Does Cholesterol (LDL) Cause Heart Disease? What is the True Cause of Heart Disease?

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A physician’s word is often taken very seriously and with little skepticism. An opinion from one or two doctors, when made in a professional office or hospital, can persuade a worried patient to take drugs with complex side-effects, or even undergo traumatic treatments such as radiation and chemotherapy. Yet, when the same doctors, with years of experience and thousands of satisfied customers, give an opinion that questions a therapy established by mainstream medicine, the mainstream media calls them irresponsible, or quacks, or even criminals.

Which brings me to Dr. Dwight Lundell. He’s an experienced heart surgeon and retired Chief of Staff and Chief of Surgery at Banner Heart Hospital in Mesa, Arizona. Not so long ago, Dr. Lundell made the following statement of confession:

“We physicians with all our training, knowledge and authority often acquire a rather large ego that tends to make it difficult to admit we are wrong. So, here it is. I freely admit to being wrong. As a heart surgeon with 25 years experience, having performed over 5,000 open-heart surgeries, today is my day to right the wrong with medical and scientific fact.

I trained for many years with other prominent physicians labeled “opinion makers.” Bombarded with scientific literature, continually attending education seminars, we opinion makers insisted heart disease resulted from the simple fact of elevated blood cholesterol. The only accepted therapy was prescribing medications to lower cholesterol and a diet that severely restricted fat intake. The latter of course we insisted would lower cholesterol and heart disease. Deviations from these recommendations were considered heresy and could quite possibly result in malpractice. It Is Not Working!

These recommendations are no longer scientifically or morally defensible.”

Many doctors are highly admirable people, but they are still human beings. They all make mistakes, they all learn from them, but the really good ones are willing to admit to them.

Cholesterol does not cause heart disease and trying to reduce it with statin drugs is a waste of time, an international group of experts has claimed.

Not surprisingly, Lundell’s statement regarding the medical establishment’s approach to treating heart disease caused a ripple in the medical industry. It challenged the validity of statins – commonly known as cholesterol-lowering medications – such as Lipitor, Crestor, Zocor, and others.

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The reason Lundell’s statement created such a buzz is because statins are big business. In the United States alone, about 25% of the population takes statin medications. They cost from as little as $53 per month to more than $600. Pfizer’s Lipitor went on sale in 1997 and its lifetime sales have surpassed $125 billion. AstraZeneca’s Crestor was the top-selling statin in 2013, generating $5.2 billion in revenue that year alone. The statin industry is estimated at around $30 billion in sales per year. Nevertheless, in the United States, more die each year of heart disease than ever before.

Lundell went on to say:

“The discovery a few years ago that inflammation in the artery wall is the real cause of heart disease is slowly leading to a paradigm shift in how heart disease and other chronic ailments will be treated. The long-established dietary recommendations have created epidemics of obesity and diabetes, the consequences of which dwarf any historical plague in terms of mortality, human suffering and dire economic consequences.

I have peered inside thousands upon thousands of arteries. A diseased artery looks as if someone took a brush and scrubbed repeatedly against its wall. Several times a day, every day, the foods we eat create small injuries compounding into more injuries, causing the body to respond continuously and appropriately with inflammation. While we savor the tantalizing taste of a sweet roll, our bodies respond alarmingly as if a foreign invader arrived declaring war. Foods loaded with sugars and simple carbohydrates, or processed with omega-6 oils for long shelf life have been the mainstay of the American diet for six decades. These foods have been slowly poisoning everyone.”

Listen to Dr. Tom Sladic, MD has he explains his understanding of the true cause of Heart Disease:

So What is the True Cause of Heart Disease?

 

A review of research involving nearly 70,000 people found there was no link between what has traditionally been considered “bad” LDL cholesterol and the premature deaths of over 60-year-olds from cardiovascular disease.

Published in the BMJ Open journal, the new study found that 92 percent of people with a high cholesterol level lived longer. (BMJ Open. Published online June 12 2016)

The authors have called for a re-evaluation of the guidelines for the prevention of cardiovascular disease and atherosclerosis, a hardening and narrowing of the arteries, because “the benefits from statin treatment have been exaggerated”.

High cholesterol is commonly caused by an unhealthy acidic lifestyle and diet, and eating high levels of processed fat in particular, as well as smoking.

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It is carried in the blood attached to proteins called lipoproteins and has been traditionally linked to cardiovascular diseases such as coronary heart disease, stroke, peripheral arterial disease and aortic disease.

Co-author of the study Dr Malcolm Kendrick, an intermediate care GP, acknowledged the findings would cause controversy but defended them as “robust” and “thoroughly reviewed”. “What we found in our detailed systematic review was that older people with high LDL (low-density lipoprotein) levels, the so-called “bad” cholesterol, lived longer and had less heart disease.”

 

Vascular and endovascular surgery expert Professor Sherif Sultan from the University of Ireland, who also worked on the study, said cholesterol is one of the “most vital” molecules in the body and prevents infection, cancer, muscle pain and other conditions in elderly people. He also stated, “lowering cholesterol with medications is a total waste of time and money”.

“Lowering cholesterol with medications for primary cardiovascular prevention in those aged over 60 is a total waste of time and resources, whereas altering your lifestyle is the single most important way to achieve a good quality of life,” he said.

Lead author Dr Uffe Ravnskov, a former associate professor of renal medicine at Lund University in Sweden, said there was “no reason” to lower high-LDL-cholesterol.

Heart Disease and Cholesterol

The graph below shows the famous 10 year Framingham correlation study between cholesterol and coronary heart disease, published in the Lancet in 1986, that big Pharma relies on and sold to the American public at large.

 

The problem though, as you see in the next graph, after 20 years the correlation shows that high cholesterol saves lives and low cholesterol is a risk factor for heart disease!

Everyone in modern society has heard about cholesterol, and how bad it is. Most do not understand why it exists, and simply see it as a menace that must be eliminated as quickly as possible. This misunderstanding is exactly what the pharmaceutical complex promotes, because it allows them to perpetually treat high cholesterol with drugs like Lipitor. These drugs are prescribed for the remainder of a patient’s lifetime, and when he/she eventually dies of a “thought attack”, family and friends will believe that the disaster was inevitable from “high cholesterol”. The death will not be attributed to other health factors or to the drugs themselves, but to the “high cholesterol”; even though there are no known deaths from cholesterol in human history. It is all very convenient for the drug companies, so long as we do not examine what is up the other sleeve.

I am reminded of restless leg syndrome, whereby the dis-ease was ‘discovered’ immediately after the pharmaceutical for it was patented, as a reason to sell us this useless pharmaceutical drug. Now, restless leg syndrome has been upgraded to a new “disease”. The cause of restless leg syndrome is also the cause of heart disease – retained metabolic and/or dietary acids in the connective and fatty tissues leading to inflammation, induration, ulceration, degeneration and finally death

“Before 1920, coronary heart disease was rare in America — so rare that when a young internist named Paul Dudley White introduced the German Electrocardiograph to his colleagues at Harvard University, they advised him to concentrate on a more profitable branch of medicine. The new machine revealed the presence of arterial blockages, thus permitting early diagnosis of coronary heart disease. But in those days, clogged arteries were a medical rarity, and White had to search for patients who could benefit from his new technology. During the next forty years, however, the incidence of coronary heart disease rose dramatically, so much so that by the mid 1950’s, heart disease was the leading cause of death among Americans.”

— Mary Enig, Ph.D.

The amount of cholesterol that you eat actually has very little relationship with the amount that you have in your blood. When you eat more cholesterol, your body produces less, and when you eat less cholesterol, your body produces more. Another way to say this is like this – when you have more metabolic or dietary acid in your blood and interstitial fluids the body produces more LDL cholesterol, and when you have less metabolic or dietary acid in your blood and interstitial fluids the body produces less cholesterol. Why? Because LDL cholesterol is a buffer or chelator of metabolic and/or dietary waste. Understand? A body usually produces between three and four times the cholesterol that one eats. The amount produced is generally related to how much is needed. Cholesterol is indeed needed and critical for optimal health. The purpose of so-called “bad cholesterol” is not to give us heart attacks, but to buffer acidic metabolic and dietary waste and to repair the damage to arteries or veins from our acidic lifestyles and diets.

Whenever a poor acidic diet and lifestyle leads to damaged arteries, a thick and sticky substance is required to patch them. That substance is known as LDL or “bad cholesterol”. When this damaging behavior is continued, multiple patches are created, leading to what we know as “clogged arteries”. The problem is not the cholesterol, which is doing its wonderful job of preventing our death from internal bleeding. The problem is the fact that the arteries or veins are damaged enough from acidic lifestyle and dietary choices to risk internal bleeding. Blocking a body’s healthy countermeasure only leads to worse problems. It is the pharmaceutical standard of symptom suppression that is like hiding the timer of a time bomb, and then expecting it not to eventually go off. Thus, that so-called “BAD” cholesterol is not “BAD” at all. In fact LDL cholesterol is saving your acidic body from internal bleeding and inevitable death. LDL cholesterol ONLY increases in the presence of excess metabolic, dietary, respiratory and/or environmental acids which increase as a result of what you eat, what you drink and what you think. High LDL cholesterol is a warning sign of your poor acidic lifestyle and dietary choices and the body is in preservation mode. It is trying to protect itself from YOU!

Cholesterol is created to save your life! The following picture is what solidified metabolic acid bound cholesterol looks like in the blood.

 

Modern medicine spends a lot of time fighting this pitch, instead of the actual causes of arterial damage. Thus, it is not surprising that cholesterol-lowering drugs cause more heart dis-ease and more heart attacks and strokes. A massive portion of the elderly population is taking cholesterol-lowering drugs, even though research shows that the higher their cholesterol levels (especially LDL) the longer that they will live and the less risk for a heart attack or stroke. The graph below illustrates this point! Low cholesterol in the elderly is actually a sign that something is seriously wrong, and a heart attack or stroke may be imminent. Modern medicine has only recently come to accept that at least some cholesterol (LDL and HDL) is good and protective! But when you mention (LDL) cholesterol as “GOOD” you better take cover from current medical savants who will attack you with their ignorance!

 

Cholesterol is still suppressed with drugs, despite what science would make prudent from the long-term Framingham Study. It also has been proven that these drugs cause high suicide rates. The drugs can lead to personality changes, in a manner similar to (but not as intense as) S.S.R.I. antidepressants.

 

The anti-cholesterol hysteria began in the 1950’s, when researcher Ancel Keys proposed the Lipid Hypothesis. It stated that cholesterol and saturated fats lead to heart disease. His beliefs were promoted heavily by the new hydrogenated oils industry, which spent obscene amounts of money to convince every one of Keys’ indisputable findings. This successful marketing campaign was on par with similar marketing for fluoride at about the same time. Studies which had oppositional findings to Keys’ were ignored or maligned. As a result of his flawed scientific methodology (subjective cherry picking results to match what he wanted to find) saturated fats like butter and eggs were used less, in exchange for the poisonous trans-fats that are in hydrogenated oils. Heart disease rates have been rising exponentially ever-since.

The French eat more fats than any other group in the world, yet they have lower rates of heart disease. The Japanese eat more fats than Americans, yet have lower rates of heart disease. There are plenty of countries with similar patterns. The French lifestyle especially counters Keys’ hypothesis, and it also provides evidence that resveratrol (found in red or purple grapes) improves heart health. Resveratrol has been shown to reverse atherosclerosis (hardening of the arteries). Maybe, just maybe its being American that causes higher rates in heart attacks.   The bottom-line medical research is subjective NOT objective!

