We have all seen someone, seemingly healthy days or hours before, suddenly slump and die. This is the kind of death or disability that heart attack visits on its victims. Of the numerous types of cardiovascular conditions, the one that is most likely to lead to a heart attack is what is known as Coronary Heart Disease (CHD) or more appropriately, Coronary Artery Disease (CAD).

Coronary arteries are the vessels (arteries) that carry oxygen-rich blood to the heart muscles or myocardium. So, as the name implies, Coronary Artery Disease is a condition that affects the coronary arteries (i.e. arteries of the heart). This condition is characterized by the slow and gradual buildup of fatty deposits (fat streaks, plaques or atheromatous streaks) in the walls of the coronary arteries. Initially, these atheromatous streaks/plaques expand into the walls of the arteries, but subsequently, they start building up and growing into the lumen of the affected arteries, narrowing such arteries and obstructing blood flow. This is known as atherosclerosis.

As the build up of the plaques continue, over the years, the plaques increase in thickness and the degree of obstruction of blood flow to the heart muscles becomes severe. Though, the buildup of the plaques takes a very long time to completely occlude the lumen of an artery and result in heart attack, however, sudden rupture of a plaque usually speeds up the process. The rupture of plaque activates the blood clotting system and the clot-plaque interaction fills the lumen of such artery to the point of sudden closure. Such sudden occlusion of a coronary artery causes irreversible death of the heart muscle supplied by that artery (myocardial infarction) and precipitates a ‘heart attack’ i.e. the sudden stop of heart beat.

Coronary heart disease, the commonest underlying cause of heart attack, as with several other cardiovascular conditions has been associated with a number of risk factors; however, a family history of coronary heart disease appears to be one of the strongest risk factors. Also, men are more likely to suffer a heart attack than women, though after menopause, the risk of women approaches that of men, especially with hormonal therapies, which tend to increase a woman’s risk of CHD. Other risk factors include: Smoking, diabetes, hypertension, obesity (especially central or female-type obesity), a chronic sub-clinical lack of vitamin C, elevated homocysteine levels, elevated blood levels of asymmetric dimethylarginine and also importantly, sedentary or inactive lifestyle.

Beside some factors which cannot be controlled, such as hereditary and gender, prevention of CHD and hence, heart attack, is usually achieved through the modification of risk factors. Leading an active life style with frequent exercise, cessation of smoking, maintaining a low-fat, low-calorie diet and decreasing blood cholesterol levels, especially Low density lipoproteins (LDL) are crucial to preventing heart attack. Exercise and healthy diet have been shown to have profound effect on cardiovascular risks, although, cessation of cigarette smoking can also profoundly reduce the risk of heart attack.

The underlying cause of heart attack is coronary heart disease (CHD) – the slow build-up of fatty deposits on the inner wall of the arteries that supply the heart muscle with blood. These fatty deposits, called plaque, gradually clog and narrow the inside channel of the arteries. It is a process that begins early in life and continues over the years.

A heart attack usually begins when an area of plaque cracks. Blood cells and other components of the blood stick over the damaged area and form a clot that suddenly and completely blocks the blood flow to the heart muscle. If the artery remains blocked, the lack of blood permanently damages the area of heart muscle supplied by that artery.

Know the signs of a heart attack, but be aware that symptoms can vary from person to person. Usual signs of a heart attack include chest pain, discomfort, heaviness or fullness in the chest, discomfort in arms, neck, jaw, stomach, shortness of breath, cold sweat or even nausea and vomiting. Sometimes these symptoms can come on suddenly but they can develop slowly. Not every chest pain is a heart attack, but it is impossible to know that before evaluation by a medical professional. Call 911 if you think you may be suffering from these symptoms. Do not drive yourself or anyone else to the hospital if these symptoms exist because during a heart attack, the possibility of life threatening rhythms exist, which can result in sudden loss of consciousness and death.

If you are rushed to hospital with a suspected heart attack, a number of tests will be performed to confirm the diagnosis and help your health care team decide on the best treatment for you.

These may include:

* Electrocardiogram (ECG) – During an ECG test, electrical leads are placed on your chest, arms and legs. These leads detect small electrical signals and produce a tracing on graph paper illustrating the electrical impulses travelling through the heart muscle.

* Blood tests

* Chest X-ray

* Angiogram – This is a special X-ray that shows whether your coronary arteries are narrowed or blocked. Under a local anaesthetic, a small tube (catheter) is inserted into an artery in your arm or groin and guided into the heart. Dye is injected through the catheter into the coronary arteries and X-rays are taken, giving detailed information about the condition of your coronary arteries.

