mammary glands.
Lipoprotein Lipase works like a detergent to emulsify excess cholesterol and triglyceride, breaking them down and enabling them to be carried safely away through the liver and bile. There's a catch however. The body requires an abundant supply of vitamin C in order to be able to produce LPL to do its job.
This ascorbate-LPL dependence may be one of the mechanisms by which most animals are protected from atherosclerosis and we humans are not. Without a sufficient high intake of vitamin C, the human body cannot produce enough LPL to prevent excess fats and cholesterol from accumulating in arterial plaque.
Lipoprotein(a)
Lipoprotein(a) is structurally similar to low density lipoproteins (LDL) and is often considered to be a marker for atherosclerotic diseases.
In other words, if there is a significant lipoprotein(a) reading in your blood work, you are theoretically considered to be at higher risk of developing atherosclerosis than if your other lipoprotein fractions are out of balance. But there is a missing link in this chain of reasoning.
Lipoprotein(a) may well indicate a genetic predisposition for elevated or distorted cholesterol readings. However, there is no conclusive scientific evidence that cholesterol or other lipoproteins actually cause atherosclerosis, plus a number of logical reasons why they cannot.
Co-enzyme Q10
Co-enzyme Q10 (ubiquinone, ubiquinol) is a vitamin-like substance that is present in ALL bodily cells and generates energy in the form of adenosine triphosphate (ATP). CoQ10 is present in large amounts in those organs with highest energy requirements, namely the heart, liver and kidneys. CoQ10 also functions as an antioxidant to protect cells against the damaging effects of oxygen free radicals. There combined actions of CoQ10 help both to strengthen the heart muscle and to prevent damage to arterial walls.
Internal production of CoQ10 is ascorbate dependant, which may be another of the reasons why most animals' bodies are protected against atherosclerosis, whereas those with hypoascorbemia are not.
If the body has sufficient high intake of vitamin C and B-vitamins, it may be capable of producing all the CoQ10 it needs - without resorting to dietary CoQ10. Large amounts of vitamin C can also supplement and even replace the antioxidant activity of CoQ10.
Cholesterol lowering drugs interfere with and deplete the body's production of CoQ10, however so anyone taking these pharmaceuticals is well advised also to take supplementary CoQ10.
Free Radicals2) vitamin C is required for the production of coenzyme Q10, an antioxidant that protects arteries from damaging oxygen free radicals
3) vitamin C itself is a powerful antioxidant.
If the human liver were capable of producing vitamin C in the same way that animals' livers do, it would probably produce a range of 2gr to 10gr per day, when converted for equivalent body weight, the higher amounts being required during times of stress.
The implication is that by taking suitably high amounts of vitamin C throughout our entire lives, we may be able to prevent atherosclerosis. It is unlikely, however, that vitamin C supplementation alone would be capable of removing arterial plaque that has been accumulating over years.
Lipoprotein Lipase
Cholesterol, triglycerides and phospholipids are LIPOPROTEINS, the molecules of which consist of fats chemically linked to proteins. Lipoproteins are classified as very low-density (VLDL), low-density (LDL), intermediate density (IDL), and high density (HDL). It is thought that individuals with high blood levels of HDL are less predisposed to coronary heart disease than those with high blood levels of VLDL or LDL. This is because the lower density lipoproteins are puffer and tend to more easily block openings in the tiny capilaries or in the arteries that have become narrowed by pre-existing plaque. The body's natural way of reducing excess lipoproteins is to make Lipoprotein Lipase (LPL).
Lipoprotein Lipase (LPL) is a water soluble, fat splitting enzyme (an emulsifier) that hydrolyze triglycerides in lipoproteins, such as those foundin very low density lipoproteins (VLDL) in the blood, into free fatty acids and one monoacylglycerol molecule. It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and free fatty acids. LPL is attached to the surface of some cells that line the capillaries and arteries, and is also distributed in adipose, heart and skeletal muscle tissue, as well as in lactating mammary glands.
