HomeVitamins and DiseaseArticles of HEALTHVITAMIN CriteriaREFERENCES/ Links
RIGHTWAY VITAMINS
Empower Healthy Choices
Natural or Synthetic Vitamins
Survive Alive
Hearts of FIRE
Hearts of FIRE 2
Radical Charges
Before You Take...
Hollow Bone Saga
BoneWorks
Soy Uncensored
Strontium and Bones
Hearts of FIRE

launched Oct 2006                                          revised Jan 2008

Hearts of FIRE

QV Summary: To combat cardiovascular heart disease, mainstream medicine picked cholesterol levels as the targeted cause. A review of the systemic facts from research shows that cholesterol is just a secondary risk factor and not a primary cause. Following are some of the facts you need to understand about this most important topic. 

Caution:  This is a general information article designed to stimulate discussion and further research. Do not make lifestyle changes without the support of your medical team. Each individual may require unique applications in their situation.

February may be Heart Health month, but heart disease continues year around to be the number one killer disease in industrialized nations. This vital topic article reveals an important concept you need to grasp. You are in control of about 75% of the causing factors, with genetics influencing the rest. The genetic part is even able to be modified by your actions to a certain degree.

Mainstream medicine has known most of these primary factors for many years, but has chosen to concentrate treatment on a secondary factor, cholesterol lowering. The heart health story you have been told is only half right. Here are some of the missing parts. First, some questions:

1. What is the history pattern of heart disease?

2. Are there any major changes to lifestyles or dietary patterns that parallel heart disease increases or decreases? 

3. What exactly is happening? 4. What parts or sections of  blood vessels are involved?

5. Are all people affected equally?

6. What does science currently say about the causes?

7. What treatments, either drugs, dietary, or lifestyle, are recommended? And for that matter, effective?

Any idea when the first recorded heart attack was?   ... From records of the Franklin Institute, in 1912 Dr James Herrick first described heart disease resulting from hardening of the arteries. And in 1938 Dr Robert Gross performed the first heart operation. Heart disease is a condition that mostly developed during the 20th century.

It is the number one cause of death today. Something mighty drastic happened in the last 100 years to allow this disease to so rapidly develop. Statistics show the most rapid increase was after 1940. Cholesterol is the factor that is blamed and targeted by the mainstream medicine machine. Thus, one would assume that dietary and plasma cholesterol levels in Americans must have increased over the last century as the heart disease rate also rose to rapidly cause this disease epidemic. What if cholesterol levels did not always parallel or match the disease rates? Remember the fifties when you were told to not use butter or lard but use vegetable oils and margarines instead? Did scientists pick the right target?

SIDEBAR: Amazingly, the history of margarine use almost parallels the rise (and fall) in heart disease rates. Developed in 1860, margarine sales reached about 120 million pounds by 1900. Then the Dairy Industry fought back and the 1902 Margarine Act amendment reduced consumption amounts down to 48 million pounds. WWI increased amounts rapidly. Again the Dairy Industry pushed legislation to reduce, but by WWII, the yellow color was added back and sales soared. Funny, about the same time as the rapid increase in heart disease. Now, might the decline observed over the last decades in heart disease be related to the improvements in margarines which lowered the levels of Trans Fats. Very Interesting! 

Look at the picture created by these references. Click on the number.

1.  The nine factors leading to Cardiovascular Disease (CVD). Of which 8 of 9 are under nutritional influences. One of the most important review articles on this website.   

2.  Calcium magnesium ratios in ground water as a risk factor.

3 Low levels of xGSH found in CVD. GSH is involved in preventing stress oxidation. Vitamin C and selenium can increase levels.

4. Fish oil omega 3 fatty acids protect against CVD. A study of levels of n-3 in fat cells verses the degree of damage found in arteries of CVD cases.

5.  The role of whole grains in reducing the risk of CHD.

6.  From Harvard on trans-fats. Double the damage to cardiovascular conditions than saturated fats. Now, would you like some margarine on that slice of bread or some butter?

THE CORE HEALTH ISSUE

These six research articles show a connection between CVD and anti-oxidant status, calcium and magnesium balance, fish omega 3 fats, fiber from whole grains, and how trans fats are far worst than saturated fats in causing CVD. Now, the question that one has to ask again. Did scientists pick the right factor to target in developing drugs to lower total cholesterol?

