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I have heart disease, so this is personal!
I had a quad-coronary bypass in January 2001; two of those grafts closed up over time and in February 2014, one was stented to reopen it while the other was abandoned and the bypassed artery stented in three places. The stented artery became re-blocked (restenosed) and was restented (a stent within a stent) in December 2014. I am currently symptom-free and can push as hard as I want during exercise with no problems.
For the last 15 years I have been researching the literature for the causes for atherosclerosis (the name for plaque buildup in arteries), and there are many, but the science of the disease has become more clear in the last few years. Still, there is considerable disagreement among authorities about the actual causes and the best strategies to avoid or heal the disease. In this category I attempt to present the known causes and strategies for avoiding or living with this disease.
The plaque-building process starts at a young age
Arterial Plaque has historically been seen in autopsies of young, deceased soldiers in our national conflicts and wars. Arterial health has improved over the last few generations, so atherosclerosis rates seen in soldiers in Korea, Vietnam and Iraq/Afghanistan has declined respectively: 77%, 44% and 8.5%. Part of this reduction is attributed to reduction in smoking rates, but also on other lifestyle and nutrition changes.  The point is that the process starts in youth, often long before we see any rise in blood pressure or cholesterol levels, so strategies for prevention need to be inculcated at a young age for the best outcomes.
However, atherosclerosis is considered a “disease of aging” and its progression accelerates with aging and becomes symptomatic typically in middle age and beyond. Most of the factors involved in this acceleration are discussed in this study reference.  The study points to cellular senescence (cells getting old and ceasing to function well) as a major factor, and details several mechanisms by which the cells involved in artery structure get old and add to the disease progress. It offers some thoughts on prevention or healing, but mostly clarifies what goes wrong unseen in our arteries.
Aged endothelial cells (ECs) and aged vascular smooth muscle cells (VSMCs) make arteries stiffer, raise blood pressure, raise vascular inflammation, encourage the formation of arterial plaque and speed up the closing down of arteries as seen in coronary artery disease. This is a very informative study – if you can wade through it; it’s well worth reading. The basic message is this: whatever we can do to slow cellular aging will also reduce the speed at which atherosclerosis progresses.
Do you see a disconnect here? Aging may accelerate the final stages of the disease, but it can’t be the cause of it because it starts in youth. We need to know what initiates the process in the first place and eliminate the cause, and we need to know how to reverse the process if it has started in our past.
I started smoking at age 12 and finally quit when I was 24. There is a mountain of evidence that the chemicals taken in by inhaling tobacco smoke make an immediate assault on the lining of our arteries, and can be an initiating element in arterial plaque development. One significant study summed it up like this:
“In conclusion, smoking can cause production of dysfunctional lipoproteins having a smaller particle size that exacerbate senescence and atherogenic progress due to oxidation and glycation.” 
The key concept here is “dysfunctional lipoproteins”. In most of the literature, the prominence of these dysfunctional lipoproteins is referred to as “Dyslipidemia”. The essential characteristic of dyslipidemia is that our lipoproteins are smaller and malformed such that they cause arterial damage and promote the buildup of plaque in our arteries.
Lipoproteins – How Fats Move Through Our Blood System (remember that oil and water don’t mix)
Lipoproteins are small, spherical protein cages that carry fats in our bloodstream. Recall that water and oils don’t mix and so to move oils and fats through our blood stream, we make these cages that are water-friendly on the outside and fat-friendly on the inside. Our liver makes most of them to transport lipids (fatty acids, triglycerides and cholesterol) to our cells for fuel, or to make functional or structural components in the cells, as well as providing the substrate for our sex hormones. They are classified according to the density with which fats, including cholesterol, are packaged in them for transport in our blood stream. So they are referred to as Very Low Density Lipoprotein (VLDL), Intermediate Density Lipoprotein (IDL), Low Density Lipoprotein (LDL), and High Density Lipoprotein (HDL).
