The 9 principal causes of CAD and how to fight against them.
Heart Attack and Stroke caused by Atherosclerotic hardening of the arteries was relatively rare up the 1900s but after the First World War things changed. People started smoking a new product called cigarettes and stopped walking and cycling and riding and started using motorized vehicles to get places. Also the common foodstuffs which came straight from farms and gardens became adulterated by mass production. This resulted in more endothelial laceration and the physiology of the plaques in everyone’s arteries changed: they became unstable with liquid cores. Ergo: the generation born in the Western world during the First World War started getting ‘Heart Attacks’ in their early middle age i.e. in the 1950s. About 60% of these First Time Heart Attacks died during the attack without reaching a hospital.
This epidemic of Arteriosclerotic based Coronary Thrombosis and Myocardial Infarction soon took over from Tuberculosis and Infectious Diseases as the most prevalent cause of death and disability in the Western world.
The research triggered by this epidemic of Coronary Heart Disease in the 1950s gave insight into the onset of the disease, the impact on the arteries, the causes and gave way to methods for prevention. The first thing that came from the epidemic was the onset of CAD. A study done after the Korean War that conducted autopsies on Western soldiers killed in action showed extensive Coronary Arteriosclerosis had already occurred in these young men in their early twenties and these findings were replicated later in Vietnam. This phenomenon was confirmed later by research such as the Bogalusa and Muscatine Heart Studies on North American teenage victims of road accidents and suicides showing a connection between risk factors and blocked arteries: between higher levels of Blood Cholesterol and Blood Pressure and Blood Sugar and Obesity and the development of advanced fibrous streaks and plaques especially if the individual had smoked. Other studies followed and now it is universally recognized that adolescent men with high risk scores will have established irreversible disease by the age of 25 and adolescent women by 10 years later.
The second thing that came out of the epidemic was research into the causes of established arteriosclerotic disease in young men and women. One of the most significant risk factors was a Family History of Premature Coronary Heart Disease, (PCHD). If a Father or Grandfather or Male Siblings had a Coronary Artery event before the age of 55, or a Mother, Grandmother or female Siblings before 65, the adolescent was at increased risk of a future event. As a Family History of Premature Coronary Artery Disease, PCHD), is the first red flag in assessing risk in young people; why not offer a free ApoB/Apo A ratio to all schoolchildren with a known Family History of PCHD.
The 2004 INTERHEART study involving 27 countries showed 9 principal, but modifiable, causes of CAD. The study found, “that nine easily measured and potentially modifiable risk factors account for an overwhelmingly large (over 90%) proportion of the risk of an initial acute myocardial infarction”.
This is huge. This study provides us with the causes of CAD and how to lower our risk and the damages we cause to our heart.
The study found the nine causes in order of importance*:
*NOTE: Those with Family History of Premature CAD (Male family member <55 years of age, Female family member <65 years of age), should have their risk monitored regularly and take control of these 9 causes as their risk is significant.
1. High Apolipoprotein B/Apolipoprotein A ratio
Lipoproteins are the carriers of LDL Cholesterol and HDL Cholesterol in the blood stream. They are indicators of how damaging the particle size of high LDLC and low HDLC is to the artery wall. Small LDLC particles are like machine gun bullets, large LDLC particles bounce off. Additionally, Blood Lipid or Cholesterol levels: if the level of Low Density Lipoprotein, (‘bad”), Cholesterol was abnormally high or the level of High Density Lipoprotein, (“good”) Cholesterol was abnormally low the risk increased exponentially. The famous Framingham Heart Study in Massachussetts showed that for every 1% that “bad” cholesterol was lowered the risk was lowered by 2%.
2. Smoking Behaviours
Smoking, the number of cigarettes per day and the years of smoking increases the risk of myocardial infarction. INTERHEART (2004) found that individuals who smoked 40 cigarettes per day had a 9.16 odds ratio of myocardial infarction and smoking even five cigarettes per day increased risk. Added with other risk factors the odds increased. Smoking and high ApoA/ApoB ratios are shown to be the two highest causes and risk factors associated with CAD. Smoking adds unstable Arteriosclerotic lesions, increasing the build up on the arteries.
3. Diabetes Mellitus
Diabetes is a metabolic disease that leads to high blood sugar levels, which can damage organs, blood vessels and nerves. (Diabetes Canada). Like smoking, Diabetes adds unstable Arteriosclerotic lesions, increasing the build up on the arteries. Diabetes also affects the micro vasculatures causing damages to the heart, often causing heart failure. The study found Diabetes to play a significant role in the increased risk for CAD.
Hypertension is the medical term used to describe high blood pressure. Blood pressure is the force of the blood pumped from the heart against the blood vessels. This force makes blood flow possible, delivering nutrients and oxygen to organs and tissues throughout the body. Hypertension occurs when there is too much pressure in your blood vessels. This can damage your blood vessels and cause health problems. Anyone can develop high blood pressure, but it becomes more common as you get older. (Hypertension Canada). The study found Hypertension was a cause of CAD and when present with other causes accounted a significant risk of CAD, including Heart Attack and Stroke.