Just recently the Food and Drug Administration issued new safety warnings about a popular class of drugs used to control and lower cholesterol levels. The FDA says the drugs, known as statins, can cause several side effects, including cognitive problems such as memory lapses and confusion. But the agency is stressing that the side effects appear to be rare and not serious. I have suggested that taking any drug, like statin drugs that lowers LDL cholesterol without removing acidic lifestyle and dietary choices is a risk for heart attack, stroke and other dis-eases like diabetes. I have lowered cholesterol successfully in all cases of hyper-chlolesterolemia without drugs by just changing the diet and lifestyle to an alkaline pH Miracle lifestyle and diet that restores the alkaline design of the body.

One of my research clients Maren Hale was diagnosed with familial hypercholesterolemia and hyper-triglycerides with LDL’s over 400 mg/dl and triglycerides over 200 mg/dl. She was also overweight. Over a period of four years Maren lost over 70 pounds and lowered her cholesterol and triglycerides to healthy normal ranges on the pH Miracle Lifestyle and Diet. Maren and her family and extended family have been a research study of the University of Utah for familial hypercholesterolemia for over 60 years. Maren was the first of all family members to lower her cholesterol and triglycerides to normal ranges due to her commitment to living a pH Miracle Lifestyle and Diet.

 

High cholesterol levels should be a warning to most people who inflammation caused by metabolic and dietary acid is present. It is a risk marker, and a symptom that can save your life! Eliminating the LDL cholesterol through drugs is the equivalent to eliminating the thermometer in a room that is too hot. It is illogical, and it does nothing to eliminate the dangerous cause of the symptom being expressed.

LDL cholesterol levels naturally drop whenever the body’s becomes less acidic and more alkaline in the interstitial fluids where acids are stored! And LDL cholesterol should never be forced lower with drugs because they WILL cause a heart attack or stroke! The pH Miracle alkaline lifestyle and diet can reduce LDL cholesterol, but it is never because of a lowered cholesterol intake.

The natural drop in cholesterol and triglycerides happens only when a person stops eating toxic acidic foods, drinking toxic acidic drinks and stops toxic acidic thoughts that produce toxic acidic waste products that destroy the arteries and veins!

Do YOU Understand?

Because healthy arteries and veins do not need patching. Remember that a body typically produces 3-4 times the amount of LDL cholesterol than consumed. The fats that a person eats are therefore comparatively insignificant. Cholesterol will rise whenever the body’s need for cholesterol rises and in direct relationship to the level of acidic thoughts, words and deeds. So acidic trans-fats and inflammatory acidic substances are what need to be avoided. These toxic acidic wastes are what damage the arteries and veins, and a body will be required to do a great deal of patching as a consequence. I will reference to alkalizing or chelating herbs and minerals that lower cholesterol levels naturally later, but alkalizing and chelating herbs and minerals do it by lowering the body’s need for LDL cholesterol, not by forcefully lowering it like pharmaceuticals do.

 

Studies on the link between cholesterol and heart health have been manipulated for decades. The first studies on eggs showed elevated cholesterol levels because they had used dehydrated eggs, and studies of coconut oil yielded similar results because they had used partially hydrogenated coconut oil to get the results that they wanted. That is why I state that ALL scientific research is subjective NOT objective!!!!!!!!!!!!!!!!!!!!!! Read about it here: http://wp.me/p5ggLY-a5

It is Simple – Cholesterol DOES NOT CAUSE Heart Disease!

Simply stated, without acid caused inflammation being present in the body, there is no way that cholesterol would accumulate on and in the wall of the blood vessel and cause heart disease and strokes. Without acid caused inflammation, cholesterol would move freely throughout the body as nature intended. It is acid caused inflammation from acidic lifestyle and dietary choices that causes cholesterol to become trapped.

Acid caused inflammation is not complicated. The cycle of metabolic and dietary acid inflammation is perfect in how the body releases cholesterol to bind acids that cause inflammation in the first place. However, if we chronically expose the body to injury to acidic poisonous toxins from acidic foods and drinks the human body was never designed to process, a condition occurs called systemic latent tissue acidosis that is the cause of ALL inflammation. Chronic acidic inflammation is just as harmful as acute acidic inflammation and are both caused by an increase of dietary and metabolic acids.

What thoughtful person would willfully expose himself or herself repeatedly to acidic foods, drinks, drugs or other substances that are known to cause injury to the body? Well, smokers, alcohol, coffee black tea, soda pop, energy and sport beverage drinkers perhaps, but at least they made that choice willfully.

The rest of us have simply followed the recommended mainstream acidic diet that is low in polyunsaturated fats, high in acidic carbohydrates and highly acidic animal flesh, not knowing we were causing repeated acidic injury to our blood vessels. This repeated injury creates chronic acidic inflammation leading to heart disease, stroke, diabetes and obesity.

 

Let me repeat: The injury and inflammation caused from acidic foods, drinks and metabolism in our blood vessels is the cause of stokes, heart attacks, diabetes and obesity and NOT the increase of cholesterol. A low healthy fat and salt diet recommended for years by mainstream medicine will cause strokes, heart attacks, diabetes and obesity.

What are the biggest culprits of chronic acidic inflammation? Quite simply, they are the overload of simple, highly processed carbohydrates (sugar, dairy products, animal flesh, chocolate, coffee, tea, including green tea, alcohol, soda pops, vinegar, peanuts, mushrooms, flour and corn and all the products made from them) and the excess consumption of saturated vegetable oils like soybean, corn and sunflower that are found in many processed foods.

Take a moment to visualize rubbing a stiff brush repeatedly over soft skin until it becomes quite red and nearly bleeding if you kept this up several times a day, every day for five years. If you could tolerate this painful brushing, you would have a bleeding, swollen infected area that became worse with each repeated acid causing injury. This is a good way to visualize dietary and metabolic acids as the brush leading to the inflammatory process that could be going on in your body right now.

 

Regardless of where the acidic inflammatory process occurs, externally or internally, it is the same. Using Ultrasound I have peered inside thousands upon thousands of arteries. A diseased artery looks as if someone took a brush and scrubbed repeatedly against its wall. Several times a day, every day, the acidic foods we eat create small injuries compounding into more injuries, causing the body to respond continuously and appropriately with increased acid caused inflammation.

While we savor the tantalizing taste of a sweet roll, chocolate or a carbonated drink our body responds alarmingly as if a foreign invader arrived declaring war. ACIDIC foods loaded with sugars and simple carbohydrates, or processed with saturated oils for long shelf life have been the mainstay of the American diet for six decades. These acidic foods have been slowly poisoning everyone.

How does eating a simple sweet roll or a piece a chocolate create a cascade of acid causing inflammation to make you sick?

Imagine spilling acidic sugary syrup on your keyboard and you have a visual of what occurs inside the cell. When we consume simple carbohydrates such as sugar, blood sugar rises rapidly. In response, your pancreas secretes insulin and sodium bicarbonate whose primary purpose is to bind and solidify acids so they do NOT destroy healthy body and blood cells and cause internal bleeding. In addition, the body releases cholesterol to help solidify excess dietary and/or metabolic acids that have NOT been properly eliminated through the four channels of elimination – urination, perspiration, respiration and defecation.

 

The body solidifies acids to protect healthy tissues, glands and organs from ulceration and then degeneration. After years of an acidic lifestyle and diet solidified acids will build-up on the wall of the arteries and veins leading to atherosclerosis, stroke and heart attack.

What does all this have to do with inflammation? Blood sugar which is a metabolic acid is controlled in a very narrow range. Extra acidic sugar molecules that are not solidified and eliminated through the four channels of elimination will injure the blood vessel wall. This repeated acidic injury to the blood vessel wall causes irritation, inflammation, ulceration and eventual degeneration or heart disease and/or cancer. When you spike your blood sugar levels or acid levels several times a day, every day, with acidic foods or thoughts it is exactly like taking sandpaper to the inside of your delicate blood vessels.

While you may not be able to see it, rest assured, tissue, gland and organ acidosis is present. I have seen it in over 40,000 client/patients spanning over 30 years who all shared one common denominator — dietary and metabolic acid caused inflammation in their veins, arteries, glands, tissues and organs. This is what retained physiological acid looks like in the tissues using full-body thermography to show the acidic red and white hot spots.

 

Let’s get back to the sweet roll and chocolate. These innocent looking goodies not only contain the acid sugar, they are also fermented and processed in one of many saturated oils. Chips and fries are soaked in soybean oil; processed foods are manufactured with saturated oils for longer shelf life.

If the balance shifts by consuming excessive sugar, animal protein, vinegar, coffee, tea, alcohol, corn, peanuts and saturated oil, the cell membranes will be damaged and the body and blood cells will begin to degenerate causing even more acids leading to greater risk of inflammation and dis-ease.

Today’s mainstream American ACIDIC diet has produced an extreme imbalance in the alkaline design of the body and an increase in dietary and metabolic acids that cause ALL sickness and dis-ease. You read this correctly – ALL sickness and dis-ease is caused by metabolic, dietary, respiratory and/or environmental ADIDS! There are no other causes. Germs and viruses are the symptoms of cellular breakdown and NOT the cause of ANY disease. Simply said, germs do NOT cause dis-ease!

 

To make matters worse, eating these acidic foods and drinks causes the body to hold on to more fat as a depository for these excess acids that are NOT being properly eliminated through the four channels of elimination. That is why people get fat. The increase in fat is in direct relationship to the increase of acidic foods, drinks and lifestyle choices. The process that began with a sweet roll or a cup of coffee, or a piece of chocolate or a glass of wine turns into a vicious cycle over time that creates heart disease, stroke, high blood pressure, diabetes, obesity and finally, Alzheimer’s disease, as the acid caused inflammatory process continues unabated.

 

There is no escaping the fact that the more we consume prepared and processed acidic foods, the more we increase the inflammation switch little by little each day. The human body cannot process, nor was it designed to consume, foods packed with sugars, animal flesh, dairy products, vinegar, alcohol, coffee, tea, chocolate, soda pop, mushrooms, peanuts, corn, flour and saturated processed oils.

There is but one answer to quieting acid caused inflammation, and that is returning to foods closer to their natural alkaline state. To build muscle, eat more chlorophyll concentrated alkaline foods.

 

Choose carbohydrates that are very complex such as colorful fruit and vegetables. Cut out of your diet saturated oils from corn or soybean.

One tablespoon of corn oil contains 7,280 mg of saturated oil; soybean contains 6,940 mg. Instead, use olive oil, avocado oil, hemp oil or fax oil.

Forget the “science” that has been drummed into your head for decades. The science that saturated fat alone causes heart disease is non-existent. The science that saturated fat raises blood cholesterol is also very weak. Since we now know that cholesterol is not the cause of heart disease, the concern about saturated fat having no place on its hydrogen chain to buffer metabolic and dietary acid is real science. It is acid that causes disease and ALL polyunsaturated oils help to buffer excess acids by the carbon chain picking up the hydrogen ion or acid on its unsaturation. In other words, all polyunsaturated fats whether Omega 1, 3, 6 or 9 buffer or neutralize all dietary and/or metabolic acids on their unsaturated carbon.

The cholesterol theory led to the no-fat, low-fat recommendations that in turn created the very acidic foods now causing an epidemic of acid caused inflammation,induration, ulceration and degeneration. Mainstream medicine made a terrible mistake when it advised people to avoid foods high in cholesterol. We now have an epidemic of arterial acidic caused inflammation leading to heart disease and other silent killers.

Government nutrition guidelines recommend a diet high in carbohydrate regardless of the ample evidence of the health risks it promotes. Yet, heart disease and obesity rates have risen in correlation with a reduced intake of dietary fat. The Food Standards Agency states all individuals’ diets should contain “plenty of starchy foods such as rice, bread, pasta and potatoes”. In addition to this, “just a little saturated fat”. This recommendation is a recipe for heart disease and stroke because of its high level of dietary acid.

While science has moved on, nutritional advice lags behind. And in a study published in Open Heart, a group of researchers conclude that national dietary advice on fat consumption issued to millions in the 1970s to reduce the risk of heart disease which suggested that fat should form no more than 30% of daily food intake lacked any solid trial evidence and shouldn’t have been introduced.