SIDEBAR: It is important to understand that there are two different processes in artery blockage. In the first case (atherosclerosis) fatty plaque containing among other things, cholesterol and calcium, begins to build up WITHIN the walls of arteries. As more plaque is developed, the inner lining of the blood vessel begins to bulge into the vessel open space and obstruct blood flow.  A heast attack occurs when these build ups get large enough to block proper blood flow. Also, the inner blood vessel lining can tear open and some of the exposed plaque breaks off and travels down the vessel until the vessel narrows and traps the plaque blocking blood flow causing a stroke if the blockage is in the brain or a heart attack if in the heart.

The other situation that can occur, often coupled with the above conditions, small elements called platelets can become sticky and clump together causing them to adher to blood vessel walls. Clots formed this way can have the same results. To find out how to avoid this, read on.

 

 CHOLESTEROL CONNECTION

Any discussion of Heart Health currently centers around CHOLESTEROL levels. The lower the better according to the American Heart Association. This logically should equate to everyone with high cholesterol levels getting cardiovascular disease and those with low levels being free of CVD. Unfortunately, the facts beg to differ with this logic. The cholesterol levels of people who suffer heart attacks are basically nearly the same as people who do not develop CVD. Yes, at the higher end numbers there is more CVD mortality which might largely be explained by genetic variations, one is called familial hypercholesterolemia, a fancy term meaning your body produces higher cholesterol. People with low cholesterol levels still can have heart attacks and some people with very high cholesterol don't develop CVD. How do these factors exist with the current cholesterol theory? The generalities the public has been lead to believe don't tell the whole story. This remarkable story needs to be told, and told correctly, and you needed to hear it yesterday.

SIDEBAR: This theory has been proposed and may have some merit. To explain the rapid rise and then fall of the CHD rates over the last century, the Spanish Flu of 1918 could have changed the subclass of genotypes to a higher cholesterol pool as these are the ones who showed a greater resistence to the infection and had higher survival rates.

The truth is that cholesterol is absolutely essential to life. There should never have been names of "good" and "bad" given to cholesterol, it is all good and necessary, although it can get out of balance due to dietary and lifestyle transgressions or hereditary factors. Without cholesterol you couldn't produce certain hormones, protect nerve cells, or make vitamin D from the action of sunlight on skin. It forms part of the bile salts necessary for digesting fats and absorbing the fat soluble vitamins A, D, E, and K. Cholesterol along with phospholipids form cell walls, or membranes that regulate entry of building nutrients and exit of wastes necessary for proper cell metabolism. Cholesterol helps support a healthy immune system. Cholesterol is vital to life.

Cycle of CHOLESTEROL

Dietary cholesterol used to be blamed for much of heart disease. Eggs became taboo since they have over 200 mg. The truth is that the source really doesn't matter to the body. There is an example of a man eating 24 eggs a day for many years and his cholesterol level varied very little. Cholesterol is built in the liver to a set amount the body needs, either programmed by genetics or influenced by dietary and lifestyle factors. YES, as seen in the movie, Supersize Me, you can overwhelm the system and create chaos. But usually, under more normal eating conditions, If you consume cholesterol in the diet, the liver just lowers the amount it produces via a feedback loop and the levels remain nearly the same.  ref 

After the liver produces cholesterol, it is packaged with Apo B onto a fat protein combination, called VLDL for very low density lipoprotein,  and carried out into the body via the blood vessels. VLDLs are mainly triglycerides with about 25% cholesterol esters. This VLDL has to be activated by Apo C2 and Apo E, which arrive with HDLs (high density lipoproteins). In the blood vessels, VLDLs  react with lipoprotein lipase, an enzyme, which forms IDL, or intermediate density lipoproteins, with the help of Apo C2 and Apo E which the VLDLs just acquired from HDLs. The IDLs have less triglycerides and more cholesterol than the VLDLs. With the aid of various other proteins called apolipoproteins (listed as apoA, B, C, D, or E) and hepatic lipase (a liver enzyme) some IDLs spin off into LDLs while the rest, about 50%, go back to the liver where the IDLs are picked up by Apo B receptors for reprocessing. Each one of these steps releases essential fatty acids into the body to perform their many vital functions. This also increases the LDL's cholesterol percentage packaged with Apo B. The apo C2 and apo E are released and sent back to HDL to begin the cycle again. ref 

The important point to remember here is these processes have just one function, to get cholesterol to the cells where it is vitally needed. Because cholesterol is fat soluble and doesn't easily mix with water or blood, these many steps overcome that barrier.