Not every chest pain is a heart attack, but it is impossible to know without being evaluated by a medical professional. When having chest pain or related symptoms, it is best and safest to call 911. For those who have a history of coronary disease, previous coronary interventions (stents, angioplasty or open-heart surgery), transport to a PCI center is imperative. Primary PCI in the shortest amount of time is the best chance for survival and limiting of heart muscle damage.

In comparison to HDL, which has been privileged with the name ‘good’ cholesterol, LDL and VLDL are relatively large cholesterol molecules; in fact, they are the richest in cholesterol. There is good reason for their large size. Unlike their smaller cousin, which easily passes through blood vessel walls, the LDL and VLDL versions of cholesterol are meant to take a different pathway; they leave the blood stream in the liver.

The blood vessels supplying the liver have a very different structure from the ones supplying other parts of the body. They are known as sinusoids. Their unique, grid-like structure permits the liver cells to receive the entire blood content, including the large cholesterol molecules. The liver cells rebuild the cholesterol and excrete it along with bile into the intestines. Once the cholesterol enters the intestines, it combines with fats, is absorbed by the lymph and enters the blood, in that order. Gallstones in the bile ducts of the liver inhibit the bile flow and partially, or even fully, block the cholesterol’s escape route. Due to back-up pressure on the liver cells, bile production drops. Typically, a healthy liver produces over a quart of bile per day. When the major bile ducts are blocked, barely a cup of bile, or even less, will find its way to the intestines. This prevents much of the VLDL and LDL cholesterol from being excreted with the bile.

Gallstones in the liver bile ducts distort the structural framework of the liver lobules, which damages and congests the sinusoids. Deposits of excessive protein also close the grid holes of these blood vessels (see the discussion of this subject in the previous section). Whereas the ‘good’ cholesterol HDL has small enough molecules to leave the bloodstream through ordinary capillaries, the larger LDL and VLDL molecules are more or less trapped in the blood. The result is that LDL and VLDL concentrations begin to rise in the blood to levels that seem potentially harmful to the body. Yet even this scenario is merely part of the body’s survival attempts. It needs the extra cholesterol to patch up the increasing number of cracks and wounds that are formed as a result of the accumulation of excessive protein in the blood vessel walls. Eventually, though, the life-saving cholesterol begins to occlude the blood vessels and cut off the oxygen supply to the heart.

In addition to this complication, reduced bile flow impairs the digestion of food, particularly fats. Therefore, there is not enough cholesterol made available to the cells of the body and their basic metabolic processes. Since the liver cells no longer receive sufficient amounts of LDL and VLDL molecules, they (the liver cells) assume that the blood is deficient in these types of cholesterol. This stimulates the liver cells to increase the production of cholesterol, further raising the levels of LDL and VLDL cholesterol in the blood.

The ‘bad’ cholesterol is trapped in the circulatory system because its escape routes, the bile ducts and the liver sinusoids, are blocked or damaged. The capillary network and arteries attach as much of the ‘bad’ cholesterol to their walls as they possibly can. Consequently, the arteries become rigid and hard.

It seems there’s something about carrying all that extra weight that contributes, on its own, to heart problems. So you might have perfect blood pressure, be free of diabetes, have normal cholesterol and no sign of arterial disease yet your weight still ups your chances of a fatal heart attack.

This finding comes from work by the British Heart Foundation’s Cardiovascular Researcher Centre. A heart attack happens when blood vessels that bring blood to the heart itself are blocked, stopping enough oxygen from getting to the heart. The muscle is then starved for oxygen and its cells start to die off.

The team spent almost 15 years following 6,082 men who had high cholesterol but without a history of diabetes or heart disease. As the study went forward, the researchers saw 214 heart disease deaths, just over a 1000 heart attacks and/or strokes where the patient survived the event. The research confirmed the long held medical belief obesity is associated with a greater chance of having all the risk factors normally associated with heart disease.

The thing was, even after accounting for factors like age and whether the participants were smokers, the risk of dying among the obese men (BMI 30.0 to 39.9) was three quarters higher than for men of normal weight.

Obese men in their middle years were found to have a 60% greater chance of dying due to a heart attack than those of the same age, but who fell into more normal weight bands, even after excluding the risk factors commonly recognized for heart disease. Obesity itself appears to play some role in fatal heart attacks.