Lipoprotein Lipase works like a detergent to emulsify excess cholesterol and triglyceride, breaking them down and enabling them to be carried safely away through the liver and bile. There's a catch however. The body requires an abundant supply of vitamin C in order to be able to produce LPL to do its job.
This ascorbate-LPL dependence may be one of the mechanisms by which most animals are protected from atherosclerosis and we humans are not. Without a sufficient high intake of vitamin C, the human body cannot produce enough LPL to prevent excess fats and cholesterol from accumulating in arterial plaque.
Lipoprotein(a)
Lipoprotein(a) is structurally similar to low density lipoproteins (LDL) and is often considered to be a marker for atherosclerotic diseases.
In other words, if there is a significant lipoprotein(a) reading in your blood work, you are theoretically considered to be at higher risk of developing atherosclerosis than if your other lipoprotein fractions are out of balance. But there is a missing link in this chain of reasoning.
Lipoprotein(a) may well indicate a genetic predisposition for elevated or distorted cholesterol readings. However, there is no conclusive scientific evidence that cholesterol or other lipoproteins actually cause atherosclerosis, plus a number of logical reasons why they cannot.
Co-enzyme Q10
Co-enzyme Q10 (ubiquinone, ubiquinol) is a vitamin-like substance that is present in ALL bodily cells and generates energy in the form of adenosine triphosphate (ATP). CoQ10 is present in large amounts in those organs with highest energy requirements, namely the heart, liver and kidneys. CoQ10 also functions as an antioxidant to protect cells against the damaging effects of oxygen free radicals. There combined actions of CoQ10 help both to strengthen the heart muscle and to prevent damage to arterial walls.
Internal production of CoQ10 is ascorbate dependant, which may be another of the reasons why most animals' bodies are protected against atherosclerosis, whereas those with hypoascorbemia are not.
If the body has sufficient high intake of vitamin C and B-vitamins, it may be capable of producing all the CoQ10 it needs - without resorting to dietary CoQ10. Large amounts of vitamin C can also supplement and even replace the antioxidant activity of CoQ10.
Cholesterol lowering drugs interfere with and deplete the body's production of CoQ10, however so anyone taking these pharmaceuticals is well advised also to take supplementary CoQ10.
A free radical is an unstable, highly reactive molecular fragment that contains an odd number of electrons and an open bond or half bond. If 2 radicals meet, both are eliminated. If a radical reacts with a nonradical, another free radical is produced. This type of event may become a chain reaction and may contribute to the development of ischemic injury, such as myocardial infarction (heart attach). Cascading free radical reactions appear to be the most significant cause of arterial damage.
Blood Sugar
All of the various sugars we consume are broken down in the digestive tract into simple sugars glucose (dextrose) and fructose (levulose), then immediately absorbed through the intestinal wall directly into the bloodstream. The LIVER converts fructose into glucose, so ultimately every king of sugar ends up as glucose (blood sugar). If we consume too much sugar, our blood becomes flooded with excess level of glucose. If our PANCREAS, LIVER and ADRENAL GLANDS are in fine working order, then this spike in blood sugar is only temporary. If our endocrine system is out of balance and we push our sugar consumption, then we may develop hypoglycemia or diabetes. (some forms of diabetes are caused or aggravated by genetic weakness).
Hypoglycemia is characterized by compulsive sugar consumption which triggers multiple highs and lows in blood sugar throughout the day. In diabetes, blood sugar is constantly too high. Unfortunatelly, high glucose levels accelerate free radical damage - the degree of which damage is most probably in direct proportion to how high the glucose level and for how much of the day. In the development of arterial damage:
a) diabetes is a hugely accelerating factor
b) hypoglycemia is probably an aggravating factor
c) in otherwise healthy people, high sugar meals may cause some degree of arterial stress.