Now, about 75% of LDLs go directly back to the liver, 24% goes to the cells and tissues which use the cholesterol to rebuild the cell walls or perform other tasks. This leaves only a small amount which could get into artery cells where radicals might oxidize them. Another lipoprotein, HDL for high density lipoprotein, picks up any excess cholesterol from cells and transports it back to the liver. Proper levels of HDLs are able to handle the lingering LDLs and get them back to the liver before oxidation can happen. But in low HDL ratios or higher oxidation conditions, more LDL could get oxidized into a form that can participate in damaging artery wall cells. 

Why this long and complex description?  Stay tuned. Let's get back to overall levels for a moment. Remember it's only a small amount that gets in artery wall cells and only a small percent of that amount would likely participate in oxidation reactions, given that certain conditions have to be concurrently present. One of these conditions is created by long term chronic inflammation, an all too common state from today's food patterns. Immune cells called macrophages rush in and hang out in inflamed tissues, ready to handle waste or infectious materials usually generated at injury sites. These macrophages tend to readily take in oxidized LDLs. This is a protective action for the body. If it was only an occasional event it would not present the degree of artery disease seen today. The macrophages swollen with oxidized LDLs are not able to leave the cells and as they gather in numbers, they cause the cells to turn into foam cells, the next stage in plaque development.

Thus, maybe overall total cholesterol levels are not really the main factor, but rather maintaining  proper HDL levels to make sure that any excess LDLs are quickly escorted back to the safety of the liver before they GET OXIDIZED and stored in artery cells. If you lower your total cholesterol without increasing the HDL to Total Cholesterol ratio, you may not have gained much of an advantage. LDLs can still oxidize and participate in cellular damage even with low total cholesterolref  Yes, this would lower the anti-oxidant needs necessary to protect the new lower amount of LDLs, which might be the only saving grace. In fact, the current news about statins is not about lowering cholesterol, but rather about their anti-oxidant and anti-inflammatory properties. Very interesting. See statin section  in part 2.

SIDEBAR: Omega-3 fats such as from fish oils offer protection against CVD by increasing HDL levels, lowering triglycerides and VLDLs, and reducing blood platelet activity. Platelets, along with fibrinogen, participate in forming blood clots. ref

NATURE'S BALANCE 

If LDL and HDL lipoproteins are in nature's balance, regardless of the overall cholesterol level, maybe everything is in harmony. Half of CVD occurs in people with normal range LDL cholesterol. An unbalanced ratio is where the "good HDL" and the "bad LDL" come into play. Dietary cholesterol only affects about 20% of cholesterol amounts. The liver builds the other 80%. So, the dietary 20% part is largely influenced by the ratio and amounts of dietary saturated fats and triglyceride levels to polyunsaturated fats. It appears that trans fats, saturated fats and the overall fat level of the diet all can influence cholesterol levels somewhat. Although the influence of saturated fat from studies on increasing cholesterol is rather modest, maybe at most 12% with on average of only 4-5%. And, not included here is the fact that many studies show NO significant changes. These are largely ignored and not published. Plus, saturated fat, in studies showing some increase, influences both LDL and HDL the same so any influence on heart attacks is very modest.

Many other factors also have an effect, such as activity level (exercise), smoking, obesity, alcohol, diabetes, some medicines, and genetics. Both LDL and HDL levels can be somewhat altered by most of these factors. Just knowing the numbers is often not enough to evaluate your CVD risk level. 

NOTE: Higher LDL, of course, still must be protected from oxidation, so an adequate supply of antioxidants is necessary, within certain ranges. Too many antioxidants is just as detrimental as not enough according to new research. BALANCE. It is also important to know that a low HDL number is not enough by itselt to increase or predict risk. A high triglyceride level is also needed with a low HDL to increase risk of heart events.