The liver initially makes VLDL as the empty carrier for various fats and then, as the liver is the primary processor of all dietary fats, it packages fats into these particles at various densities, depending on their purpose and sends them into the blood stream for transport. The liver also makes HDL particles, also made by the cells lining the intestines, which are empty of any form of cholesterol.
HDL is different in that it is involved in bringing unused fats back to the liver and also functions as an antioxidant in the process. When it returns cholesterol from the body, that is called Reverse Cholesterol Transport, and is the primary way that HDL reduces or prevents arterial plaque buildup. 
For many decades science has mistakenly thought that the more LDL we produced, the faster our arteries plug up; but the process proves to be much more complex. Under a variety of stress conditions, our liver can make smaller, more dense lipoproteins, primarily LDLs, which are dysfunctional in that they can be easily damaged.
Damaged LDLs become invasive in the artery walls, burrowing under the endothelial cells lining all arteries, creating local inflammation that brings immune cells into the artery wall which become part of the plaque. The question now being settled is whether immune cells are first attracted to damaged LDLs (and other damaged lipoprotein elements) and then invade the artery lining, or rather are gobbled up by immune cells which then burrow into the artery wall?
The starting point for prevention of heart disease, it seems to me, is to understand how dyslipidemia gets started in the first place.
Causes of Dyslipdemia
Hypothyroidism and Dyslipidemia
Hypothyroidism is the most common pathologic hormone deficiency among the endocrine disorders. It is characterized by declining levels of thyroid hormones T4 and T3, with rising TSH. Hypothyroidism may be due to primary disease of the thyroid gland itself or hypo-secretion of the pituitary TSH. Thyroid hormones have significant effects on synthesis, mobilization and metabolism of lipids. Overt hypothyroidism is associated with elevated cholesterol, but more importantly, with elevated levels of small-dense LDL (sdLDL) and oxidized LDL (oxLDL), which are proving to be causative factors in artery disease initiation and progression. 
It remains to be seen whether thyroid deficiency is a primary initiating cause of dyslipidemia, but the latest research shows that it is a contributing factor.
Metabolic Syndrome and Dyslipidemia
Metabolic Syndrome is a set of multiple risk factors that lead to atherosclerotic cardiovascular disease and type 2 diabetes. These include atherogenic (builds plaque in arteries) dyslipidemia, elevated blood pressure, insulin resistance and elevated blood sugar, a pro-thrombotic state, and a pro-inflammatory state. Excess energy intake (eating too much or too often) and resulting excess body fat storage (obesity) are the major drivers of the syndrome.
The latest science has led to this conclusion; metabolic syndrome is caused by excess food intake over a long time period, during which these metabolic malfunctions manifest and worsen. It is hastened by eating high-glycemic foods that excessively and repeatedly raise blood sugar until insulin receptors in many of our tissues and organs become insensitive to insulin and glucose levels in the blood remain constantly elevated.
This study cited above shows that the primary mechanisms that damage LDL are oxidation and glycation, and these encourage it to invade artery walls and build plaque. It is important to understand that these same mechanisms (oxidation and glycation) are inflicting damage in every body; they just damage us much faster if we smoke or eat a diet that leads us to have chronically high blood sugar.
Oxidation is a byproduct of using oxygen for energy production; we breath it in and exhale carbon dioxide, our red blood cells carry it to every cell in the body, where it is used to burn our food to make energy for cellular operation. Unfortunately it also interacts in varied ways to break things in the process. The damage accumulates with age, and some of that damage is to our lipoproteins – the small spherical protein cages that carry fats in our bloodstream; VLDL, IDL and LDL.
When oxidized, these particles attract immune cells (monocyte-derived macrophages) which engulf these damaged lipoproteins and are prone to invade our artery structures, become foam cells, leading to plaque formation. HDL prevents plaque formation by binding to macrophages and removing the damaged cholesterol, both in circulating blood plasma and in the space below the endothelium in the artery walls .
More to come – work in process.