While more circumspect, cardiologist Rahul Bahl wrote in a linked editorial:

“There is certainly a strong argument that an over-reliance in public health on saturated fat as the main dietary villain for cardiovascular disease has distracted from the risks posed by other nutrients, such as carbohydrates.”

Fat and High-Carbohydrate Foods

Some fats aren’t good – trans fats, for example, which are mostly man-made – while others, such as monounsaturated fats found in olive oil are seen as having beneficial qualities.

Today, government guidelines recommend that fats should compose no more than 35% of an individual’s daily calorie intake – and that saturated fat, in particular, ought to supply less than 11%.

Fat intake decreased from 36.6% to 33.7% from 1971 to 2006, while the intake of carbohydrates rose from 44.0% to 48.7%. Yet obesity levels have escalated.

There is evidence to also show that carbohydrates can lead to feelings of increased hunger. A recent study in The American Journal of Clinical Nutrition found that eating carbohydrate foods with a high glycemic index (bread, rice, pasta) caused effects on the brain that led to feelings of increased hunger, which could in turn lead to eating more.

Another study in 2013 found high-carb meals could leave you feeling hungrier hours later compared to a low-carb meal with more fibre, protein and fat. The team behind the research attributed this to the plummeting levels of blood sugar that regularly follows high-carb meals.

The Diet-Heart Hypothesis

At the University of Hull they have been also looking at the effects of saturated fats on triglyceride levels – a type of fat (lipid) found in the blood. Using coconut oil because of its high (90%) saturated fat content, we found that when coupled with exercise, it significantly reduced triglyceride levels. A recent Brazilian rat study also found that coconut oil and exercise could lower blood pressure.

So where does our unshakable idea that fat leads to heart disease come from? The diet-heart hypothesis, that low density lipoproteins (LDL) cholesterol is raised in the blood by eating saturated fat, which then leads to clogged arteries and eventual heart disease, is not a credible claim.

 

This theory linking saturated fat and heart disease has been around since 1955 when Ansel Keys introduced his lipid hypothesis. Despite it being the foundation of dietary recommendations, it has never been proven and we have been advised to avoid certain foods including meat, dairy products and coconuts. And these myths are so deeply embedded in our minds, that recent science advocates have seen how hard it is to challenge established thinking.

 Saturated Fat and Cholesterol

When we talk about high-density lipoprotein (HDL) or LDL – often referred to as good and bad cholesterol – we aren’t actually referring to cholesterol itself. These lipoproteins actually carry cholesterol, fat and fat soluble vitamins in the bloodstream. It appears that elevated levels of cholesterol (or more accurately, cholesterol which is transported around the blood by lipioproteins) is correlated with an increase in the risk of heart disease.

However, correlation does not mean causation. Very low cholesterol is linked with an increased risk of death (though not from heart disease). And in the very old, research suggests cholesterol can be protective. So it’s fair to say the relationship between cardiovascular disease and total cholesterol is complex.

Type of cholesterol is important. The “good” (HDL) cholesterol is strongly linked with a reduced risk of heart disease. However, LDL, the “bad” cholesterol, is associated with an increased risk of heart disease. But it turns out that there are in fact subtypes of LDL which make this black and white picture more complicated. The actual size of the LDL particle is significant. Individuals are at a heightened risk of heart disease if they have most small, dense LDL particles, that may more easily lodge in the arteries, as opposed to those who have large LDL particles.

Your blood lipid profile is frequently used as a medical screening tool for abnormalities in lipids (including triglycerides and cholesterol). These blood lipid profile tests can identify approximate risks for cardiovascular disease and specific genetic diseases. Studies have also shown that saturated fats do not harm your blood lipid profile – and can actually improve it. Saturated fats could lower the risk of heart disease by shifting LDL cholesterol from dense small LDL to large LDL.

Numerous short-term feeding trials have shown that an increase in saturated fat consumption leads to a rise in overall LDL. Nevertheless, the result is inconsistent and weak. The methods used in a number of these research studies have been criticised – and plenty of studies support the contrary, that no association exists between total LDL and saturated fat consumption.

Cause and Correlation

If it was true that saturated fat did cause heart disease, then it follows that people who consume more would be at higher risk. But observational studies – again only illustrative of correlation not cause – haven’t shown this. One study looked at a population of 347,747 subjects from a total of 21 studies and concluded that there was “no significant evidence for concluding that dietary saturated fat is associated with an increased risk of coronary heart or cardiovascular disease”. This has also been the conclusion of other reviews.

So What About Randomized Controlled Trials?

One such study divided 12,866 male subjects at a high risk of heart disease into a low-fat or Western diet group. After six years, no difference was found between them. The Women’s Health Imitative, the biggest randomized controlled trial in diet history, comprised of 48,835 postmenopausal women who were also divided into two similar groups and came up with similar findings.

The Cold-Pressed Organic Coconut Oil Connection

If you don’t care for the science, then take an everyday example. Look at the large populations of the Masai in Africa who consume large amounts of saturated fat but have low levels of coronary heart disease. Or the Tokelauans of New Zealand who consume a massive amount of saturated fat through coconuts: more than 60% of their daily calories come from coconuts. These populations have no history of heart disease. And the health benefits of coconut oil are now becoming known more widely.

 

We are learning so much more about fats and that there is no evidence that saturated fat causes heart disease. Leading nutrition experts have been calling for an amendment to dietary recommendations for more than ten years. But despite these calls and the high-quality evidence assembled throughout the past decade, doctors, governments – and by extension the public – still take extraordinarily little notice. But a decade of research to the contrary would suggest it’s time we moved away from entrenched thinking, towards a more enlightened attitude to saturated fat.

 

What you can do is choose whole, organic, raw, NON-GMO, alkaline foods your grandmother served and not those your mom turned to as grocery store aisles filled with manufactured acidic foods and drinks. By eliminating acidic causing inflammatory foods and adding essential nutrients from fresh, raw, organic, alkaline unprocessed food, you will reverse years of damage in your arteries and throughout your body from consuming the typical American ACIDIC diet.

To learn more read the following article, THE PH MIRACLE FOR HEART DISEASE – DISCOVER THE TRUTH ABOUT HEART DISEASE, CONGESTIVE HEART FAILURE, ATHEROSCLEROSIS, CHOLESTEROL, HYPERTENSION, STROKE AND MORE! –

https://phoreveryoung.wordpress.com/2015/08/06/a-self-care-to-a-self-cure-for-heart-disease-a-number-1-killer/

 

To learn more read the following article: https://www.amazon.com/gp/product/B01KBMFRA4/ref=dbs_a_def_rwt_hsch_vapi_taft_p2_i8

 

 

 

 

To learn more about the work, research, findings of publications of Robert O Young CPT, MSc, DSc, PhD and Naturopathic Practitioner go to: http://www.drrobertyoung.com