SIDEBAR: There is an interesting disease that occurs in children where they are genetically programmed to produce low cholesterol levels. This compromises their immune system. Giving cholesterol to these children improves their resistance to infectious diseases. Therefore cholesterol participates in building immunity. Since it is known that low choesterol levels compromise immunity as seen in this condition, is it wise to lower it to the levels suggested today for cardiovascular protection?

On the other side of the coin, some people are programmed to produce high cholesterol levels. From the available stats for the first 30 years of the last century, these people actually had a slightly lower motrality rate compared to normal cholesterol producers. During the years from 1930 to 1960, the mortality for high producers increased to almost double that of the regular producers. Since infectious diseases were responsible for most of the deaths during the first thirty year period, could the higher immunity protection from increased cholesterol levels been responsible for the lower mortality rate?

IMPORTANCE OF BILE

Every cell in the body needs cholesterol, including the cells lining the artery walls. Half of the cycle of cholesterol is going from the liver to the cells and the excess returning back to the liver. The other half is completed by looking at the pathway of bile salts. Bile salts are made in the liver from cholesterol. They are sent to the gallbladder where they are concentrated and stored until sent into the intestinal tract to digest fats from your last meal.

The pool of available bile salts has to be kept within certain levels for proper body functioning. Almost 95% of bile salts can be reabsorbed and go back to the liver so the cholesterol can be reused. It is this vital. Only small amounts are eliminated. In the liver, further steps can be taken to push more cholesterol into bile for elimination if needed to balance the available pool. Up to 50% of the total cholesterol in the body can be used for this purpose. Thus, bile is the method the body uses to eliminate excess cholesterol, albeit very slowly. Studies show that giving bile salts orally has actually lowered cholesterol levels. Fibers also aid this removal process of bile and cholesterol. This completes the cycle of cholesterol.

What happens to make a vital and absolutely necessary ingredient of the body turn into a savage disease causing monster?

Let's cut right to the chase. Cholesterol is an innocent and vital worker for health. According to the referenced study in picture 1 above, there is really just one initial cause of CVD, damage to blood vessel wall cells, called endothelial dysfunction. Here are some of the ways this damage can occur. 1. From LDL cholesterol or other fats oxidizing. 2. From the formation of advanced glycation end products (AGES), common in diabetes and high sugar diets. 3. From lowered nitric oxide production 4. From the action of DNA damaging toxic chemicals or pathogenic germs.  5. From chronic inflammatory cellular stress (increases number of macrophage in cells). 6. From genetic mistakes.  And perhaps one of the current theories that fits more of the known facts better than the cholesterol theory, 7. Hemodynamics.   Now, four out of the seven are set up by dietary choices and genetic mistakes might be somewhat modified by prudent nutrition as well.

LDL cholesterol dosen't have to get oxidized if enough anti-oxidants such as vitamin E and C or anti-oxidant foods, like pomegranates, are available to protect. Thus, it is not the cholesterol level which should shoulder all the blame, but the lack of anti-oxidant protection to safeguard LDL cholesterol. LDL cholesterol can be easily oxidized, especially the smaller size particles created by trans fats. ref  This is why vegetable and fruit supplied anti-oxidants are so vital. A note of interest is that this is where the protein homocysteine levels come into play. Higher blood levels participate in the oxidation process.

Note: This from Berkeley Wellness Alert June 2011: 
Saturated fat (as in meat, butter and milk) is the leading dietary culprit behind high blood cholesterol and heart disease. Right? Well, maybe not, recent research suggests.

Though saturated fat raises LDL ("bad") cholesterol, this is offset somewhat by the fact that it mostly increases levels of larger LDL particles, which are now known to be less dangerous than smaller ones. This finding comes in part from research by Dr. Ronald Krauss, director of Atherosclerosis Research at Children's Hospital Oakland Research Institute and a member of the (Berkeley) Wellness Letter Editorial Board."  ---end  

Advanced glycation end products are formed when sugars are allowed to react with proteins. This is a major contributor to the aging process. Again, it is not the AGES which should be blamed, but the high sugar level in the blood from either diet or insulin resistance.