Our bodies can getall of the glucose we need for optimal functioning from gradual breakdown of complex carbohydrates (eg: whole grains, starchy vegetables), thus avoiding spikes in blood sugar.
Blood Fats
The body has a very clever way of assuring that fats in the bloodstream stay within an acceptable range. The fats that we consume are broken down by the action of bile and amylase enzymes into simpler fatty acids that are absorbed into the lymphatic system rather than the bloodstream. To absorb fats directly into the blood would be fatal. Instead, fats circulate throughout the lymphatics and are transferred into the blood on an "as needed" basis. Thus, the quantity of fats in the blood is strictly regulated and is of no consequence to atherosclerosis. The quality of fats most assuredly is, however. Unstable polyunsaturated oils, rancid fats and trans fats circulating in our lymphatic system find their way into cellular membranes, thus increasing their vulnerability to free radical damage.
Hypoglycemia is characterized by compulsive sugar consumption which triggers multiple highs and lows in blood sugar throughout the day. In diabetes, blood sugar is constantly too high. Unfortunatelly, high glucose levels accelerate free radical damage - the degree of which damage is most probably in direct proportion to how high the glucose level and for how much of the day. In the development of arterial damage:
a) diabetes is a hugely accelerating factor
b) hypoglycemia is probably an aggravating factor
c) in otherwise healthy people, high sugar meals may cause some degree of arterial stress.
Our bodies can getall of the glucose we need for optimal functioning from gradual breakdown of complex carbohydrates (eg: whole grains, starchy vegetables), thus avoiding spikes in blood sugar.
Blood Fats
The body has a very clever way of assuring that fats in the bloodstream stay within an acceptable range. The fats that we consume are broken down by the action of bile and amylase enzymes into simpler fatty acids that are absorbed into the lymphatic system rather than the bloodstream. To absorb fats directly into the blood would be fatal. Instead, fats circulate throughout the lymphatics and are transferred into the blood on an "as needed" basis. Thus, the quantity of fats in the blood is strictly regulated and is of no consequence to atherosclerosis. The quality of fats most assuredly is, however. Unstable polyunsaturated oils, rancid fats and trans fats circulating in our lymphatic system find their way into cellular membranes, thus increasing their vulnerability to free radical damage.
Niacin (vitamin B3)
When there is a need for additional support to dietary and lifestyle practices that can lower cholesterol, it simply makes sense to use natural compounds, which are actually safer and more effective than the prescription drugs commonly used for that purpose.
Niacin, or vitamin B3, has long been used to lower cholesterol. In fact niacin is recommended by the National Cholesterol Education Program as the first "drug" to use. Unlike many cholesterol-lowering drugs, which have actually been shown to reduce life expectancy, niacin can lower cholesterol safely and extend life. Its effects are long-lasting. (The dose of niacin usually required to lower cholesterol is 1gram/3 times per day).
NOTE: Besides safely reducing harmful cholesterol levels, another niacin feature is its ability to greatly reduce anxiety and depression. Yet another feature is that it dilates blood vessels and creates a sensation of warmth, called a "niacin flush." (reaction that is totally harmless). This is often accompanied with a blushing of the skin. It is this "flush" or sensation of heat that indicates a temporary saturation of niacin.
When you flush, you can literally see and feel that you've taken enough niacin. The idea is to initially take just enough niacin to have a slight flush. This means a pinkness about the cheeks, ears, neck, forearms and perhaps elsewhere. A slight niacin flush should end in about fifteen minutes or so. If you take too much niacin, the flush may be more pronounced and longer lasting. If you flush beet red for half an hour and feel weird, well, you took too much. And a large dose of niacin on an empty stomach is certain to cause profound flushing.
The dose required to reduce harmful cholesterol can result in flushing of the skin so you might want to buy a slow-released product. (forms of B3 that don't create flushing like inositol hexaniacinate).
Source: www.rowlandpub.com/
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