DOES HIGH CHOLESTEROL CAUSE HEART ATTACKS and STROKES?

DOES HIGH CHOLESTEROL CAUSE HEART DISEASE?

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.

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.

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.”

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 where inflammation is 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 criticized – 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 is 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 Dr. Robert O. Young's book, The Cause and Cure for Atherosclerosis and Coronary Heart Disease.

To order the Kindle version go to: https://www.amazon.com/gp/product/B01KBMFRA4/ref=dbs_a_def_rwt_hsch_vapi_taft_p2_i8

What Causes Cancer, Heart Disease and Diabetes?

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.