Cardiovascular Disease (CVD) is still the number one killer in the western world! Despite this being the case for the last 60+ years and despite the figures actually falling since the 1970’s, mainstream medical research is still looking for the ‘magic bullet’, the elusive ‘cure’ that is deemed to be in a pill form, for this number one cause of death in the developed world. The best that they have been able to come up with, regarding treatment, is a whole wrath of new ant-hypertensive drugs and perhaps the biggest scourge of the 21st century – the statin family of drugs for lowering cholesterol!
In 2014 over 45,000 deaths were attributed to CVD in Australia, whilst in the US over 610,000 deaths were caused by CVD – most of these preventable. Interestingly, there are measurable variations in community sectors when influencing factors such as ethnicity, socio-economic status and geographic placement are considered. But when meta-analyses are studied and the data correlated, most of the reporting emphasis (to the public) is placed on areas that drug therapy can be applied (to generate huge profits for the Big Pharma who funded the study), rather than high-lighting, and thus accentuating, the more fundamental (but not so profitable) and vitally critical influences that diet and lifestyle have on the treatment and prevention of CVD!
Even today with there being so much available published scientific evidence indicating that there has been far too much emphasis placed on the influence that cholesterol has on the progression of CVD, the general medical fraternity still throws a spotlight on lowering cholesterol levels as the major combatant in the fight to treat and prevent CVD. This is clearly a case of big pharma’s influence on grass roots general medical practice and their agenda to maximise statin drug sales.
But let’s turn our focus towards what really are the major indicators we should be looking at when establishing CVD risk analysis and what natural protocols and frameworks you can put in place to make sure that your risk factors are minimal.
So let’s look at some Quick Facts pertaining to Your Health and CVD:
- Saturated fat is an excellent source of energy and supports healthy cellular function, since your cellular membranes are comprised mainly of saturated fat and many hormonal and metabolic processes utilize saturated fat. There has never been any scientific evidence presented to confirm that consuming saturated fat by itself is unhealthy.
- Saturated fat, primarily from animal products, has been a dominant source of calories for humans throughout evolution.
- Modern medicine has promoted a false association between high levels of fat in the diet and high levels of fat in the blood (aka, high triglycerides). High triglycerides in a fasted state are confirmed to be unhealthy, but are associated with excess carbohydrate intake, not fat intake.
- Low density lipo-protein (LDL) converts from very low density lipo-protein (VLDL) into either small, dense LDL or large, fluffy LDL. Small dense LDL is more inclined to be dangerous because it can lodge in the arterial wall and become oxidized and inflamed. Traditional blood readings for LDL are of little to no value when assessing heart disease risk. Interestingly, the majority of heart attack victims have a ‘safe’ LDL value.
- High density lipo-protein (HDL) cholesterol protects against heart disease by cleansing the blood stream of potentially damaging small dense LDL molecules. Consuming saturated fat helps elevate LDL levels, since HDL is used to digest fat. A sensible exercise program has also been shown to elevate HDL.
- Statins have minimal impact on the most important heart disease risk factors and have numerous problematic side effects that can compromise health. Dietary and lifestyle modification can quickly and dramatically reduce CVD risk factors, as revealed in blood values for HDL, triglycerides, assorted inflammation markers like C-reactive protein and small, dense LDL.
- The true catalysts for CVD – oxidation and inflammation – occur from adverse dietary habits and lifestyle practices that are totally unrelated to saturated fat and cholesterol intake, but closely related to excess carbohydrate intake/excess insulin production and excess intake of easily oxidized polyunsaturated fats.
- Some other lifestyle practices that promote oxidation and inflammation in the blood stream are smoking, poor stress management, insufficient sleep, excess alcohol consumption and chronic, overly stressful exercise patterns.
The CVD Process
The delicate and sensitive Endothelial Cell Layer (ECL) of your arteries has been damaged due to systemic inflammation and oxidation. This inflammatory damage makes it easier for small, dense LDL loaded with triglyceride (excess insulin = excess triglyceride = a pattern of fat storage instead of fat burning) to lodge in the ‘gap junction’ between the cells in the damaged ECL. As Dr. Sinha explains in The South Asian Health Solution, “Your ECL is in constant contact with your blood and can detect even the most subtle chemical disturbances arising from poor nutrition or negative emotions. It responds to any damage or perceived threats by sounding the inflammation alarm. In a healthy body the inflammation crew is remarkably effective in making repairs and keeping the ECL in great condition. However, in an unhealthy body, this pro-inflammatory emergency response system often does more damage than good.”