Why the increased risk?

No one is sure, though experts suspect the long-term inflammation that comes with carrying lots of weight might be the real reason of the increased risk. More work is needed, though experts who didn’t take part in the study aren’t at all surprised that the heart risk of all those extra pounds isn’t explained by traditional cardiovascular risk factors.

Experts believe the answer might lie in chemicals the fat cells release, or perhaps that those suffering from obesity tend to have bigger heart muscles in order to handle the added stress of their enlarged bodies. It may be that a heart so stressed struggles to keep going during an adverse heart event.

The findings also suggest that treating cholesterol and blood pressure, managing diabetes in people and addressing their weight issues are all key steps to reducing heart disease risk in men. Losing weight (or not gaining it in the first place) needs to get more attention, more resources and more support.

What you may not know is the true cause of heart disease… the real culprits.

Is it cholesterol?

Is it saturated fats?

The AMA (American Medical Association) and the AHA (American Heart Association) as well as the food industry have been telling us so forever. Okay, maybe not forever, but a long time!

If we know what the cause is, why have heart disease escalated into becoming our nation’s #1 killer?

3 Reasons Why Cholesterol and Saturated Fats Are Not the True Causes of Heart Disease

1. How can it be that as the consumption of saturated fats and cholesterol declined sharply from the levels it used to be, heart disease increased proportionately? It appears that the statistics are telling a different story than what the AMA, AHA, and the food industry has been telling us.

2. Just look at significant role that saturated fats and cholesterol play in our bodies. It will probably surprise you to know that saturated fats comprise at least 50% of your cell membranes (every single one of your trillions of cells), giving them stiffness and integrity. Cholesterol also makes up part of the cell membrane, regulating its fluidity (what passes in and out) as well as giving stiffness and stability to the cell membrane. Additionally, cholesterol is a precursor to bile (which is produced in the liver and gall bladder to emulsify fats), Vitamin D, the steroid hormones (that help us deal with stress), and the sex hormones. Cholesterol is also very important for proper development of the brain and nervous system, so mother’s milk is very cholesterol-rich, and contains a special enzyme to help the baby utilize this nutrient. How can saturated fats and cholesterol possibly be the bad guys in light of this information?

3. HDL and LDL are NOT forms of cholesterol! That’s right, HDL and LDL are really lipoproteins, carrier molecules for cholesterol and other fats. Because cholesterol and other fats are not water-soluble, they require a carrier molecule to transport them through the blood stream. Even more interestingly, these carrier molecules have built-in cell-targeting signals, directing them to specific target cells. Don’t you wonder why?

Over Twenty Years of Research Has Established Inflammation’s Key Role in Atherosclerosis

But what’s causing the inflammation?

Is it cholesterol or saturated fats, as the AMA, AHA and food industry has led us to believe? It is NOT. We already proved it above.

The mechanism by which periodontal disease causes inflammation via free radicals produced by the immune system is well-known and accepted. But the role saturated fats and cholesterol play in inflammation is unknown to medical doctors. That’s because something else is causing the inflammation leading to atherosclerotic plaques. That something else happens to be the very polyunsaturated oils touted as “heart healthy” by the AMA, AHA, and the food industry. All of this information is well supported and detailed in my book, Revolutionizing Your Health.

How the Supposedly “Heart Healthy” Oils Are the True Causes of Heart Disease…

Polyunsaturated oils go rancid and become oxidized very easily by heat and light, which mean they become a free radical. Free radicals are very unstable molecules missing an electron. In the body, they try to stabilize themselves by “stealing” an electron from neighboring cells. This continues in a domino effect, wreaking cellular destruction and producing inflammation. In fact, the high heat used in processing these oils often creates free radicals before the oil even leaves the processing plant. Additionally, when these oils are used for cooking, and especially for frying, they produce tremendous amounts of free radicals.

Earlier, it was discussed that saturated fats make up at least 50% of cell membranes, along with cholesterol. The trouble is that our bodies don’t distinguish between saturated fats and polyunsaturated oils. A diet high in polyunsaturated oils will then be incorporated into cell membranes in place of the more stable and functional saturated fats. In effect this makes weaker cell membranes that are loaded with free radicals. This produces the inflammation that cardiologists now know to be at the root of heart disease. Cholesterol is simply the “repair substance” the body uses to repair the cellular damage produced by the free radicals in polyunsaturated oils.