Nitric oxide (NO) is a free radical gas that helps blood vessels relax and expand when the heart pumps. If the production of NO is reduced, blood pressure increases. While this normally occurs slowly as one ages, dietary factors might hasten. Calcium participates in NO production as well as plant lignands, as in flaxseeds. NO has a body life of just a few seconds but is an important stimulator of many vital functions. As a free radical, it's life can be shortened by anti-oxidants.  ref   An interesting note, Viagra increases a down stream element that NO stimulates to help relax blood vessels. It also has anti-platelet adhesion properties. Here is a list of conditions where NO participates from the referenced site above:

  • Hypertension

  • Obesity

  • Dyslipidemias (particularly hypercholesterolemia and hypertriglyceridemia)

  • Diabetes (both type I and II)

  • Heart failure

  • Atherosclerosis

  • Aging

  • Cigarette smoking

Chemicals added to foods or from residues of environmental overloads, or inhaled chemical additives from numerous manufactured products, and bacteria produced diseases (including gum infections) can all participate in cellular DNA damage, the master coding material necessary for the exact duplication during cell division.  

Lowering cholesterol, which does help give the body a better chance to maintain a positive anti-oxidant balance, may not be as valuable in the long run if ratio changes between the types and sizes of cholesterol, the oxidation of LDLs, and the formation of AGES are not prevented through proper dietary and lifestyle pattterns.  Read on.

Further clarifications:

1. Lack of sufficient exercise or body muscle movement to increase HDL levels. This action could even compensate for the ingestion of some dietary animal saturated fat increasing cholesterol levels. Balanced ratios! So in a sense, the more calories you burn, the more saturated fats you could safely eat. Maybe this is what protected the early 20th century farmers and ranchers. They sure loved their bacon and lard fried foods. And milk was always full fat.

Exercise also increases the proper particle size of both LDL and HDL which increases their efficiency to move more cholesterol and lowers their oxidized damage potential. LDLs have a higher fat content than HDL and oxidize more readily. The antioxidants from vegetables and fruits plus those produced naturally in cells are helpful to prevent this action. In fact, they are essential.

Exercising also strengthens the heart muscle and increases artery wall elasticity and integrity. A strong heart doesn't have to beat as often. This lowers blood pressure, a marker for CVD. Exercise is also needed to strengthen the abdominal wall muscles to prevent the excess pooling of blood around and in the liver and other digestive organs which could interfere with their vital functions as well as hinder overall blood circulation, especially to the brain. This occurs from prolonged sedentary occupations and is all too common in America. Get off the sofa and start dancing. 

2. Chronic inflammatory processes. When tissues get inflamed, macrophage cells from the immune system rush into the affected cells. While this process is vital when the body is injured, it should not happen just anywhere and chronically. How does chronic inflammation affect artery cells?  The macrophages have an affinity to attract and hold oxidized LDLs.  Oxidized LDLs can lead to INJURY of the cell tissue of vessel walls. Dietary factors involving either unbalanced omega 6 and 3 levels or / and low anti-oxidant status can initiate this process.  You now have a recipe for the start of CVD.

If you want to lower your risks for CVD, you have to build immune antioxidant capacity to stop oxidation radicals and balance fat types to reduce chronic inflammatory processes. It appears that what you eat is largely to blame here. A note of interest, C-reactive protein levels indicate inflammation is present somewhere in the body. While it has a very high coorelation to CVD, it can also be elevated from gum infections, in men from prostatitis, in women from urinary tract infections, also from digestive gastric inflammations, and from a few other conditions. 

Read Survive Alive. Eat right and exercise for lifelong heart health. 

3. There is a factor that solves a rather bizarre mystery. Why are only certain sections in arteries usually attacked? Scientists have been studying this process for quite some time. The process is called hemodynamics. Simply this has to do with the speed the blood is moving and the shape of the arteries it is passing through. Artery wall shear stresses are greater at certain locations, such as after a blood vessel separates into two channels or where it bends which create turbulence in blood flow. These areas have increased forces or stresses put on the walls. The endothelial cells lining the inside of the arteries, called the intima, with the help of a thin elastic membrane take most of this force. These mighty cells need all the support you can give them to handle the job. High fat meals are especially damaging. In fact, if you could peek into your arteries after one of these meals, you would see these cells turn bright red, not from embarrassment, but from inflammation caused by the body reacting to high animal saturated and trans fats. Thus the damage this structural factor can induce is also somewhat under the influence of dietary factors too, especially in controlling blood thickness and stickiness. Factors that aspirin and certain foods help limit. This process condition is included under HIGH BLOOD PRESSURE. Cholesterol is one of the factors, along with vitamin C, protein, and silica, that helps build strong cellular membranes and artery walls. 

