I found this to-the-point excerpt in a health book I’m reading: Transcend. It does a good job of explaining a heart attack on a cellular level. It’s becoming more clear as I refine my sources that inflammation, sugar, bad cholesterol, and perhaps excess iron are some big bad baddies in our body – though these processes, fats, and minerals necessary, in excess we are killing ourselves (and everything is in excess and processed for easy consumption this day and age). This would mean eating an anti-inflammatory, antioxidant/phytonutrient rich, low glycemic-index super-food diet would be our best bet to undo a lot of damage we’ve done to our bodies (Dr.Greger’s food videos have an excellent approach at getting you to eat whole foods the very night you watch them). I’m trying it for 30 days and am noticing some positive results – some too embarrassing to mention 
It usually takes about 30 days to adopt a good habit, and to spark that habit it sometimes takes a jolt – an emotional imprint to show how truly fragile the situation is. So here is a quick point-by-point summary on what will/is killing our close friends and family (on a cellular level):
We now know that most heart attacks do not result from arteries blocked with the hard calcified deposits, or calcified plaque, that patients are shown by their surgeons. In fact, this type of hard plaque is rarely the cause of heart attacks; rather, it appears to be the result of the body’s attempt to wall off the real cuplrit, which is soft, noncalcified, or vulnerable, plaque. Soft or vulnerable plaque is flexible and dynamic. It rarely produces symptoms, does not appreciably block arteries, and is difficult to see on angiograms. Yet, vulnerable plaque is the real villain in the story.
This new understanding replaces the old model of heart disease and looks at it instead as a dynamic multistep process in which inflammation (the overactivation of the immune system) works first to create vulnerable plaque and then to lead it through an intricate and insidious cascade of events that ultimately ends in a heart attack. It is worthwhile to review the steps in the process that leads up to a heart attack because it guides our thinking on how to thwart this process at every stage.
The common wisdom used to be that only men need to be concerned about heart diseases. A 2002 survey by the society for Women’s Health Research showed that 60 percent of women fear cancer the most, compared with only 5 percent who were afraid of heart disease. So it may come as a surprise that heart disease is the number one killer of both men and women. Of the 1.1 million heart attacks each year, almost half occur in women.
The story begins with LDL (low density lipoprotein) cholesterol particles – the aptly named “bad” cholesterol We should note that LDL is not all bad; indeed we could not survive without it. LDL transports cholesterol from the liver to the body’s tissues, where it is needed to keep cell membranes healthy. It is also a precursor of our sex hormones. But when levels of LDL are higher than we need for these vital life processes, it accumulates inside the artery walls, where it can undergo pathological changes. LDL can react with oxygen to become oxidized and with excess glucose in a process called glycation (binding with sugar molecules). Once modified in this way, the LDL particles take on a different appearance. They no longer look friendly to the immune system and are easily mistaken for foreign invaders. The immune system responds by sending in different types of white blood cells, including monocytes and T lymphocytes, in an attempt to destroy the pathological LDL molecules.
After the monocytes encounter the LDL deposits, they become macrophages and begin to gobble up these deposits. These macrophages (from the Latin macro for big and phage for eater) have such big appetites, they eventually become stuffed with the LDL particles and become “foam cells,” so named because they look like bubbles of foam. This is the beginning of vulnerable plaque, which at this stage is called a fatty streak. Autopsies of soldiers killed in battle have shown that this early form of vulnerable plaque is quite common in 20-year-olds, and can even be found in children.
Note that the entire process above is associated with inflammation, basically an overactivation of the immune system. Inflammation, in fact, underlies every stage of this process. In the next step, inflammation causes the blood vessel’s smooth muscle cells to grow over the foam cells and form a fibrous cap. This is now a mature vulnerable plaque, which typically does not restrict bloodflow but just appears as a slight bulge in the outer diameter of the blood vessel. Vulnerable plaque has been notoriously difficult to visualize, but we have recently begun to be able to see images of it in the arteries of a beating heart using a new generation of noninvasive scanners, which are emerging as promising diagnostic tools.
The stage is now set for the coup de grace event of a heart attack, and is again fueled by inflammation. Prompted by substances produced by an overactive immune system, the fibrous cap can rupture, spilling the contents of the foam cells and other dangerous chemicals that they have produced. Specific elements in the bloodstream respond by forming a blood clot or thrombus to keep the contents of the foam cells from entering the bloodstream If the thrombus that forms is large enough to completely block the coronary artery, that’s a heart attack. The region of the heart normally supplied by this artery is now deprived of oxygen and other nutrients and will die if the blockage is not quickly reversed. It is important to note that, in most cases, until just moments before the heart attack, the artery was not significantly blocked by the vulnerable plaque. The thrombus formed suddenly after the rupture of the fibrous cap, with devastating consequences.