References

  1. https://www.ahajournals.org/doi/abs/10.1161/circ.130.suppl_2.1898\
  2. Ravnskov U, Diamond DM, Hama R, et al. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review
  3. Office Of Dietary Supplements Fact Sheet: Folate
  4. Doshi SN, McDowell IF, Moat SJ, Payne N, Durrant HJ, Lewis MJ, Goodfellos J. Folic acid improves endothelial function in coronary artery disease via mechanisms largely independent of homocysteine. Circulation. 2002;105:22-6.
  5. Doshi SN, McDowell IFW, Moat SJ, Lang D, Newcombe RG, Kredean MB, Lewis MJ, Goodfellow J. Folate improves endothelial function in coronary artery disease. Arterioscler Thromb Vasc Biol 2001;21:1196-1202.
  6. Wald DS, Bishop L, Wald NJ, Law M, Hennessy E, Weir D, McPartlin J, Scott J. Randomized trial of folic acid supplementation and serum homocysteine levels. Arch Intern Med 2001;161:695-700.
  7. Jennings E. Folic acid as a cancer preventing agent. Med Hypothesis 1995;45:297-303.
  8. Freudenheim JL, Grahm S, Marshall JR, Haughey BP, Cholewinski S, Wilkinson G. Folate intake and carcinogenesis of the colon and rectum. Int J Epidemiol 1991;20:368-74.
  9. Giovannucci E, Stampfer MJ, Colditz GA, Hunter DJ, Fuchs C, Rosner BA, Speizer FE, Willett WC. Multivitamin use, folate, and colon cancer in women in the Nurses’ Health Study. Ann Intern Med 1998;129:517-24.
  10. A Paoloni-Giacobino, R Grimble, C Pichard. Genetics and nutrition. Clinical Nutrition Volume 22, Issue 5, Pages 429-435 (October 2003)
  11. Corradaa MM, Kawasab CH, Hallfrischc J, Mullerd D, Brookmeyere R. Reduced risk of Alzheimer?s disease with high folate intake: The Baltimore Longitudinal Study of Aging. Alzheimer’s and Dementia Volume 1, Issue 1, Pages 11-18 (July 2005).
  12. Wang HX, Wahlin Å, Basun H, Fastbom J, Winblad B, Fratiglioni L. Vitamin B12 and folate in relation to the development of Alzheimer?s disease. Neurology May 8, 2001 vol. 56 no. 9 1188-1194.
  13. Office Of Dietary Supplements Fact Sheet
  14. Appel LJ. Nonpharmacologic therapies that reduce blood pressure: A fresh perspective. Clin Cardiol 1999;22:1111-5.
  15. Simopoulos AP. The nutritional aspects of hypertension. Compr Ther 1999;25:95-100.
  16. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997;336:1117-24.
  17. Saris NE, Mervaala E, Karppanen H, Khawaja JA, Lewenstam A. Magnesium: an update on physiological, clinical, and analytical aspects. Clinica Chimica Acta 2000;294:1-26.
  18. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. National Academy Press. Washington, DC, 1999.
  19. Paolisso G, Sgambato S, Gambardella A, Pizza G, Tesauro P, Varricchio H, D’Onofrio F. Daily magnesium supplements improve glucose handling in elderly subjects. Am J Clin Nutr 1992;55:1161-7.
  20. Altura BM and Altura BT. Magnesium and cardiovascular biology: An important link between cardiovascular risk factors and atherogenesis. Cell Mol Biol Res 1995;41:347-59.
  21. Ford ES. Serum magnesium and ischaemic heart disease: Findings from a national sample of US adults. Intl J of Epidem 1999;28:645-51.
  22. Liao F, Folsom A, Brancati F. Is low magnesium concentration a risk factor for coronary heart disease? The Atherosclerosis Risk in Communities (ARIC) Study. Am Heart J 1998;136:480-90.
  23. Ascherio A, Rimm EB, Hernan MA, Giovannucci EL, Kawachi I, Stampfer MJ, Willett WC. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation 1998;98:1198-204.
  24. Elisaf M, Milionis H, Siamopoulos K. Hypomagnesemic hypokalemia and hypocalcemia: Clinical and laboratory characteristics. Mineral Electrolyte Metab 1997;23:105-12.
  25. Xing JH and Soffer EE. Adverse effects of laxatives. Dis Colon Rectum 2001;44:1201-9.
  26. Mauskop A, Altura BM. Role of magnesium in the pathogenesis and treatment of migraines. Clin Neurosci. 1998;5(1):24-27.
  27. Peikert A, Wilimzig C, Kohne-Volland R. Prophylaxis of migraine with oral magnesium: results from a prospective, multi-center, placebo-controlled and double-blind randomized study. Cephalalgia. 1996;16(4):257-263.
  28. Pfaffenrath V, Wessely P, Meyer C, et al. Magnesium in the prophylaxis of migraine–a double-blind placebo-controlled study. Cephalalgia. 1996;16(6):436-440.
  29. Wang F, Van Den Eeden SK, Ackerson LM, Salk SE, Reince RH, Elin RJ. Oral magnesium oxide prophylaxis of frequent migrainous headache in children: a randomized, double-blind, placebo-controlled trial. Headache. 2003;43(6):601-610.
  30. Bendich A. The potential for dietary supplements to reduce premenstrual syndrome (PMS) symptoms. J Am Coll Nutr. 2000;19(1):3-12.
  31. Rude RK. Magnesium deficiency: A cause of heterogeneous disease in humans. J Bone Miner Res 1998;13:749-58.
  32. Rude KR. Magnesium metabolism and deficiency. Endocrinol Metab Clin North Am 1993;22:377-95.
  33. Kelepouris E and Agus ZS. Hypomagnesemia: Renal magnesium handling. Semin Nephrol 1998;18:58-73.
  34. Ramsay LE, Yeo WW, Jackson PR. Metabolic effects of diuretics. Cardiology 1994;84 Suppl 2:48-56.
  35. Kobrin SM and Goldfarb S. Magnesium Deficiency. Semin Nephrol 1990;10:525-35.
  36. Lajer H and Daugaard G. Cisplatin and hypomagnesemia. Ca Treat Rev 1999;25:47-58.
  37. Tosiello L. Hypomagnesemia and diabetes mellitus. A review of clinical implications. Arch Intern Med 1996;156:1143-8.
  38. Paolisso G, Scheen A, D’Onofrio F, Lefebvre P. Magnesium and glucose homeostasis. Diabetologia 1990;33:511-4.
  39. Elisaf M, Bairaktari E, Kalaitzidis R, Siamopoulos K. Hypomagnesemia in alcoholic patients. Alcohol Clin Exp Res 1998;22:244-6.
  40. Abbott L, Nadler J, Rude RK. Magnesium deficiency in alcoholism: Possible contribution to osteoporosis and cardiovascular disease in alcoholics. Alcohol Clin Exp Res 1994;18:1076-82.
  41. Rude RK, Shils ME. Magnesium. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, eds. Modern Nutrition in Health and Disease. 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006:223-247.
  42. Food and Nutrition Board, Institute of Medicine. Magnesium. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington D.C.: National Academy Press; 1997:190-249.
  43. Schwartz R, Walker G, Linz MD, MacKellar I. Metabolic responses of adolescent boys to two levels of dietary magnesium and protein. I. Magnesium and nitrogen retention. Am J Clin Nutr. 1973;26(5):510-518.
  44. Shils ME. Magnesium. In Modern Nutrition in Health and Disease, 9th Edition. (edited by Shils, ME, Olson, JA, Shike, M, and Ross, AC.) New York: Lippincott Williams and Wilkins, 1999, p. 169-92.
  45. Spencer H, Norris C, Williams D. Inhibitory effects of zinc on magnesium balance and magnesium absorption in man. J Am Coll Nutr. 1994;13(5):479-484.
  46. Torsten Bohn, Lena Davidsson*, Thomas Walczyk and Richard F. Hurrel Fractional magnesium absorption is signi?cantly lower in human subjects from a meal served with an oxalate-rich vegetable, spinach, as compared with a meal served with kale, a vegetable with a low oxalate content. Laboratory for Human Nutrition, Institute of Food Science and Nutrition, Swiss Federal Institute of Technology, Zurich, Switzerland (Received 27 May 2003 – Revised 7 November 2003 – Accepted 28 November 2003
  47. FDA Drug Safety Communication: Low magnesium levels can be associated with long-term use of Proton Pump Inhibitor drugs (PPIs)
  48. Leach RM, Harris ED. Manganese. In: O’Dell BL, Sunde RA, eds. Handbook of nutritionally essential minerals. New York: Marcel Dekker, Inc; 1997:335-355.
  49. Freeland-Graves J, Llanes C. Models to study manganese deficiency. In: Klimis-Tavantzis DL, ed. Manganese in health and disease. Boca Raton: CRC Press, Inc; 1994.
  50. Reginster JY, Strause LG, Saltman P, Franchimont P. Trace elements and postmenopausal osteoporosis: a preliminary study of decreased serum manganese. Med Sci Res. 1988;16:337-338.
  51. Odabasi E, Turan M, Aydin A, Akay C, Kutlu M. Magnesium, zinc, copper, manganese, and selenium levels in postmenopausal women with osteoporosis. Can magnesium play a key role in osteoporosis? Ann Acad Med Singapore. 2008;37(7):564-567.
  52. Keen CL, Zidenberg-Cherr S. Manganese. In: Ziegler EE, Filer LJ, eds. Present Knowledge in Nutrition. 7th ed. Washington D.C.: ILSI Press; 1996:334-343.
  53. Carl GF, Gallagher BB. Manganese and epilepsy. In: Klimis-Tavantzis DL, ed. Manganese in health and disease. Boca Raton: CRC Press, Inc; 1994:133-157.
  54. Blaurock-Busch, E. Wichtige Nahrstoffe fur Gesunde Haut und Haare, Kosmetik Internat. 3/87.
  55. Collipp, P.J., et al. Manganese in infant formulas and learning disability. Ann. Nutr. Metab. 27(6):488-494, 1983.
  56. “Guidelines for Niacin Therapy For the Treatment of Elevated Lipoprotein a (Lpa)”. Rush Hemophilia & Thrombophilia Center. August 15, 2002, Revised July 27, 2005. Retrieved 20 November 2009. “facial flushing is a common side effect of niacin therapy that usually subsides after several weeks of consistent niacin use”
  57. Katzung, Bertram G. (2006). Basic and clinical pharmacology. New York: McGraw-Hill Medical Publishing Division. ISBN 0071451536.
  58. Greenbaum CJ, Kahn SE, Palmer JP. Nicotinamide’s effects on glucose metabolism in subjects at risk for IDDM. Diabetes. 1996;45(11):1631-1634.
  59. Lampeter EF, Klinghammer A, Scherbaum WA, et al. The Deutsche Nicotinamide Intervention Study: an attempt to prevent type 1 diabetes. DENIS Group. Diabetes. 1998;47(6):980-984.
  60. Hageman GJ, Stierum RH. Niacin, poly(ADP-ribose) polymerase-1 and genomic stability. Mutat Res. 2001;475(1-2):45-56.
  61. Jacobson EL, Shieh WM, Huang AC. Mapping the role of NAD metabolism in prevention and treatment of carcinogenesis. Mol Cell Biochem. 1999;193(1-2):69-74.
  62. Weitberg AB. Effect of nicotinic acid supplementation in vivo on oxygen radical-induced genetic damage in human lymphocytes. Mutat Res. 1989;216(4):197-201.
  63. Tang AM, Graham NM, Saah AJ. Effects of micronutrient intake on survival in human immunodeficiency virus type 1 infection. Am J Epidemiol. 1996;143(12):1244-1256.
  64. Brown RR, Ozaki Y, Datta SP, Borden EC, Sondel PM, Malone DG. Implications of interferon-induced tryptophan catabolism in cancer, auto-immune diseases and AIDS. Adv Exp Med Biol. 1991;294:425-435.
  65. Murray MF, Langan M, MacGregor RR. Increased plasma tryptophan in HIV-infected patients treated with pharmacologic doses of nicotinamide. Nutrition. 2001;17(7-8):654-656.
  66. Office of Dietary Supplements Fact Sheet: Vitamin B6
  67. New SA, Bolton-Smith C, Grubb DA, Reid DM. Nutritional influences on bone mineral density: a cross-sectional study in premenopausal women. Am J Clin Nutr. 1997;65(6):1831-1839.
  68. New SA, Robins SP, Campbell MK, et al. Dietary influences on bone mass and bone metabolism: further evidence of a positive link between fruit and vegetable consumption and bone health? Am J Clin Nutr. 2000;71(1):142-151.
  69. Tucker KL, Hannan MT, Chen H, Cupples LA, Wilson PW, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr. 1999;69(4):727-736.
  70. Ascherio A, Rimm EB, Hernan MA, et al. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation. 1998;98(12):1198-1204.