5. Abdominal Obesity
Abdominal Obesity in the INTERHEART study included the waist/hip ratio, more important for children than BMI. Waste Circumfrence should be half you height or less inches. Most Obese individuals have a genetic base to their condition. Either Mother or Father was also Obese. There is in fact a Familial condition in many people at birth where the bacteria in the colon absorb every calorie of carbohydrate. In recent years the amount of sugar and adulterated fat used by the Food Manufacturing industry is enormous. So those with a genetic absorption of carbohydrates will have a lifelong struggle with their weight because the digested carbohydrate is turned into glucose for energy and any excess glucose is converted to glycogen and stored in fat cells which will not release it unless there no more carbohydrate is available. Which in today’s world is generally never. Obesity is a disease of adipose cells; either Adipose hypertrophy, (fat cells are too large), or Adipose hyperplasty, (fat cells are too many). If obesity is confronted in childhood it can be held in check for a lifetime. Trying to reverse Obesity as an adult is a morass of complexities: yoyo dieting, activity, inactivity, metabolic rate, insulin resistance, mental condition, job satisfaction, response to hunger. It rarely is successful.
6. Psycho-social factors
The study found psycho-social factors including depression, locus of control, perceived stress, and life events played a role in increasing CAD in individuals. Findings indicate there is a great impact of psycho-social on women than men, 45·2% vs 28·8%, yet have a significant impact the risk of CAD for both groups.
7. Fruit and vegetable consumption
INTERHEART found regular consumption of fruits and vegetables was associated with a 30% relative risk reduction. The other CAD villains are synthetic Trans, (or cis ), Fatty Acids. These are found in almost all the fast food and prepackaged food we eat today. The end point of these digested particles of fatty acid is Very Low Density Cholesterol, (VLDL), which should be cleared by the liver but if in excess is converted into the “bad” form of LDLC which is what creates the sandbars which stick in the artery wall. Again the LDLC clearance rate is genetic. Some people clear their LDLC no matter how much fast food they eat. The aim is to start life by choosing a lifestyle which creates arterial walls whose endothelium resembles ‘teflon’: where everything slides along it. Not ‘Velcro’ where everything sticks to it.
The Glycogen storage problem and the LDLC clearance rate problem are two inherited conditions which divide young people into groups. One group can eat what they like and never put on weight; one group can eat what they like and never get hardened arteries. The other groups puts on weight by looking at food or have hardened arteries by the age of 25 by eating the wrong things and choosing the wrong lifestyles. It is hard for the latter groups to accept that they are different from the former groups. Especially as no-one informs them of it. To get the Food Industry to change their products why not recruit the groups of the population to whom their present products are toxic rather than lecture everyone on eating better every February.
8. Physical Activity
Physical Inactivity (excessive sedentary behaviour) has been shown to increase rates of CAD as a result of increase weight gain, lowered muscle tone, reduced stamina and use of the heart muscle to circulate blood flow.
9. Alcohol Consumption
According to INTERHEART (2004) Promotion of the consumption of moderate alcohol to prevent myocardial infarction might also not be acceptable to many populations, for cultural or religious reasons, and might increase the proportion of heavy drinkers and thereby enhance the risk of other diseases such as strokes, some cancers, cirrhosis of the liver, or injuries. The overall PAR without alcohol included in the model is 89·7%; adding alcohol increases it by less than 1% because of the substantial overlap in contributions of other risk factors. Lower on the causes of CAD, yet when present with additional risk factors can cause more damage.
How to avoid CAD?
The answer is clear
1. Know your family history
2. Know your Cholesterol numbers, ask if your Doctor if you need to know your ApoB/ApoA1
3. Live Smoke Free
4. Eat a non-atherogenic diet including daily consumption of fruit and vegetable and avoiding processed, trans-fat foods
5. Be active and avoid excessive sedentary behaviours
Based on what we know about the causes of the disease, the onset of the disease and how to reduce our risk, it is clear we need to being in adolescence before the damage is too great and irreversible. Education of risk factors and the awareness of the potential fatal outcomes of CAD must be taught to the whole population before it is too late. By following the steps above, eating fruit and vegetables, taking exercise, and avoiding smoking, INTERHEART suggests, could lead to about 80% lower relative risk. We know this. It is time we do something about it.
We need to take this research as seriously as a heart attack. It is never to early to address our risks for CAD.
To stop hardening our hearts, we need to lead a healthy lifestyle and know our numbers . We must take care of our arteries.We must start before the damage is too severe and irreversible. This means addressing CAD in adolescences. In order to reach the whole population, we need to go where we can provide all adolescents the same benefits and opportunities. Schools are the only place where we can see the whole adolescent population.