Interestingly, in a healthy body, cholesterol molecules can be used as a temporary band-aid to cover lesions in the ECL. When the state of inflammation subsides the cholesterol leaves the now healed ECL lesion and is recycled back to the liver by HDL. When inflammation is chronic, problems can breed with small, dense LDL on the ECL as described above. They remain in place for too long and the inflammation is exacerbated by an inflammatory white blood cell (macrophage) immune response, and the LDL molecules become oxidized by the constant exposure to haemoglobin on the arterial wall.
It’s likely, that the original flawed association between cholesterol and CVD came about from the simple observation of cholesterol molecules forming plaque on the arterial walls of deceased heart attack victims. In other words blame was placed on the band-aid (cholesterol attached to the ECL) rather than examining the cause of the original wound, and why it became ‘infected’ (inflamed and oxidized) and eventually fatal.
When small, dense LDL molecules become lodged in the ECL, they are exposed to oxygenated blood (haemoglobin) passing through the arteries. This constant oxidative exposure causes the area to become inflamed and to form the familiar plaque on the arterial walls that characterizes atherosclerosis.
The immune system, reacting to this undesirable plaque formation, sends macrophages (scavenging white blood cells designed to engulf and digest cellular debris) to the area in an effort to mitigate the damage. The macrophages rush to the scene and attempt to devour the small, dense LDL. While well intentioned to begin with, the macrophages become overwhelmed by the major effort and expand in size to become what are known as Foam Cells. These foam cells produce a chemical known as myeloperoxidase, which further oxidize LDL particles. Foam cells also release chemicals called cytokines into the blood stream which attract more macrophages to the area to cause further inflammatory damage.
Coagulation (clot formation) eventually causes a significant obstruction – a fat-filled tumour known commonly as ‘plaque’ – on the ECL. As oxidation and inflammation continue, the plaque becomes stiff and calcified and more susceptible to rupture. Once a rupture occurs it can block the artery on the spot, or more commonly detach from the artery wall, drift into circulation and eventually cause a stroke (blockage of an artery on route to the brain) or a heart attack – aka myocardial infarction (blockage of a coronary artery).
Importantly again, the real heart disease catalysts are:
- Excess Insulin (caused by a high carbohydrate diet) – promotes inflammation, stiff arteries, sticky platelets.(clot formation) and oxidized small, dense LDL.
- High Triglycerides (from a high carbohydrate diet) – promotes conversion of VLDL to small, dense LDL instead of large fluffy LDL and locking into fat storage pattern (promoting weight gain).
- Excess Cortisol (from poor diet, chronic exercise, insufficient sleep and chronic emotional stress) – chronic stress promotes an inflammatory environment in the blood stream and damage to the sensitive ECL.
- Insufficient HDL (from poor diet , statin use and chronic exercise) – the body is less efficient at clearing oxidized cholesterol from the blood stream leading to further ECL damage.
LDL blood test readings are minimally relevant to CVD risk. More relevant blood tests to track CVD risk are:
- Triglyceride : HDL ratio (3.5:1 or less is imperative but 1:1 or better is ideal)
- Blood Pressure (too high = poor ECL function)
- Vitamin D
- HbA1C (average blood glucose long term)
- Fasted glucose
- LDL particle count (breakdown of small, dense and large, fluffy LDL and also VLDL)
- Systemic inflammatory markers like C-Reactive protein, Homocysteine and CPK
- Coronary calcium score – a scan that reveals the amount of arterial calcification around the heart
It is now becoming more widely accepted that excess carbohydrate consumption drives high triglycerides in the blood and that consuming saturated fat – long maligned as a heart disease catalyst – is entirely healthy and in fact a centre piece of the human diet for hundreds of thousands of years.
Next week let’s examine the ideal dietary and lifestyle patterns to adopt for maximum cardio-vascular system support!