  71. Iso H, Stampfer MJ, Manson JE, et al. Prospective study of calcium, potassium, and magnesium intake and risk of stroke in women. Stroke. 1999;30(9):1772-1779.
  72. Fang J, Madhavan S, Alderman MH. Dietary potassium intake and stroke mortality. Stroke. 2000;31(7):1532-1537.
  73. Bazzano LA, He J, Ogden LG, et al. Dietary potassium intake and risk of stroke in US men and women: National Health and Nutrition Examination Survey I epidemiologic follow-up study. Stroke. 2001;32(7):1473-1480.
  74. Green DM, Ropper AH, Kronmal RA, Psaty BM, Burke GL. Serum potassium level and dietary potassium intake as risk factors for stroke. Neurology. 2002;59(3):314-320.
  75. Barri YM, Wingo CS. The effects of potassium depletion and supplementation on blood pressure: a clinical review. Am J Med Sci. 1997;314(1):37-40.
  76. Hajjar IM, Grim CE, George V, Kotchen TA. Impact of diet on blood pressure and age-related changes in blood pressure in the US population: analysis of NHANES III. Arch Intern Med. 2001;161(4):589-593.
  77. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med. 1997;336(16):1117-1124.
  78. Gennari FJ. Hypokalemia. N Engl J Med. 1998;339(7):451-458.
  79. http://lpi.oregonstate.edu/infocenter/minerals/potassium/potassiumrefs.html
  80. Shearer MJ. The roles of vitamins D and K in bone health and osteoporosis prevention. Proc Nutr Soc. 1997;56(3):915-937.
  81. Booth SL. Skeletal functions of vitamin K-dependent proteins: not just for clotting anymore. Nutr Rev. 1997;55(7):282-284.
  82. Suttie JW. Vitamin K. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, eds. Modern Nutrition in Health and Disease. 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006:412-425.
  83. Allison (2001). The possible role of vitamin K deficiency in the pathogenesis of Alzheimer’s disease and in augmenting brain damage associated with cardiovascular disease. Medical hypotheses 57 (2): 151?5. doi:10.1054/mehy.2001.1307. PMID 11461163.
  84. ODS Fact Sheet on Coumadin – http://ods.od.nih.gov/pubs/factsheets/coumadin1.pdf
  85. Office of Dietary Suppliments Face Sheet: Vitamin C
  86. Gokce N, Keaney JF, Jr., Frei B, et al. Long-term ascorbic acid administration reverses endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation. 1999;99(25):3234-3240.
  87. Audera, C (2001). “Mega-dose vitamin C in treatment of the common cold: a randomised controlled trial”. Medical Journal of Australia 389: 175.
  88. Hemilä, Harri; Chalker, Elizabeth; Douglas, Bob; Hemilä, Harri (2007). “Vitamin C for preventing and treating the common cold”. Cochrane database of systematic reviews (Online) (3): CD000980.
  89. Fleming DJ, Tucker KL, Jacques PF, Dallal GE, Wilson PW, Wood RJ (December 2002). “Dietary factors associated with the risk of high iron stores in the elderly Framingham Heart Study cohort”.
  90. The American Journal of Clinical Nutrition 76 (6): 1375?84.Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: National Academy Press, 2000.
  91. Weinstein M, Babyn P, Zlotkin S. An orange a day keeps the doctor away: scurvy in the year 2000. Pediatrics 2001;108:E55.
  92. Hoffman FA. Micronutrient requirements of cancer patients. Cancer. 1985;55 (1 Suppl):295-300.
  93. Deicher R, Hörl WH. Vitamin C in chronic kidney disease and hemodialysis patients. Kidney Blood Press Res 2003;26:100-6.
  94. Aishah Al-Jarallah, Fatima Igdoura, Yi Zhang, Christine B Tenedero, Elizabeth J White, Melissa E Macdonald, Suleiman A Igdoura, Bernardo L Trigatti. The effect of pomegranate extract on coronary artery atherosclerosis in SR-BI/APOE double knockout mice. Atherosclerosis. 2013 May ;228(1):80-9. Epub 2013 Mar 7. PMID: 23528829
  95. Michael Aviram, Mira Rosenblat, Diana Gaitini, Samy Nitecki, Aaron Hoffman, Leslie Dornfeld, Nina Volkova, Dita Presser, Judith Attias, Harley Liker, Tony Hayek. Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation. Clin Nutr. 2004 Jun;23(3):423-33. PMID: 15158307
  96. GreenMedInfo.com, Pomegranate’s Anti-Inflammatory Properties
  97. Mahalaxmi Mohan, Harshal Waghulde, Sanjay Kasture. Effect of pomegranate juice on Angiotensin II-induced hypertension in diabetic Wistar rats. Phytother Res. 2009 Dec 17. PMID: 20020514
  98. Filomena de Nigris, Maria Luisa Balestrieri, Sharon Williams-Ignarro, Francesco P D’Armiento, Carmela Fiorito, Louis J Ignarro, Claudio Napoli. The influence of pomegranate fruit extract in comparison to regular pomegranate juice and seed oil on nitric oxide and arterial function in obese Zucker rats. Nitric Oxide. 2007 Aug ;17(1):50-4. Epub 2007 May 5. PMID: 17553710
  99. Filomena de Nigris, Sharon Williams-Ignarro, Vincenzo Sica, Lilach O Lerman, Francesco P D’Armiento, Russell E Byrns, Amelia Casamassimi, Daniela Carpentiero, Concetta Schiano, Daigo Sumi, Carmela Fiorito, Louis J Ignarro, Claudio Napoli. Effects of a pomegranate fruit extract rich in punicalagin on oxidation-sensitive genes and eNOS activity at sites of perturbed shear stress and atherogenesis. Cardiovasc Res. 2007 Jan 15;73(2):414-23. Epub 2006 Sep 1. PMID: 17014835
  100. Yasunori Sawayama, Kyoko Okada, Shinji Maeda, Hachiro Ohnishi, Norihiro Furusyo, Jun Hayashi. Both hepatitis C virus and Chlamydia pneumoniae infection are related to the progression of carotid atherosclerosis in patients undergoing lipid lowering therapy. Fukuoka Igaku Zasshi. 2006 Aug;97(8):245-55. PMID: 17087362
  101. M Aviram, L Dornfeld, M Rosenblat, N Volkova, M Kaplan, R Coleman, T Hayek, D Presser, B Fuhrman. Pomegranate juice consumption reduces oxidative stress, atherogenic modifications to LDL, and platelet aggregation: studies in humans and in atherosclerotic apolipoprotein E-deficient mice. Am J Clin Nutr. 2000 May ;71(5):1062-76. PMID: 10799367
  102. Adde FV, Rodrizues JC, Cardoso AL. Nutritional follow-up of cystic fibrosis patients: the role of nutrition education. J Pediatr (Rio J). 2004;80(6):475-82.
  103. Beckles Willson N, Elliot TM, Everard ML. Omega-3 fatty acids (from fish oils) for cystic fibrosis. Cochrane Database Syst Rev. 2002;(3):CD002201.
  104. Bope. Conn’s Current Therapy 2010. 1st ed. Philadelphia, PA: Saunders, An Imprint of Elsevier; 2009.
  105. Bruzzese E, Raia V, Gaudiello G, et al. Intestinal inflammation is a frequent feature of cystic fibrosis and is reduced by probiotic administration. Aliment Pharmacol Ther. 2004;20(7):813-9.
  106. Cabrera C, Artacho R, Gimenez R. Beneficial effects of green tea — a review. J Am Coll Nutr. 2006;25(2):79-99.
  107. Campbell, T.M. The China Study, BenBella Books; First Paperback Edition edition (May 11, 2006).
  108. Caramia G, Cocchi M, Garliardini R, et al. Fatty acids composition of plasma phospholipids and triglycerides in children with cystic fibrosis. The effect of dietary supplementation with an olive and soybean oils mixture. Pediatr Med Chir. 2003;25(1):42-9.
  109. Chin J. Intestinal microflora: negotiating health outcomes with the warring community within us. Asia Pac J Clin Nutr. 2004;13(Suppl):S24-5.
  110. Cvetnic Z, Vladimir-Knezevic S. Antimicrobial activity of grapefruit seed and pulp ethanolic extract. Acta Pharm. 2004;54(3):243-50.
  111. D’Agostino, Russell MW, Huse DM et al. ‘Primary and subsequent coronary risk appraisal: new results from the Framingham Study’, American Heart Journal 2000.
  112. D’Agostino, Russell MW, Huse DM et al. ‘Primary and subsequent coronary risk appraisal: new results from the Framingham Study’, American Heart Journal 2000.
  113. D’Agostino, Vasan, Pencina, Wolf, Cobain, Massaro, Kannel. ‘A General Cardiovascular Risk Profile for Use in Primary Care: The Framingham Heart Study’.
  114. D’Agostino, Wolf, Belanger, Kannel ‘Stroke Risk Profile: Adjustment for Antihypertensive Medication’, Stroke 1994.
  115. Dolinoy D.C., Weidman J.R., Waterland R.A., Jirtle R.L. (2006). Maternal Genistein Alters Coat Color and Protects Avy Mouse Offspring from Obesity by Modifying the Fetal Epigenome. Environmental Health Perspectives, 114:567-572.
  116. Dolinoy D.C., Huang D., Jirtle R.L. (2007). Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. PNAS, 104: 13056-13061.
  117. Doron S, Gorbach SL. Probiotics: their role in the treatment and prevention of disease. Expert Rev Anti Infect Ther. 2006;4(2):261-75.
  118. Farrell P, Rosenstein B, White T, et al. Guidelines for Diagnosis of Cystic Fibrosis in Newborns through Older Adults: Cystic Fibrosis Foundation Consensus Report. Journal of Pediatrics. 2008;153(2)
  119. Ferri. Ferri’s Clinical Advisior 2010. 1st ed. Philadelphia, PA: Mosby, An Imprint of Elsevier; 2009.
  120. Gonclaves C, Dinis T, Batista MT. Antioxidant properties of proanthocyanidins of Uncaria tomentosa bark decoction: a mechanism for anti-inflammatory activity. Phytochemistry. 2005;66(1):89-98.
  121. Grey V, Mohammed SR, Smountas AA, et al. Improved glutathione status in young adult patients with cystic fibrosis supplemented with whey protein. J Cyst Fibros. 2003;2(4):195-8.
  122. Guo R, Pittler MH, Ernst E. Herbal medicines for the treatment of COPD: a systematic review. Eur Respir J. 2006;28(2):330-8.
  123. Hale LP, Greer PK, Trinh CT, James CL. Proteinase activity and stability of natural bromelain preparations. Int Immunopharmacol. 2005;5(4):783-93.
  124. Harlan M. Krumholz, MD; Teresa E. Seeman, PhD; Susan S. Merrill, PhD; Carlos F. Mendes de Leon, PhD; Viola Vaccarino, MD; David I. Silverman, MD; Reiko Tsukahara, MD; Adrian M. Ostfeld, MD; Lisa F. Berkman, PhD. Lack of Association Between Cholesterol and Coronary Heart Disease Mortality and Morbidity and All- Cause Mortality in Persons Older Than 70 Years. JAMA. 1994;272(17):1335-1340. doi:10.1001/jama.1994.03520170045034.
  125. Heggers JP, Cottingham J, Gussman J, et al. The effectiveness of processed grapefruit-seed extract as an antibacterial agent: II
  126. Mechanism of action and in vitro toxicity. J Altern Complement Med. 2002;8(3):333-40.
  127. Huang SH, Schall JI, Zemel BS, Stallings VA. Vitamin E status in children with cystic fibrosis and pancreatic insufficiency.J Pediatr. 2006;148(4):556-559.
  128. Infante P, Redecillas F, Torrent V, et al. Improvement of intestinal function in cystic fibrosis patients using probiotics. An Pediatr. 2008;69(6):501-5.
  129. Jonsdottir B, Bergsteinsson H, Baldursson O. Cystic Fibrosis–Review. Laeknabladid. 2008;94(12):831-7.
  130. Kannel, D’Agostino, Silbershatz, Belanger, Wilson, Levy. ‘Profile for Estimating Risk of Heart Failure’ – Arch Intern. Med. 1999.
  131. Kaati G., Bygren L.O., Pembrey M., Sjostrom M. (2007). Transgenerational response to nutrition, early life circumstances and longevity. European Journal of Human Genetics, 15: 784-790.
  132. Kormosh N, Laktionov K, Antoshechkina M. Effect of a combination of extract from several plants on cell-mediated and humoral immunity of patients with advanced ovarian cancer. Phytother Res. 2006;20(5):424-5.
  133. Kucharski R., Maleszka J., Foret S., Maleszka R. Nutritional Control of Reproductive Status in Honeybees via DNA Methylation (2008). Science, 319: 1827-1830 (registration required)
  134. McCabe H. Riboflavin deficiency in cystic fibrosis: three case reports. J Hum Nutr Diet. 2001;14(5):365-70.
