What is a Heart Attack?

Below is an overview of the mechanism that leads to cardiac myocardial infarctions (or heart attack).  It took many decades for a basic understanding of this process.

The consensus at the beginning of the 20th century was that heart disease is a normal part of aging.  In 1913, a 28 year old pathologist, Nikolay Anitschkow (or Anichkov), working at the Military Medical Academy in St. Petersburg, showed that by feeding rabbits cholesterol dissolved in sunflower oil induced vascular lesions closely resembling those of human atherosclerosis, both grossly and microscopically. Controls fed only the sunflower oil showed no lesions. [1]

Another difficulty in understanding heart disease is that there are a number of factors involved.  Researchers, practitioners and the public become attached to one aspect.  Some argue passionately regarding one aspect of heart disease and become blind to other factors.

By the 1950s, a number of important advances had been made including the discovery of the mechanism for cholesterol transportation in the blood (via lipoproteins) and the mechanism for cholesterol to enter the artery wall from the blood.  Dr John Gofman was a leading pioneer researcher in the field of lipoproteins who was familiar with Anitschkow’s work.  His work showed that both cholesterol and low-density lipoproteins were both indicators of coronary heart disease risk.  This work and other evidence convinced Gofman that blood cholesterol, and the dietary determinants of blood cholesterol, was centrally important in atherosclerosis.  His wife, Dr. Helen F. Gofman co-authored a low-fat, low-cholesterol diet book [2] that was published in 1951.  John Gofman wrote the preface for the book.

Russell Ross and John Glomset wrote a two-part paper that was published in the New England Journal of Medicine in 1976 (31, 32).  Their paper proposed that an injury caused endothelial damage.  Later studies showed that the endothelial layer overlying the lesions was actually unbroken and the lesions were formed underneath the endothelial layer.  Even though it was not clear on the cause of the injury, the inflammatory response to this injury is an important factor.

In the early 1970s, Earl and John Benditt from the same department at the University of Washington proposed that the smooth muscle cells in each atherosclerotic lesion was a benign tumor originating from a single cell. [1]

Today, particularly in popular books, magazines and websites, a number of people argue passionately for a single cause of heart disease such as the inflammatory response to injury and deny that multiple factors (such as cholesterol) are involved in heart disease.

It is “Normal” to Die from Heart Disease

One difficulty in accepting the role of cholesterol in heart disease is that the “normal” ranges in Western countries are unhealthy.  It is also normal to die from heart disease.  30% of Australians (that is, 45,053 people) died from cardiovascular diseases in 2014. [2]

According to the Mayo Clinic, cholesterol should be below 200 mg/dL (5.2 mmol/L).

However, the following authorities have stated that they have never seen a heart disease fatality when cholesterol levels are below 150 mg/dL (3.9 mmol/L).

  • Dr William Roberts is a leading cardiovascular pathologist. He is the current editor (at 2016) of the American Journal of Cardiology—a position he has held since 1982.
  • Dr William Castelli served as the third director of the Framingham Heart Study from 1979-1995
  • Dr Caldwell Esselstyn has been associated with the Cleveland Clinic since 1968. He currently directs the cardiovascular prevention and reversal program at The Cleveland Clinic Wellness Institute.

Autopsies of 300 male soldiers killed in action in Korea showed 77.3% of the soldiers had gross evidence of heart problems.  The average age was 22 years, fit and active and had not been diagnosed with heart problems. [3]

Professor Lew Kuller from the University of Pittsburgh School of Public Health states, “All males who are 65 and all females who are 70 who have been exposed to the traditional Western diet have cardiovascular disease and should be treated as such.”

What is a Heart Attack?

Endothelial cells line all blood (arteries, veins, capillaries as well as the heart) and lymphatic vessels.  The endothelium is one cell thick.

  • When we start eating a high fat (or even a medium fat) Standard Western Diet, it increases the viscosity of the blood.  White and red blood cells, platelets, endothelial cells and low-density lipoprotein (LDL) particles containing cholesterol become adhesive – our blood becomes “sticky”.
  • The LDL particles that contain cholesterol enter into the space beneath the endothelium.
  • Plaques develop in the sub-endothelial space.  Plaques consist of macrophages, foam cells, dead foam cells, fats, cholesterol and smooth muscle tissue.  The plaques intrude into the arterial space.
  • Thrombosis (blood clot inside a blood vessel) at the site of a ruptured plaque precipitates most heart attacks (myocardial infarctions).
  • The vessel is completely blocked. If this is a small blood vessel within the brain, the person may not be aware of the situation. If it is a large vessel, the person will have a heart attack or a stroke.

How do you damage your endothelial cells?

