HOW CHOLESTEROL MOVES IN THE BODY.
[This is an exact excerpt from my new book… “Youthing: Look Younger, Stay Healthier, Live Longer”.]
Dr Andrew Saul used the analogy of a bus line, which is an apt one.
Since cholesterol is an oily substance that travels through a watery bloodstream, it must be carried to various destinations in the body. He explained that HDL cholesterol contains more protein than lipid or ‘oil’ material. Protein is denser than lipid, hence the name ‘high density lipoprotein’. The HDL carries this dense cholesterol as cargo straight to the liver and is eliminated via the gall bladder and intestines. The LDL ‘Bus Line’ contains more lipid or ‘oil’ than protein, hence the name ‘low-density lipoprotein’. The LDL Bus Line transports cholesterol to a variety of sites in the body, where it is used to repair or protect tissues or to be used in the synthesis of many vital compounds.
LDL cholesterol’s role is so important that nature lets the LDL Bus Line transport twice the number of cholesterols ‘passengers’ as the HDL Bus Line does.
LDL cholesterol is thus taken to important destinations in the body such as:
- Skin, cholesterol reacts with sunlight to produce the ‘best kind’ Vitamin D.
- Sex hormones (oestrogens, testosterone, and progesterone).
- Nerve cells so they are well-insulated and don’t short circuit.
- Scar tissue to repair tissue injuries.
- Cell walls to ‘waterproof’ us so we don’t melt in the rain or when we take a bath.
- Blood vessels for vital cardiovascular repairs, as well.
God designed the body exquisitely, and clearly contrary to the well-advertised scaremongering belief that LDL cholesterol is bad and we must lower it with statin drugs. Cholesterol’s real mission is to save our lives, not to kill us.
Lipoprotein A or Lp(a) – The Real Culprit
Lipoprotein A, otherwise known as Lp(a), is another special cholesterol carrier found only in the few species that do not produce their own ascorbic acid, such as humans.
Its mission is to patch up damaged blood vessels. Lp(a)’s protein coat is very sticky — think of the ‘a’ as meaning ‘adhesive.’ The ‘sticky’ Lp(a) particle circulates through the vessels and adheres to spots where a blood vessel wall is damaged.
Due to the Velcro-like surface of Lp(a), circulating LDL particles also will adhere where Lp(a) is busy patching, escalating the process of atherosclerosis formation.
When there are higher ascorbic or Vitamin C concentrations, the amount of Lp(a) is less because this leads to less production of the sticky Lp(a) particles.
Dr Ron Kennedy wrote some interesting Facts About Lp(a) in his book Lipoprotein(a), Vascular disease and Vitamin C.
- Lp(a) levels are influenced by genetics (inheritance).
- Diet does not influence Lp(a) levels.
- Cholesterol-lowering drugs have not been shown to lower Lp(a) levels.
- Both ascorbate (vitamin C) and niacin (vitamin B-3) have been shown to lower Lp(a) levels.
- Natural amino acids, L-lysine and L-proline, prevent the outer coat (apo-a) of a Lipoprotein A carrier from being sticky. These amino acids convert apo-a from a ‘Velcro’ to a ‘Teflon’ quality. L-lysine and L-proline also help remove plaque that is already present in blood vessels displacing Lp(a) cholesterol from artery walls.
CHOLESTEROL – THE HIGHS and LOWS
HIGH LDL – A relatively high LDL reading may indicate the body needs to repair a lot of things and transport cholesterol to areas of stress or disrepair. 179
LOW HDL – A low HDL reading may mean the body needs to hold on to cholesterol to both make repairs and to synthesise molecules that are scarce.
Lower LDL and High HDL — when we ‘artificially’ lower our cholesterol through pharmacological inhibitors (like ‘statin’ drugs), we really cannot infer anything about our state of health with regards to cholesterol levels.
With drugs, we can make less cholesterol available to block our blood vessels, but at the same time, we will make less cholesterol available to perform vital functions (like converting sunlight to vitamin D, insulating nerve cells, healing scars, etc.).
Dr. William Castelli, director of the prestigious Framingham Study, wrote:
“Total cholesterol, as it turns out, has never been an indicator of who is more likely to suffer a heart attack. The more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower peoples’ serum cholesterol…we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active.’
The ongoing Framingham population study also found that there was virtually no difference in coronary heart disease events for individuals with high cholesterol or low cholesterol levels. Even for those with extremely high cholesterol levels.
Now that being said, please do not take this as carte blanche to consume as much saturated fat and calories as you want, but because cholesterol supports so many essential physiological processes, it doesn’t make a lot of sense to pharmacologically inhibit cholesterol production 180 to ‘get our numbers right.’ In fact, in study after study, the group with the lowest cholesterol levels had the highest mortality (death due to all causes).
I find the mortality rates for those with the lowest cholesterol readings particularly troubling. I believe it’s far better to help our bodies make necessary repairs and let the numbers ‘fix’ themselves. Nature ultimately does not waste energy, so when less cholesterol is needed, less cholesterol will be produced.”
Let’s look at the number one cause of death – Heart Disease:
Heart Disease and Cholesterol:
The lipid theory is disproven, your body needs cholesterol to protect nerve tissue, to act as an anticoagulant, to buffer cells from toxic agents, to protect cell membranes, to help maintain memory, and to assist in production of vitamin D3.
THE FRAMINGHAM HEART STUDY: This began in 1948 and is ongoing to date.
The Framingham Heart Study is a long-term, ongoing cardiovascular study of residents of the city of Framingham. Massachusetts. It was a study that was initiated by the United States Public Health Service to investigate the epidemiology and risk factors for cardiovascular disease.