  135. McGowan P.O., Meaney M.J., Szyf M. (2008).  Diet and the epigenetic (re)programming of phenotypic differences in behavior. Brain Research, 1237: 12-24 (subscription required).
  136. Mizejewski GJ, Pass KA. Fatty acids, alpha-fetoprotein, and cystic fibrosis. Pediatrics. 2001;108(6):1370-3.
  137. Murray KL, Lee CK, Mogayzel PJ Jr, Zeitlin PL, Rosenstein BJ. Dietary supplement use in pediatric patients with cystic fibrosis. Am J Health Syst Pharm. 2008;65(6):562-5.
  138. National Institutes of Health (U.S. Department of Health and Human Services) www.nih.gov.
  139. Nutrition Reviews 54: 1-30, 1996. Raised glutathione levels fight the oxdiation of fats circulating in the bloodstream including cholesterol, retarding the process of plaque formation in the arteries leading to most heart attacks and strokes.
  140. Olveira G, Olveira C. Nutrition, cystic fibrosis and the digestive tract. Nutr Hosp. 2008;23(2):71-86.
  141. Paterson PG, Juurlink BH. Nutritional Regulation of Glutathione in Stroke. Neurtox Res. 1999 Dec; 1(2): 99-112.
  142. Parikh, Pencina, Wang, Benjamin, Lanier, Levy, D’Agostino, Kannel, Vasan. ‘A Risk Score for Predicting Near-Term Incidence of Hypertension: The Framingham Heart Study’, Annals of Internal Medicine 2008.
  143. Pencina, D’Agostino, Larson, Massaro, Vasan. ‘Predicting the 30-Year Risk of Cardiovascular Disease: The Framingham Heart Study’, Circulation 2009.
  144. Proesmans M, Vermeulen F, De Boeck K. What’s new in cystic fibrosis? From trating symptoms to correction of the basic defect. Eur J Pediatr. 2008;167(8):839-49.
  145. RahmanI, MacNee W. Oxidative Stress and Regulation of Glutathione in Lung Inflammation. Eur Respir J. 2000 Sep; 16(3):534-54.
  146. Roum JH, Buhl R, McElvaney NG, et al. Systemic Deficiency of Glutathione in Systic Fibrosis. J Appl Physiol 1993; 75:19-24.
  147. Rubin BK. The pharmacologic approach to airway clearance: Mucoactive agents. Paediatr Respir Rev. 2006;7 Suppl 1:S215-9.
  148. Schnabel RB, Sullivan LM, Levy D, Pencina MJ, Massaro JM, D’Agostino RB, Sr., Newton-Cheh C, Yamamoto JF, Magnani JW, Tadros TM, Kannel WB, Wang TJ, Ellinor PT, Wolf PA, Vasan RS, Benjamin EJ. Development of a risk score for atrial fibrillation (Framingham Heart Study): a community-based cohort Lancet 2009;373:739-745.
  149. Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002;21(6):495-505.
  150. The Adult Treatment Panel III, JAMA. 2001.
  151. Wilson, Meigs, Sullivan, Fox, Nathan, D’Agostino. ‘Prediction of Incident Diabetes Mellitus in Middle-aged Adults: The Framingham Offspring Study,’ Archives of Internal Medicine 2007.
  152. Young, RO, Sick and Tired, Woodland Publishing, Orem, Utah, 2001.
  153. Yoon JH, Baek SJ. Molecular targets of dietary polyphenols with anti-inflammatory properties. Yonsei Med J. 2005;46(5):585-96.
  154. Young, RO, Young, SR, Young, The pH Miracle Revised and Updated, Grand Central Publishing, New York, NY, 2010Pollak O J. 1952, An Etiologic Concept of Atherosclerosis Based on Study of Intimal Alterations after Shock. Circulation;5;539-550. Full free paper at:http://circ.ahajournals.org/cgi/reprint/5/4/539.pdf
  155. 148. Ross R, Glomset J, Harker L. 1977. Response to injury and atherogenesis. Am J Pathol. Mar;86(3):675-8
  156. Press release. 2006. New Explanation For The Cause Of Atherosclerosis: The Acidity Theory, Medical News Today, Aug 10 at http://www.medicalnewstoday.com/articles/49244.php
  157. Press release. 2006. Beyond Lipids: Understanding the Mechanics of Atherosclerosis (press release). UCSD News, July 12. at: http://www.jacobsschool.ucsd.edu/news/news_releases/release.sfe?id=554
  158. Kaunas R, Usami S, Chien S. 2006 Regulation of stretch-induced JNK activation by stress fiber orientation. Cellular Signalling, Nov;18(11):1924-31 at http://www.ncbi.nlm.nih.gov/pubmed/16581230
  159. Haga JH, Li Yi-Shuan J. and Chien S. 2007. Molecular basis of the effects of mechanical stretch on vascular smooth muscle cells, Journal of Biomechanics, 40(5):947-60.
  160. Mesquita QHde. 1979. Myogenic Theory of Myocardial Infarction (Teoria Miogênica do Enfarte do Miocárdio, Gemini, Sao Paulo, SP – Brazil Book in Portuguese language with a summary in English at: http://www.infarctcombat.org/LivroTM/parte8.htm
  161. Mesquita QHde, Baptista CAS. 1994. Why Myogenic Theory not Thrombogenic Theory. Arq Bras Cardiol, V. 62 (4) – (Official Journal of Brazilian Cardiology Society). Full translated paper at http://www.infarctcombat.org/MTxTT-ABC.pdf
  162. Fernandes VS et al. 2006, Subclinical atherosclerosis and incipient regional myocardial dysfunction in asymptomatic individuals. The Multi-Ethnic Study of Atherosclerosis (MESA), J Am Coll Cardiol 47: 2420-8 Full free paper at http://content.onlinejacc.org/cgi/content/full/j.jacc.2005.12.075v1
  163. Marwah R, Doux J, Lee P and Yun A. 2007. Is atherosclerosis a neurogenic phenomenon? Medical Hypotheses, V 69, I 4: 884-887
  164. Selye H. 1950. The physiology and pathology of exposure to stress: A treatise based on the concepts of the general-adaptation-syndrome and the diseases of adaptation”, Montreal, Acta, Inc. / Selye H et al. 1970 Experimental Cardiovascular Diseases, Volume 1 (History, Cardiovascular Disease, Factors Influencing Cardiovascular Disease); Volume 2 (Histology and Histochemistry, Chemical and Functional Changes, References), Springer-Verlag, Berlin New York
  165. Cannon WJ. 1914. The emergency function of the adrenal medulla in pain and the major emotions. Am J Physiol. 33:356-372
  166. Benson JC, Eckert SP, McCleskey EW. 1999. Acid-Evoked Currents in Cardiac Sensory Neurons – A possible mediator of myocardial ischemic sensation, Circulation Research, 84:921-928. Full free paper at http://circres.ahajournals.org/cgi/content/full/84/8/921
  167. Gianni M et al. 2006. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review, European Heart Journal, V27,N13: 1523-1529
  168. Akashi YJ et al. 2002. Reversible left ventricular dysfunction “takotsubo” cardiomyopathy related to catecholamine cardiotoxicity, J. Electrocardiol 2002; 35:351-356
  169. Arora S et al. 2006. Transient left ventricular apical ballooning after cocaine use; is catecholamine cardiotoxicity the pathologic link? Mayo Clin Proc. 2006; 81:820-832. Full free paper at http://www.mayoclinicproceedings.com/pdf/8106/8106cr2.pdf
  170. Wittstein IS et al. 2005. Neurohumoral features of myocardial stunning due to sudden emotional stress, New Engl J Med, Feb 10, V352: 539-548
  171. Graham LN, Smith PA et al. 2004. Sympathetic neural hyperactivity and its normalization following unstable angina and acute myocardial infarction, Clin Sci (Lond), Jun;106(6):605-11
  172. Gazes PC, Richardson JA et al. 1959. Plasma catecholamine concentrations in myocardial infarction and angina pectoris, Circulation 19:657-661
  173. Waldenstrom AP et al. 1978. A possible role of noradrenaline in the development of myocardial infarction, Am Heart J. 95:43-51
  174. Nadeau RA, de Champlain J. 1979. Plasma catecholamine in acute myocardial infarction, Am Heart J, 98: 548-554
  175. McCance AJ, Thompson PA, Forfar JC. 1993. Increased cardiac sympathetic nervous activity in patients with unstable coronary heart disease, Eur Heart J, Jun;14(6):751-7
  176. Makikalio A. 2005. Cardiovascular autonomic and hormonal dysregulation in ischemic stroke with an emphasis on survival, International Journal of Circumpolar Health 64:5
  177. Korner P. 2007. Essential Hypertension and Its Causes: Neural and Non-Neural Mechanisms. New York, Oxford University Press
  178. Rainforth MV, Schneider RH, Nidich SI, Gaylord-King C, Salerno JW, Anderson JW. 2007. Stress Reduction Programs in Patients with Elevated Blood Pressure: A Systematic Review and Metaanalysis. Curr Hypertens Rep Dec;9(6):520-8. Full free paper at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18350109
  179. Barnett PA, Spence JD, Manuck SB, et al. 1997. Psychological stress and the progression of carotid artery disease, J Hypertens 15:49–55
  180. Kamarck TW, Everson SA, Kaplan GA, et al. 1997. Exaggerated blood pressure responses during mental stress are associated with enhanced carotid atherosclerosis in middle-aged Finnish men: findings from the Kuopio ischemic heart disease study. Circulation,96:3842–8 Full free paper at: http://circ.ahajournals.org/cgi/content/full/96/11/384210
  181. Jennings JR, Kamarck TW et al. 2004. Exaggerated blood pressure responses during mental stress are associated with enhanced carotid atherosclerosis in middle-aged Finnish men: findings from the Kuopio ischemic heart disease study, Circulation;110:2198-2203. Full free paper at: http://circ.ahajournals.org/cgi/content/full/110/15/2198
  182. Hauss WH et al. 1990. Adrenaline and noradrenaline as possible chemical mediators in the pathogenesis of arteriosclerosis. Ann N Y Acad Sci 598:91-101
  183. Matthews KA et al. 1998. Stress-Induced Pulse Pressure Change predicts women’s carotid atherosclerosis, Stroke 29:1525-1530
  184. Matthews KA, Zhu S, Tucker DC, Whooley MA. 2006. Blood pressure reactivity to psychological stress and coronary calcification in the Coronary Artery Risk Development in Young Adults Study, Hypertension, Mar; 47(3):391-5. Full free paper at http://hyper.ahajournals.org/cgi/content/full/47/3/391
  185. Ghiadone L et al. 2000. Mental stress induces transient endothelial dysfunction in humans, Circulation102:2473. Full free paper at http://circ.ahajounals.org/cgi/content/full/102/20/2473
  186. Steptoe A. et al. 2006. Delayed blood pressure recovery after psychological stress is associated with carotid intima-media thickness. Arterioscler. Thromb. Vasc. Biol. Nov, 26(11):2547-51
  187. Eller NH, Netterstrom. 2007. Psychosocial factors at home and at work and four-years progression in intima-media thickness. In J Behav Med 2007; 14 (1):21-29
  188. Faramawi et al. 2007. Relation between depressive symptoms and common carotid artery atherosclerosis in American persons > 65 years of age, Am J Cardiol; 99:1610-1613
  189. Schoner W. 2002. Endogenous cardiac glycosides, a new class of steroid hormones. Eur J Biochem. 268, 2440-2448, Full free paper at http://www.ejbiochem.org/cgi/content/full/269/10/2440
  190. Nesher M, Shpolansky U, Rosen H, Lichtstein D. 2007.The digitalis-like steroid hormones: New mechanisms of action and biological significance. Life Sci. May 15;80(23):2093-107
  191. Sophocleus A et al. 2003. Circulating endogenous digitalis-like factors (EDLF) in man is derived from the adrenals and its secretion is ACTH-dependent. J Endocrinol Invest Jul;26(7):668-74
  192. Weidemann H et al. 2004. Diverse effects of stress and additional adrenocorticotropic hormone on digitalislike compounds in normal and nude mice, Journal of Neuroendocrinology, Vol 16, 458-463. Full free paper at http://physiology.huji.ac.il/pdf/lichtstein/weiden-et-al04.pdf
  193. Hassan M. AM Qazzaz et al. 2004. De Novo Biosynthesis and Radiolabeling of Mammalian Digitalis-Like Factors. Clin Chem. Mar;50(3):612-20. Full free paper at http://www.clinchem.org/cgi/content/full/50/3/612
  194. Rose AM, Valdes RJ. 1994. Understanding the sodium potassium pump and its relevance to disease, Clin. Chem. 40/9: 1674-1685 Full free paper at: http://www.clinchem.org/cgi/reprint/40/9/1674