We have all seen someone, seemingly healthy days or hours before, suddenly slump and die. This is the kind of death or disability that heart attack visits on its victims. Of the numerous types of cardiovascular conditions, the one that is most likely to lead to a heart attack is what is known as Coronary Heart Disease (CHD) or more appropriately, Coronary Artery Disease (CAD).

Coronary arteries are the vessels (arteries) that carry oxygen-rich blood to the heart muscles or myocardium. So, as the name implies, Coronary Artery Disease is a condition that affects the coronary arteries (i.e. arteries of the heart). This condition is characterized by the slow and gradual buildup of fatty deposits (fat streaks, plaques or atheromatous streaks) in the walls of the coronary arteries. Initially, these atheromatous streaks/plaques expand into the walls of the arteries, but subsequently, they start building up and growing into the lumen of the affected arteries, narrowing such arteries and obstructing blood flow. This is known as atherosclerosis.

As the build up of the plaques continue, over the years, the plaques increase in thickness and the degree of obstruction of blood flow to the heart muscles becomes severe. Though, the buildup of the plaques takes a very long time to completely occlude the lumen of an artery and result in heart attack, however, sudden rupture of a plaque usually speeds up the process. The rupture of plaque activates the blood clotting system and the clot-plaque interaction fills the lumen of such artery to the point of sudden closure. Such sudden occlusion of a coronary artery causes irreversible death of the heart muscle supplied by that artery (myocardial infarction) and precipitates a ‘heart attack’ i.e. the sudden stop of heart beat.

Coronary heart disease, the commonest underlying cause of heart attack, as with several other cardiovascular conditions has been associated with a number of risk factors; however, a family history of coronary heart disease appears to be one of the strongest risk factors. Also, men are more likely to suffer a heart attack than women, though after menopause, the risk of women approaches that of men, especially with hormonal therapies, which tend to increase a woman’s risk of CHD. Other risk factors include: Smoking, diabetes, hypertension, obesity (especially central or female-type obesity), a chronic sub-clinical lack of vitamin C, elevated homocysteine levels, elevated blood levels of asymmetric dimethylarginine and also importantly, sedentary or inactive lifestyle.

Beside some factors which cannot be controlled, such as hereditary and gender, prevention of CHD and hence, heart attack, is usually achieved through the modification of risk factors. Leading an active life style with frequent exercise, cessation of smoking, maintaining a low-fat, low-calorie diet and decreasing blood cholesterol levels, especially Low density lipoproteins (LDL) are crucial to preventing heart attack. Exercise and healthy diet have been shown to have profound effect on cardiovascular risks, although, cessation of cigarette smoking can also profoundly reduce the risk of heart attack.

The underlying cause of heart attack is coronary heart disease (CHD) – the slow build-up of fatty deposits on the inner wall of the arteries that supply the heart muscle with blood. These fatty deposits, called plaque, gradually clog and narrow the inside channel of the arteries. It is a process that begins early in life and continues over the years.

A heart attack usually begins when an area of plaque cracks. Blood cells and other components of the blood stick over the damaged area and form a clot that suddenly and completely blocks the blood flow to the heart muscle. If the artery remains blocked, the lack of blood permanently damages the area of heart muscle supplied by that artery.

Know the signs of a heart attack, but be aware that symptoms can vary from person to person. Usual signs of a heart attack include chest pain, discomfort, heaviness or fullness in the chest, discomfort in arms, neck, jaw, stomach, shortness of breath, cold sweat or even nausea and vomiting. Sometimes these symptoms can come on suddenly but they can develop slowly. Not every chest pain is a heart attack, but it is impossible to know that before evaluation by a medical professional. Call 911 if you think you may be suffering from these symptoms. Do not drive yourself or anyone else to the hospital if these symptoms exist because during a heart attack, the possibility of life threatening rhythms exist, which can result in sudden loss of consciousness and death.

If you are rushed to hospital with a suspected heart attack, a number of tests will be performed to confirm the diagnosis and help your health care team decide on the best treatment for you.

These may include:

* Electrocardiogram (ECG) – During an ECG test, electrical leads are placed on your chest, arms and legs. These leads detect small electrical signals and produce a tracing on graph paper illustrating the electrical impulses travelling through the heart muscle.

* Blood tests

* Chest X-ray

* Angiogram – This is a special X-ray that shows whether your coronary arteries are narrowed or blocked. Under a local anaesthetic, a small tube (catheter) is inserted into an artery in your arm or groin and guided into the heart. Dye is injected through the catheter into the coronary arteries and X-rays are taken, giving detailed information about the condition of your coronary arteries.