The endothelial cells produce nitric oxide.  It only exists for a few milliseconds.   Nitric oxide dilates blood vessels and it also prevents cells in your blood from becoming adhesive.

Nitroglycerine is used to treat vascular conditions as it produces nitric oxide in the body.

A number of factors prevent endothelial cells from producing nitric oxide.

  • Hypertension (high blood pressure)
  • High cholesterol
  • High homocysteine
  • High triglycerides – all oils and fats including “healthy” oils such as olive, coconut and omega 3 fatty acids (fish oils and flaxseed oil).
  • Insulin resistance – which is caused by high fat content in muscle cells
  • Smoking

If you have a high fat meal then it compromises your ability to produce nitric oxide and at takes several hours to recover – just in time for your next high fat meal.

Healthy endothelial cells are essential to our health so doing everything possible to keep them from being damaged is imperative for our well-being.

Steps to Take

Keeping our blood vessels healthy is a key to many diseases and conditions.

Our kidneys are rich in fine blood vessels.  Kidneys are involved with filtering of the blood, absorption of nutrients, blood pressure regulation and maintaining correct pH levels of blood.

We can limit our risk of heart disease and other “diseases of affluence” by taking a number of steps.  Addressing only one issue, such as taking a tablet to reduce cholesterol, does not address other factors that are essential for optimal health.

Reduce Serum Cholesterol

Some dietary changes that diminish the amount of cholesterol in the blood are:

  • reducing saturated fats consumption
  • reducing animal protein consumption
  • reducing cholesterol consumption

Increase Anti-oxidants

Colourful fruit, beans and vegetables have high level of vitamins, minerals and phytochemicals that act as anti-oxidants that assist in preventing the inflammation stage.

Remove Added Oils from Diet

Dr Caldwell Esseltyn is a former surgeon who now treats people through diet.  He is adamant that there is no place in the diet for any added oils.

NO OIL! Not even olive oil, which goes against a lot of other advice out there about so-called good fats. The reality is that oils are extremely low in terms of nutritive value. They contain no fiber, no minerals and are 100% fat calories. And above all they contain saturated fat which immediately injures the endothelial lining of the arteries when eaten.

Olive oil, canola oil, coconut oil, sunflower oil, soybean oil, peanut oil, avoid any oil – They injure the endothelium, the innermost lining of the artery, and that injury is the gateway to vascular disease.

Prevent and Reverse Heart Disease – Caldwell Esselstyn

Check Homocysteine Levels

Homocysteine is a non-protein amino acid.  It is synthesised in the body from methionine which is a sulphur containing amino-acid.  Methionine is more prevalent in animal products than plant products.

A high level is of homocysteine is associated with an increased risk for chronic inflammation, cardiovascular disease and Alzheimer’s disease.

High levels indicate vitamin B12, B6 or folic acid (B9) deficiency. It can also be caused by smoking, alcoholism, hypothyroidism, kidney disease and diabetes.  There are also genetic conditions that result in high homocysteine levels.

Optimal level of homocysteine is 6 μmol/L or lower.  This may be lower than the reference range given by your pathology laboratory.

Maintain Correct Omega-6:Omega-3 ratio

The amount of omega-6 fatty acids in the food supply has increased and that of omega-3 fatty acids has decreased during human evolution from an estimated ratio of approximately 1:1 for omega-6:omega-3 to 25:1, based on various estimates. Omega-3 fatty acids decrease platelet aggregation, blood viscosity and fibrinogen (involved in blood clot formation). [4]

Decreasing the amount of omega-6 oils (found in grains, corn, safflower, sunflower and cottonseed) is a better way of decreasing the omega-6:omega-3 ratio than increasing the amount of omega-3 rich foods such as fish, fish oil and flaxseed oil.

To ensure an adequate amount of omega-3 oil in the diet, grind 20ml (1 tablespoon) of flaxseed in a spice grinder and add to meals each day.  In order to be digested, the flaxseed needs to be ground.  It is best to grind the flaxseed each day to prevent the oils from becoming oxidised.

Footnotes

  1. Steinberg, D. (2007) The Cholesterol Wars:  The Skeptics vs. the Preponderance of Evidence. San Diego, CA: Academic Press.
  2. National Heart Foundation (n.d.) Heart disease in Australia [online]. Available from www.heartfoundation.org.au/about-us/what-we-do/heart-disease-in-australia (Accessed 28 October 2016).
  3. Campbell, T. C. & Campbell, T. M. (2006) The China Study. Dallas USA: Benbella Books.
  4. Simopoulos, A. P. (1991) Omega-3 fatty acids in health and disease and in growth and development. The American Journal of Clinical Nutrition. (August), p112

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