  195. Vasilyev A, Khater K, and Rakowski RF. 2004. Effect of Extracellular pH on Presteady-State and SteadyState Current Mediated by the Na+/K+ Pump,. J Membr Biol. March 15; 198(2):65–76. Full free paper at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1357233
  196. Li C, Geering K, Horisberger JD. 2006. The Third Sodium Binding Site of Na,K-ATPase Is Functionally Linked to Acidic pH-Activated Inward Current. Membr Biol. 213(1):1-9.
  197. Mesquita QHde, Baptista CAS. 2002. Cardiotônico: insuperável na preservação da estabilidade miocárdica como preventivo das síndromes coronárias agudas e responsável pela prolongada sobrevida, Ars Cvrandi, maio 35:3. Full free paper at http://www.infarctcombat.org/28anos/digitalicos.html . Summary in English at: http://www.infarctcombat.org/heartnews-16.html
  198. Mesquita QHde, Baptista CAS et al. 2002. Efeitos do cardiotônico + dilatador coronário na coronáriomiocardiopatia crônica estável, com e sem enfarte prévio, a longo prazo. Ars Cvrandi, setembro;35:7. Full free paper at http://www.infarctcombat.org/qhm/cme.pdf Summary in English athttp://www.infarctcombat.org/heartnews-16.html
  199. Kern B. 1970. Der Myokard-Infarkt. Haug-Verlag, Heidelberg.
  200. Gao JRS et al. 2002. Isoform specific stimulation of cardiac Na/K pumps by nM concentrations of glycosides, J Gen Physiol 119:297-312. Full free paper at http://www.jgp.org/cgi/content/full/119/4/297
  201. Schobel HP et al. 1991.Contrasting effects of digitalis and dobutamine on baroreflex sympathetic control in normal humans, Circulation V84, 1118-1129. Full free paper at: http://circ.ahajournals.org/cgi/reprint/84/3/1118
  202. Gutman Y, Boonyaviroj P. Naunyn Schmiedebergs. 1977. Mechanism of inhibition of catecholamine release from adrenal medulla by diphenylhydantoin and by low concentration of ouabain (10 (-10) M). Arch Pharmacol Feb;296(3):293-6
  203. von Ardenne M. 1978. Die Hemmung der mikrozirculation beim myokardinfarkt und das perlingual applizierte g-strophanthin, Arzneimittel-Forsch. 28; 202:
  204. Pierre SV et al. 2007. Ouabain triggers preconditioning through activation of the NA+, K+-ATPase signalling cascade in rat hearts, Cardiovasc Res, Feb 1;73(3): 488-96
  205. Pugin J, Dunn-Siegrist I, Dufour J, Tissieres P, Charles PE, Comte R. 2007. Cyclic Stretch of Human Lung Cells Induces an Acidification and Promotes Bacterial Growth, Am J Respir Cell Mol Biol. Oct 5 doi:10.1165/rcmb.2007-0114OC
  206. Levy B, Gibot S, Franck P, Cravoisy A, Bollaert PE. 2005. Relation between muscle Na+K+ ATPase activity and raised lactate concentrations in septic shock: a prospective study. Lancet. Mar 5-11;365(9462):871-5.
  207. Schade DS.1982. The role of catecholamines in metabolic acidosis. Ciba Found Symp;87:235-53
  208. Abarquez RF Jr. 1967. Digitalis in the treatment of hypertension. A preliminary report. Acta Med Philipp. Jan-Mar;3(3):161-70
  209. Yuan CM, Manunta P, Hamlyn JM et al. 1993. Long-term ouabain administration produces hypertension in rats. Hypertension, 3;22;178-187 Full free paper at: http://hyper.ahajournals.org/cgi/reprint/22/2/178
  210. Manunta, P., Hamilton, J., Rogowski, A.C., Hamilton, B.P., Hamlyn, J.M. 2000. Chronic hypertension induced by ouabain but not digoxin in the rat:antihypertensive effect of digoxin and digitoxin. Hypertension Research 23 (Suppl), S77–S85.
  211. Yang Q, Huang W, Jozwik C, Lin Y, Glasman M et al. 2005. Cardiac glycosides inhibit TNF-alpha/NF-kappaB signaling by blocking recruitment of TNF receptor-associated death domain to the TNF receptor. Proc Natl Acad Sci USA Jul 5;102(27):9631-6. Full free paper at http://www.pnas.org/cgi/content/full/102/27/963111
  212. Sternberg EM. 2001. Neuroendocrine regulation of autoimmune/inflammatory disease, J Endocrinol Jun; 169(3):429-35. Full free paper at http://joe.endocrinology-journals.org/cgi/reprint/169/3/429
  213. Brum PC, Kosek J, Patterson A et al. 2002. Abnormal cardiac function associated with sympathetic nervous system hyperactivity in mice. Am J Physiol Heart Circ Physiol 283: H1838-H1845. Full free paper at http://ajpheart.physiology.org/cgi/content/full/283/5/H1838#B4
  214. F. E. Demartini, P. J. Cannon, W. B. Stason, and J. H. Laragh. 1965. Lactic Acid Metabolism in Hypertensive Patients. Science 11 June, Vol. 148. no. 3676, pp. 1482 – 1484
  215. Sharda S, Gupta SN and Khuteta KP. 1975. Effect on mental stress on intermediate carbohydrate-and lipidmetabolism. Indian J Physiol Pharmacol. Apr-Jun;19(2):86-9.
  216. Hall JB, Brown DA. 1979. Plasma glucose and lactic acid alterations in response to a stressful exam. Biol Psychol. May;8(3):179-88.
  217. von Ardenne M, Reitnauer PG. 1989. Increase of perfusion pressure at constant perfusion rate caused by low pH values, Biomed Biochim Acta, 48(4):317-23
  218. Yasushi Horai et al. 2005. Changes in pH increase perfusion pressure of coronary arteries in the rat. J Pharmacol Sci 97; 400: 407
  219. Austin C, Wray S. 2000. Interactions Between Ca2+ and H+ and Functional Consequences in Vascular Smooth Muscle, Mini Review, Circulation Research 86:355. Full free paper at: http://circres.ahajournals.org/cgi/content/full/86/3/355
  220. Kim YM et al. 2005. Contribution of Na_-K_ pump and KIR currents to extracellular pH-dependent changes of contractility in rat superior mesenteric artery, Am J Physiol Heart Circ Physiol 289:792-800 Full free paper at http://ajpheart.physiology.org/cgi/reprint/289/2/H792
  221. Carter G, Gavin JB. 1989. Endocardial damage induced by lactate, lowered pH and lactic acid in nonischemic beating hearts. Pathology Apr;21(2):125-30
  222. Sharma AM, Kribben A et al. 1990. Salt sensitivity in humans is associated with abnormal acid-base balance. Hypertension; 16, 407-413. Full free paper at http://hyper.ahajournals.org/cgi/reprint/16/4/407
  223. Harold T. Edwards, Edward H. Bensley, David B. Dill and Thorne M. Carpenter. 1944. Human Respiratory Quotients in Relation to Alveolar Carbon Dioxide and Blood Lactic Acid After Ingestion of Glucose, Fructose, or Galactose. Journal of Nutrition Vol. 27 No. 3 March, pp. 241-251. Full free paper at http://jn.nutrition.org/cgi/reprint/27/3/241
  224. Hallfrisch J. 1990. Metabolic effects of dietary fructose. FASEB J, Vol 4; Jun: 2652-2660. Full free paper at http://www.fasebj.org/cgi/reprint/4/9/2652.pdf
  225. Mesquita QHde. 1982. Aspectos angiográficos coronários e ventriculograficos do primeiro enfarte do miocárdio em coronariopatia crônica silenciosa. Rev. Bras. Med., V 39: N7
  226. LA Naves and McCleskey EW. 2005. An acid-sensing ion channel that detects ischemic pain. Braz J Med Biol Res, 38 (11) 1561-69 http://www.scielo.br/pdf/bjmbr/v38n11/v38n11a01.pdf
  227. Vogt AM, Ackermann C, Yildiz M, Schoels W, Kübler W. 2002. Lactate accumulation rather than ATP depletion predicts ischemic myocardial necrosis: implications for the development of lethal myocardial injury, Biochim Biophys Acta Mar 16;1586(2):219- 26.
  228. Todd GL, Baroldi G, Pieper GM, Clayton FC, Eliot RS. 1985. Experimental catecholamine- induced myocardial necrosis. I. Morphology, quantification and regional distribution of acute contraction band lesions. J Mol Cell Cardiol. Apr 17(4):317- 38.
  229. Henning RJ, Well MH, Weiner F. 1982. Blood lactate as prognostic indicator of survival in patients with acute myocardial infarction. Circ Shock, 9(3):307-15
  230. Vikhert AM, Cherpachenko NM. 1985. Histoenzymological characteristics of the myocardium in sudden cardiac death. Arkh Patol 47(7):29-34
  231. Huang Y, McNamara JO. 2004. “Ischemic Stroke: “Acidotoxicity” Is a Perpetrator”, Cell, Volume 118, Issue 6, 17 September, Pages 665-666Tennant R. 1935. Factors concerned in the arrest of contraction in an ischemic myocardial area. Am J Physiol: 133; 677-682
  232. Katz AM, Hecht H. H. 1969. The early pump failure of the ischaemic heart. Am J Med: 47; 497-502
  233. Elharrer V, Zipes D.P. 1977. Cardiac electrophysiologic alterations during myocardial ischaemia. Am J Physiol: 233: H329-345
  234. Pan HL et al. 1999. Role of protons in activation of cardiac sympathetic C-fibre afferents during ischaemia in cats. J Physiol. Aug 1;518 ( Pt 3):857-66. Full free paper at http://jp.physoc.org/cgi/content/full/518/3/857
  235. Leake DS. 1997. Does an acidic pH explain why low density lipoprotein is oxidised in atherosclerotic lesions? Atherosclerosis. Mar 21;129(2):149- 57
  236. Gown MA, Benditt PE. 1982. Lactate dehydrogenase (LDH) isozymes of human atherosclerotic plaques. Am J Pathol 1982, 107:316-321
  237. Morgan J, Leake DS. 1995. Oxidation of low density lipoprotein by iron or copper at acidic pH. J Lipid Res. Dec;36(12):2504- 12. Full free paper at: http://www.jlr.org/cgi/reprint/36/12/2504
  238. Patterson RA, Leake DS. 1998. Human serum, cysteine and histidine inhibit the oxidation of low density lipoprotein less at acidic pH. FEBS Lett. Sep 4;434(3):317- 21.
  239. Naghavi M et al. 2002. pH Heterogeneity of human and rabbit atherosclerotic plaques; a new insight into detection of vulnerable plaque. Atherosclerosis Sep, V 164; 1:27-35
  240. Khan T, Soller B, Naghavi M, Casscells W. 2005. Tissue pH determination for the detection of metabolically active inflamed vulnerable plaques using near-infrared spectroscopy: an in-vitro feasibility study. Cardiology.; 103(1): 10-6.
  241. Sneck M, Kovanen PT, Oorni K. 2005. Decrease in pH strongly enhances binding of native, proteolysed, lipolysed, and oxidized low density lipoprotein particles to human aortic proteoglycans, Journal of Biological Chemistry, 280;45: Nov. Full free paper at http://www.jbc.org/cgi/reprint/280/45/37449
  242. Oorni K and Kovanen PT. 2006. Enhanced extracellular lipid accumulation in acidic environments. Curr Opin Lipidol 17(5);534-40: Oct
  243. Patterson RA, Horsley ETM, Leake DS. 2003. Prooxidant and antioxidant properties of human serum ultrafiltrates toward LDL: important role of uric acid. Journal of Lipid Research, Vol. 44, 512-521, March Full free paper at http://www.jlr.org/cgi/reprint/44/3/51212
  244. Hayden MR, Tyagi SC. 2004. Uric acid: A new look at an old risk marker for cardiovascular disease, metabolic syndrome, and type 2 diabetes mellitus: The urate redox shuttle. Nutr Metab (Lond). 1: 10, October 19. Full paper at http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=529248
  245. McCully KS. 1969. Vascular pathology of homocysteinemia: implications for the pathogenesis of atherosclerosis. Am J Pathology 56:111:28
  246. Stoney CM. 1999. Plasma homocysteine levels increase in women during psychological stress, Life Sci 64(25):2359-65
  247. Stoney CM and Engebretson TO. 2000. Plasma homocysteine concentrations are positively associated with hostility and anger, Life Sci 66(23):2267-75
  248. Hapuarachchi JR, Chalmers AH et al. 2003. Changes in clinically relevant metabolites with psychological stress parameters. Behav Med. Summer;29(2):52-9
  249. Jerlich A et al. 1999. Correlation of low-density lipoprotein modification by myeloperoxidase with hypocholorous acid formation, Int. J. Clin, Lab, Res 29(4):155-61