4. The ratio of HDL to total cholesterol (TC) and knowing your genetics, dietary, or lifestyle influences on LDL subtypes are really important factors. Well, yes, the overall mix of fatty acids is important as well, but more on this in another article. Obviously, by deduction this information gives you your LDL level, but from research, neither the level of LDL or the total cholesterol (TC) amount are enough by themselves to positively relate to CVD, even the HDL to TC ratio fails in some cases relative to the many subtypes of LDLs and HDLs. ref  Clarification of reference study term, HL, hepatic lipase. Hepatic lipase plays a key role in the metabolism of pro-atherogenic and anti-atherogenic lipoprotein actions. Activity of HL may be related to HDL levels, but there are many gene related factors involved that determine which way.

5. There is controversy as to the value of knowing the particle sizes of LDLs and HDLs. Since smaller, denser particle size LDLs could cross artery cell membranes more and participate in oxidation quicker,  the assumption was made that increased levels would be found in CVD cases. Unfortunately, many other risk factors are usually also present such as high triglyceride levels, obesity, insulin resistance, and low HDL that it is difficult to access just one factor. Studies such as the review reference below show no direct correlation. But, a few do show influence. Since the wrong diet and lack of exercise can change the particle size from large to small in both LDls and HDls, don't you think this should be part of the treatment protocol with drugs? Not knowing your particle size may be leaving out vital information which could help in evaluating risks and measuring progress. ref  ref  ref ref

Measuring your LDL profile for the seven subtypes could become standard practice in the future. Certain small subtypes are better predictors of future artery disease progression than any of the currently measured cholesterol parameters. The wise protocol to control the fires of heart disease is to adopt a conservative approach until all the facts are discovered. Behaviors to increase HDLs and lower LDLs naturally through proper dietary and lifestyle interventions pay major health dividends even if you are one of those preconditioned by hereditary genes. ref ref High LDLs without enough HDLs lets too much cholesterol build up in the blood and cells. An event that, like teenage boys on a Friday night, tends to create mischief. 

6. Triglyceride levels are showing in some age groups to exhibit a higher risk factor than cholesterol to predict future cardiovascular events. Sugars and saturated fats increase triglyceride amounts.

Interesting SIDEBAR: Is the low fat diet craze taking a dive? Even the American Heart Association is starting to sing a different tune since current research is changing assumptions. Past recommendations were to lower fat, especially saturated fat, as much as possible. This of course left a void to be filled, one that carbohydrates were only to happy to fill, unfortunately with simple sugars and refined grains. The results are in. A moderate level of fat (33%), high in monounsaturates, creates a preferred cholesterol profile greater than a low fat high carbohydrate diet. While the very low fat DASH diet does lower total and LDL cholesterol, it also lowers HDL (not good) and does not affect triglycerides. ref  Following is the reference which includes the nuts and bolts for holding HDL levels high. Simple and to the point.   www.umassmed.edu/uploadedfiles/raisinghdl.pd   Note it is in PDF. f

Here is an interesting report from a Japanese medical journal to further this discussion from another perspective: SPECIAL REPORT Pharmaceutical Society of Japan (image placeholder) YAKUGAKU ZASSHI, Volume 125(11), pages 833-852, 2005:

 

 

 

"Dr. Harumi Okuyama, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan, has published an urgent call for physicians worldwide to back away from cholesterol reduction medications and to embrace omega-3 fish/flax oils in order to effectively reduce heart disease, cancer and all-cause mortality."  See Part 2 for the rest of this revealing abstract. 

 

 

Statins and Cholesterol  (continued in Hearts of FIRE 2)    

 

Warning: This information is presented to stimulate the learning process. If you are ill, consult with a medical professional. Your education about disease conditions helps make you a more informed, and hopefully healthier, patient. Due to the complexities of Cardiovascular disease, many factors have to be considered, monitored, and evaluated while under the care of your medical doctor.

 

 

top          next page  Hearts of FIRE 2