Not every chest pain is a heart attack, but it is impossible to know without being evaluated by a medical professional. When having chest pain or related symptoms, it is best and safest to call 911. For those who have a history of coronary disease, previous coronary interventions (stents, angioplasty or open-heart surgery), transport to a PCI center is imperative. Primary PCI in the shortest amount of time is the best chance for survival and limiting of heart muscle damage.

In comparison to HDL, which has been privileged with the name ‘good’ cholesterol, LDL and VLDL are relatively large cholesterol molecules; in fact, they are the richest in cholesterol. There is good reason for their large size. Unlike their smaller cousin, which easily passes through blood vessel walls, the LDL and VLDL versions of cholesterol are meant to take a different pathway; they leave the blood stream in the liver.

The blood vessels supplying the liver have a very different structure from the ones supplying other parts of the body. They are known as sinusoids. Their unique, grid-like structure permits the liver cells to receive the entire blood content, including the large cholesterol molecules. The liver cells rebuild the cholesterol and excrete it along with bile into the intestines. Once the cholesterol enters the intestines, it combines with fats, is absorbed by the lymph and enters the blood, in that order. Gallstones in the bile ducts of the liver inhibit the bile flow and partially, or even fully, block the cholesterol’s escape route. Due to back-up pressure on the liver cells, bile production drops. Typically, a healthy liver produces over a quart of bile per day. When the major bile ducts are blocked, barely a cup of bile, or even less, will find its way to the intestines. This prevents much of the VLDL and LDL cholesterol from being excreted with the bile.

Gallstones in the liver bile ducts distort the structural framework of the liver lobules, which damages and congests the sinusoids. Deposits of excessive protein also close the grid holes of these blood vessels (see the discussion of this subject in the previous section). Whereas the ‘good’ cholesterol HDL has small enough molecules to leave the bloodstream through ordinary capillaries, the larger LDL and VLDL molecules are more or less trapped in the blood. The result is that LDL and VLDL concentrations begin to rise in the blood to levels that seem potentially harmful to the body. Yet even this scenario is merely part of the body’s survival attempts. It needs the extra cholesterol to patch up the increasing number of cracks and wounds that are formed as a result of the accumulation of excessive protein in the blood vessel walls. Eventually, though, the life-saving cholesterol begins to occlude the blood vessels and cut off the oxygen supply to the heart.

In addition to this complication, reduced bile flow impairs the digestion of food, particularly fats. Therefore, there is not enough cholesterol made available to the cells of the body and their basic metabolic processes. Since the liver cells no longer receive sufficient amounts of LDL and VLDL molecules, they (the liver cells) assume that the blood is deficient in these types of cholesterol. This stimulates the liver cells to increase the production of cholesterol, further raising the levels of LDL and VLDL cholesterol in the blood.

The ‘bad’ cholesterol is trapped in the circulatory system because its escape routes, the bile ducts and the liver sinusoids, are blocked or damaged. The capillary network and arteries attach as much of the ‘bad’ cholesterol to their walls as they possibly can. Consequently, the arteries become rigid and hard.

It seems there’s something about carrying all that extra weight that contributes, on its own, to heart problems. So you might have perfect blood pressure, be free of diabetes, have normal cholesterol and no sign of arterial disease yet your weight still ups your chances of a fatal heart attack.

This finding comes from work by the British Heart Foundation’s Cardiovascular Researcher Centre. A heart attack happens when blood vessels that bring blood to the heart itself are blocked, stopping enough oxygen from getting to the heart. The muscle is then starved for oxygen and its cells start to die off.

The team spent almost 15 years following 6,082 men who had high cholesterol but without a history of diabetes or heart disease. As the study went forward, the researchers saw 214 heart disease deaths, just over a 1000 heart attacks and/or strokes where the patient survived the event. The research confirmed the long held medical belief obesity is associated with a greater chance of having all the risk factors normally associated with heart disease.

The thing was, even after accounting for factors like age and whether the participants were smokers, the risk of dying among the obese men (BMI 30.0 to 39.9) was three quarters higher than for men of normal weight.

Obese men in their middle years were found to have a 60% greater chance of dying due to a heart attack than those of the same age, but who fell into more normal weight bands, even after excluding the risk factors commonly recognized for heart disease. Obesity itself appears to play some role in fatal heart attacks.