  250. Podrez EA, Abu-Soud HM, Hasen SL. 2000. Myeloperoxidase-generated oxidants and atherosclerosis. Free Radic Biol Med 28:1717–172
  251. Yang J, Cheng Y, Ji R, Zhang C. 2006. Novel model of inflammatory neointima formation reveals a potential role of myeloperoxidase in neointimal hyperplasia. Am J Physiol Heart Circ Physiol. Dec;291(6):H3087- 93.
  252. Meuwese MC, Stroes ESG, Hazen SL, et al. 2007. Serum myeloperoxidase levels are associated with the future risk of coronary artery disease in apparently healthy individuals: The EPIC-Norfolk Prospective Population Study..J Am Coll Cardiol 50:159-165
  253. Wong ML et al. 2000. Acute systemic inflammation up-regulates secretory sphingomyelinase in vivo: A possible link between inflammatory cytokines and atherogenesis, PNAS 97;8681-8686 Full free paper at http://www.pnas.org/cgi/content/full/97/15/8681
  254. Abela GS. 2006. Plaque Rupture by Cholesterol Crystallization – A Novel Concept for Acute Coronary Syndrome, American College of Cardiology Annual Scientific Session, March 13, Full free paper at http://www.cardiosource.com/rapidnewssummaries/summary.asp?SumID=164
  255. Malek AM, Alper SL, Izumo S. 1999. Hemodynamic shear stress and its role in atherosclerosis JAMA 282: 2035-2042
  256. Cheng C et al. 2006. Atherosclerotic lesion size and vulnerability are determined by patterns of fluid shear stress. Circulation 113:2744-2753. Full free paper at at: http://circ.ahajournals.org/cgi/content/abstract/113/23/2744
  257. Cunningham KS and Gotlieb AI. 2005. The role of shear stress in the pathogenesis of atherosclerosis (Mini review), Laboratory Investigation 85, 9-23, Full free paper at: http://www.nature.com/labinvest/journal/v85/n1/full/3700215a.html
  258. Texon M. 1957. A hemodynamic concept of atherosclerosis, with particular reference to coronary occlusion. Arch Intern Med 99:418–42
  259. Imparato AM, Lord JW Jr, Texon M, Helpern M. 1961. Experimental atherosclerosis produced by alteration of blood vessel configuration. Surg Forum 12:245–247.
  260. Rittersma SZH, van der Wal AC, Koch KT, et al. 2005. Plaque instability frequently occurs days or weeks before occlusive coronary thrombosis. A pathological thrombectomy study in primary percutaneous coronary intervention. Circulation; 111:1160-1165. Full free paper at: http://circ.ahajournals.org/cgi/content/full/111/9/1160
  261. Ojio S, Takatsy H, et al. 2000. Considerable time from the onset of plaque rupture and/or thrombi until the onset of acute myocardial infarction in humans coronary angiographic findings within 1 week before the onset of infarction. Circulation;102:2063. Full free paper at:http://www.circ.ahajournals.org/cgi/reprint/102/17/206
  262. Ulrich E. Heidlan, Bodo E. Strauer. 2001. Left ventricular muscle mass and elevated heart rate are associated with coronary plaque disruption, Circulation 104:1477. Full free paper at: http://circ.ahajournals.org/cgi/content/full/104/13/1477
  263. Baroldi G, Bigi R, Cortigiani L. 2004. Ultrasound imaging versus morphopathology in cardiovascular diseases. Coronary collateral circulation and atherosclerotic plaque. Cardiovascular ultrasound; 3: 6. Full free paper at: http://www.cardiovascularultrasound.com/content/3/1/6
  264. Roberts W. C. 1974. Coronary Thrombosis and Fatal Myocardial Ischemia. Circulation;49;1-3 Full free paper at http://circ.ahajournals.org/cgi/reprint/49/1/1.pdf
  265. Rioufol G, Finet G, Andre-Fouet X et al. 2002. Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study. Circulation; 106:804-808. Full free paper at: http://www.circ.ahajournals.org/cgi/reprint/01.CIR.0000025609.13806.31v1
  266. Yasunori Ueda, Masanori Asakura, et al. 2001. The healing process of infarct-related plaque: Insights from 18 months of serial angioscopic follow-up. Am Coll Cardiol, 38:1916-1922.Full free paper at: http://content.onlinejacc.org/cgi/reprint/38/7/1916
  267. Giorgio Baroldi, Riccardo Bigi and Lauro Cortigiani.2005. Ultrasound imaging versusmorphopathology in cardiovascular diseases. Myocardial cell damage. Cardiovascular Ultrasound 3:32. Full free paper at http://www.cardiovascularultrasound.com/content/3/1/32
  268. Murakami T, Mizuno S, Takahashi Y, Ohsato K et al. 1998. Intracoronary aspiration thrombectomy for acute myocardial infarction, Am. J Cardiology Oct 1;82 (7):839-44
  269. Wang HX, Leineweber C, et al. 2007. Psychosocial stress and atherosclerosis: family and work stress accelerate progression of coronary disease in women. The Stockholm Female Coronary Angiography Study. Journal of Internal Medicine 261;245-254
  270. Richmond AC et al. 2000. Effects of stress reduction on carotid atherosclerosis in hypertensive African Americans, Stroke 31:568-573. Full free paper at: http://stroke.ahajournals.org/cgi/reprint/31/3/568
  271. Fields JZ et al. 2002. Effect of a multimodality natural medicine program on carotid atherosclerosis in older subjects: a pilot trial of Maharishi Vedic Medicine, American Journal of Cardiology, 89; 8:952-958
  272. Manchanda SC, Narang R, Reddy KS, Sachdeva U, Prabhakaran D, Dharmanand S, Rajani M and Bijlani R. 2002. Retardation of coronary atherosclerosis with yoga lifestyle prevention, J Assoc Physicians India Jul; 48(7): 687-94 13.
  273. Rainer Rauramaa et al. 2004. Effects of aerobical physical exercise on inflammation and atherosclerosis in men: The DNASCO Study. Annals of Internal Medicine, 15 June, 140:12:1007-1014,
  274. Lichtor T et al. 1987.The sympathetic nervous system and atherosclerosis. J Neurosurg Dec;67(6):906-1,Pauletto P et al. 1991. Sympathetic drive and vascular damage in hypertension and atherosclerosis, Hypertension Apr;17(4 Suppl):III75-81.
  275. Wikstrand J, Berglund G, Hedblad B, Hulthe, Wikstrand J. 2003.Anti-atherosclerotic effects of beta-blockers. Am J Cardiol. Jun 19;91(12A):25H-29H.
  276. Sipahi I et al. 2007. B-Blockers and progression of coronary atherosclerosis; Pooled analysis of 4 intravascular trials. Annals of Internal Medicine, 3 July, V147; Issue 1: 10-18
  277. Mesquita QHde, Kerbrie SV, Mari SM, Baptista CA, Monteiro J, Maciel MC. 1978. Preservação funcional do miocárdio isquêmico pelo cardiotonico a longo prazo: recateterização de 29 casos. Medicina de Hoje, março 1978
  278. Hansson GK. 2005. Inflammation, atherosclerosis and coronary artery disease, NEJM V 352; N16 April 21.
  279. Malcolm Kendrick. 2007. Are statins overused? Future Lipidol, 2 (5)
  280. Player MS, King DE, et al. 2007. Psychosocial Factors and Progression From Prehypertension to Hypertension or Coronary Heart Disease, Ann Fam Med ;5(5):403-411. Full free paper at http://www.medscape.com/viewarticle/565806?src=mp.
  281. Palatini P, Longo D, Zaetta V, Perkovic D, Garbelotto R, Pessina AC. 2006. Evolution of blood pressure and cholesterol in stage 1 hypertension: role of autonomic nervous system activity, J Hypertens.Jul;24(7):1375-81.
  282. Grassi G, Quarti-Trevano F, Seravalle G, Dell’Oro R. 2007. Cardiovascular risk and adrenergic overdrive in the metabolic syndrome. Nutr Metab Cardiovasc Dis Jul; 17(6): 473-81.
  283. Choi CS, Kiim YB, Lee FN, et al. 2002. Lactate induces insulin resistance in skeletal muscle by suppressing glycolysis and impairing insulin signaling. Am J Physiol Endocrinol Metab 283: E233–E240, 2002. Full free paper at: http://ajpendo.physiology.org/cgi/content/full/283/2/E233,
  284. Tentolouris N, Tsigos C, Perea D et al. 2003. Differential effects of high-fat and high-carbohydrate isoenergetic meals on cardiac autonomic nervous system activity in lean and obese women. Metabolism. Nov;52(11):1426- 32.
  285. Calynn Davis Bunol, 2005. Thesis, Autonomic nervous system modulation of the heart following a high carbohydrate liquid meal, December. Full free paper at http://etd.lsu.edu/docs/available/etd-09082005-165133/unrestricted/Bunol_thesis.pdf
  286. Erkilla AT, Matthan NR, et al. 2006. Higher plasma docosahexaenoic acid is associated with reduced progression of coronary atherosclerosis in women with CAD. J Lipid Res; 47: 2814-19 Full free paper at http://www.jlr.org/cgi/reprint/47/12/2814.
  287. Ogilve GK, Fettman MJ et al. 2000. Effect of fish oil, arginine, and doxorubicin chemotherapy on remission and survival time for dogs with lymphoma: A double-blind, randomized placebo-controlled study, Cancer; 88: 1016-28. Full free paper at: http://www3.interscience.wiley.com/cgibin/fulltext/75504731/PDFSTART
  288. Graziani Y. 1977. Regulation of cyclic AMP level and lactic acid production in Ehrlich ascites tumor cells. Biochim Biophys Acta April 27;497(2):499-506.
  289. Nazam Ansari N, Bhandari U, Pillai KK. 2007. Protective role of curcumin in myocardial oxidative damage induced by isoproterenol in rats. Hum Exp Toxicol, Dec;26(12):933-8.
  290. Dernek S et al. 2004. Cardioprotection with resveratrol pretreatment: improved beneficial effects over standard treatment in heart rats after global ischemia. Scand Cardiovasc J Aug;38(4):245-54.
  291. Al Makdessi S, Sweidan H, Müllner S, Jacob R. 1996. Myocardial protection by pretreatment with Crataegus oxyacantha: an assessment by means of the release of lactate dehydrogenase by the ischemic and reperfused Langendorff heart. Arzneimittelforschung Jan;46(1):25-7.
  292. Leor J, Goldbourt U et al. 1995. Digoxin and increased mortality among patients recovering from acute myocardial infarction: importance of digoxin dose, Cardiovasc Drugs Ther. Oct;9(5):723-
  293. Adams KF Jr, Patterson JH et al. 2005. Relationship of serum digoxin concentration to mortality and morbidity in women in the digitalis investigation group trial: a retrospective analysis. J Am Coll Cardiol. Aug 2;46(3):497-504.
  294. Wycoff C.C. 1969. New Concepts of Digitalis, Calif Med. 1969 December; 111(6): 423–432. Full free paper at http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1503737.
  295. T Bjornheden, M Levin, M Evaldsson, O Wiklund. 1999. Evidence of hypoxic areas within the arterial wall in vivo, Arteriosclerosis, Thrombosis and Vascular Biology; 19:870-87.
  296. Quick AJ. 1935. The effect of exercise on the excretion of uric acid. The Journal of Biological Chemistry. Full free paper at: http://www.jbc.org/cgi/reprint/110/1/107.pdf
  297. Flierl MA, Rittirsch D, Nadeau BA et al. 2007. Phagocyte-derived catecholamines enhance acute inflammatory injury. Nature Oct 11;449 (7163):721-5
  298. Lee KS and Klaus W. 1971. The subcellular basis for the mechanisms of inotropic action of cardiac glycosides. Pharmacol Rev 23:193-261
  299. Wen Y, Leake DS. 2007. Low density Lipoprotein oxidation undergoes within lysosome in cells. Circ.Res. 100;1337-1343. Full free paper at http://circres.ahajournals.org/cgi/content/full/100/9/1337
  300. Marshall MW and Iacono JM (1976). Changes in lactate dehydrogenase, LDH isoenzymes, lactate, and pyruvate as a result of feeding low fat diets to healthy men and women. Metabolism. 1976 Feb;25(2):169-78.
  301. Yoshimura T, Miyoshi T, et al. (1986). Effect of high carbohydrate diet on serum lactate
  302. dehydrogenase isozyme pattern in Japanese young men. Acta Biol Hung. 1986;37(3-4):243-8.

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