Why the increased risk?

No one is sure, though experts suspect the long-term inflammation that comes with carrying lots of weight might be the real reason of the increased risk. More work is needed, though experts who didn’t take part in the study aren’t at all surprised that the heart risk of all those extra pounds isn’t explained by traditional cardiovascular risk factors.

Experts believe the answer might lie in chemicals the fat cells release, or perhaps that those suffering from obesity tend to have bigger heart muscles in order to handle the added stress of their enlarged bodies. It may be that a heart so stressed struggles to keep going during an adverse heart event.

The findings also suggest that treating cholesterol and blood pressure, managing diabetes in people and addressing their weight issues are all key steps to reducing heart disease risk in men. Losing weight (or not gaining it in the first place) needs to get more attention, more resources and more support.

What you may not know is the true cause of heart disease… the real culprits.

Is it cholesterol?

Is it saturated fats?

The AMA (American Medical Association) and the AHA (American Heart Association) as well as the food industry have been telling us so forever. Okay, maybe not forever, but a long time!

If we know what the cause is, why have heart disease escalated into becoming our nation’s #1 killer?

3 Reasons Why Cholesterol and Saturated Fats Are Not the True Causes of Heart Disease

1. How can it be that as the consumption of saturated fats and cholesterol declined sharply from the levels it used to be, heart disease increased proportionately? It appears that the statistics are telling a different story than what the AMA, AHA, and the food industry has been telling us.

2. Just look at significant role that saturated fats and cholesterol play in our bodies. It will probably surprise you to know that saturated fats comprise at least 50% of your cell membranes (every single one of your trillions of cells), giving them stiffness and integrity. Cholesterol also makes up part of the cell membrane, regulating its fluidity (what passes in and out) as well as giving stiffness and stability to the cell membrane. Additionally, cholesterol is a precursor to bile (which is produced in the liver and gall bladder to emulsify fats), Vitamin D, the steroid hormones (that help us deal with stress), and the sex hormones. Cholesterol is also very important for proper development of the brain and nervous system, so mother’s milk is very cholesterol-rich, and contains a special enzyme to help the baby utilize this nutrient. How can saturated fats and cholesterol possibly be the bad guys in light of this information?

3. HDL and LDL are NOT forms of cholesterol! That’s right, HDL and LDL are really lipoproteins, carrier molecules for cholesterol and other fats. Because cholesterol and other fats are not water-soluble, they require a carrier molecule to transport them through the blood stream. Even more interestingly, these carrier molecules have built-in cell-targeting signals, directing them to specific target cells. Don’t you wonder why?

Over Twenty Years of Research Has Established Inflammation’s Key Role in Atherosclerosis

But what’s causing the inflammation?

Is it cholesterol or saturated fats, as the AMA, AHA and food industry has led us to believe? It is NOT. We already proved it above.

The mechanism by which periodontal disease causes inflammation via free radicals produced by the immune system is well-known and accepted. But the role saturated fats and cholesterol play in inflammation is unknown to medical doctors. That’s because something else is causing the inflammation leading to atherosclerotic plaques. That something else happens to be the very polyunsaturated oils touted as “heart healthy” by the AMA, AHA, and the food industry. All of this information is well supported and detailed in my book, Revolutionizing Your Health.

How the Supposedly “Heart Healthy” Oils Are the True Causes of Heart Disease…

Polyunsaturated oils go rancid and become oxidized very easily by heat and light, which mean they become a free radical. Free radicals are very unstable molecules missing an electron. In the body, they try to stabilize themselves by “stealing” an electron from neighboring cells. This continues in a domino effect, wreaking cellular destruction and producing inflammation. In fact, the high heat used in processing these oils often creates free radicals before the oil even leaves the processing plant. Additionally, when these oils are used for cooking, and especially for frying, they produce tremendous amounts of free radicals.

Earlier, it was discussed that saturated fats make up at least 50% of cell membranes, along with cholesterol. The trouble is that our bodies don’t distinguish between saturated fats and polyunsaturated oils. A diet high in polyunsaturated oils will then be incorporated into cell membranes in place of the more stable and functional saturated fats. In effect this makes weaker cell membranes that are loaded with free radicals. This produces the inflammation that cardiologists now know to be at the root of heart disease. Cholesterol is simply the “repair substance” the body uses to repair the cellular damage produced by the free radicals in polyunsaturated oils.