This new understanding motivates all of our recommendations for heart attack prevention. Since the process starts with excess LDL particles, keeping LDL at healthy low leels is our first recommendation. In addition to LDL, there is a form of cholesterol called HDL (high density lipoprotein), the “good cholesterol,” which clears LDL particles from the bloodstream and carries them back to the liver. So, keeping HDL levels high is another important approach.Keeping in mind that every stage leading to a heart attack is fueled by inflammation, we see once again another way in which our evolutionary Stone Age heritage is not on our side when we get to middle age. Infections were the most common form of death tens of thousands of years ago, so having a strong and highly reactive immune system was critical to the survival of the human species. At this earlier time in our evolution, very few people lived long enough to die from heart attacks, so there was little need to worry about the downsides of an overly active immune system that might cause a heart attack later in life. In addition, many aspects of our modern lifestyle, such as the wrong diet and excessive stress, increase the activation of the immune system and increase inflammation. So, our next perhaps most important strategy in preventing heart attacks is keeping our immune system robust enough to combat infections but avoiding its overactivation and subsequent inflammation. Each of our recommendations below fits into one of these overarching themes.
Several other risk factors have been associated with higher levels of heart disease, and removing each such factor has been shown in extensive studies to lower heart attack risk. We will discuss how each risk factor fits into the new understanding of how heart attacks arise. In addition, a stroke results from the same set of steps except that it takes place in the arteries feeding the brain rather than the heart. So, an added benefit is that by reducing your risk of a heart attack, you will also be reducing your risk of strokes.
To start, we recommend that you get a basic set of heart related blood test, which should include:
- A lipid panel, which includes total cholesterol as well as LDL, HDL, and triglycerides (a measure of fat in the blood)
- High sensitivity c reactive protein (CRP, a measure of inflammation in the body)
- Homocysteine (a measure of an independent risk factor)
Then count the number of major risk factors you have based on the 11 we list below. If you have three or more major risk factors, we recommend that you also get an exercise stress test and ultrafast computed tomographic scan of the hear, which will provide additional information on your risk of having a heart attack in the next several years.
(list of 11 questions).
…more text…
(recommendations of red yeast rice, plant sterols, policaosanol, vit E, phosphatidycholine as a supplements with dosage listed)Statin drugs
if natural supplements fail to move your cholesterol, LDL, HDL, and triglyceride levels to an ideal range, you and your physician may want to consider one of the HMG CoA reducatase enzyme inhibitors, also known as statin drugs. Statins slow down the creation of cholesterol by the liver and increase the rate at which LDL is cleared from the blood.They also appear to inhibit the oxidation of LDL, therby slowing down the first step of vulnerable plaque formation. Perhaps most important of all, statins reduce the likelihood that cholesterol in plaques will become inflamed.
Like all prescription medications, statin drugs are associated with side effects. They may have toxic effects on the liver, so your physician will want to monitor your liver enzymes periodically. The same enzyme that the body uses to make cholesterol, HMG-Coa reductase, is also used in the manufacture of coenzyme Q10. Since taking statins depletes the body of coenzyme Q10 which is needed to maintain the health of the mitochondria (the energy furnaces in every cell), it is vital to take supplemental coenzyme Q10 when taking statin drugs. You should take 50 to 150 milligrams of coenzyme Q10 twice a day or 50 milligrams of the activated form of coenzyme Q10 known as ubiquinol twice a day if you are receiving a statin drug. These are available over the counter without prescription.
(more info on lipitor and some proper nutrition)
Iron in the blood can act as a catalyst for the process of oxidizing LDL, one of the first steps in the formation of vulnerable plaque. This is one reason that premenopausal women have some level of protection since menstruation helps keep iron levels low. Women also receive protection before menopause thanks to hormone levels that may inhibit these LDL changes.
If you are a man 45 years or older or a woman over 55, then you already have one major risk factor. If you have two additional major risk factors, then you should give a high priority to adopting all of the recommendation in this chapter.
-Transcend, preview more of the April 2009 book here
1.1-1.5 million heart attacks occur each year in the US, and 37 percent of people who “experience a coronary attack in a given year die from it.” And the rest suffer from irreversible damage to their heart, sometimes with more attacks (or other responses like a stroke) to follow or even chest-cracking surgery.
So we need to take preventative steps. I guess my next step is to monitor my inflammation and get a lipid panel (see the 3 bulleted tests above). Scary 
perhaps, now that I put so much weight on these tests and know what they say about me, but I do enjoy progress and trying for a better score on each test. According to Transcend I was supposed to do this 4 years ago:
We agree with the National Cholesterol Education Program (NCEP) and the American Heart Association recommendation that everyone get a lipid panel beginning at age 20, and, if results are normal every 5 years thereafter.
I never thought of certain diseases as so preventable with aggressive nutritional habits and monitoring (but it makes sense since we put so much priority on food from eras before). My parents were always talking about diseases as just genetic or ‘just the luck of the draw’, or purely age-related, or for people who are just disease-prone (and my dad is a doctor 
). Like the only diseases to worry about are the sudden-occurrence ones and that we should take a reactive approach (rather than preventative).
Well now in the emerging field (emerging since 2005) of inflammation a lot of diseases are being linked to it (and now even my dad looks for anti-inflammatory foods and supplements). According to Transcend aging and disease are generally 80 percent environment and 20 percent genetic. I was noticing signs of aging when I started reading more about it (and imagining trying to play sports against a teenager version of myself). You may say, “Well I’m going to burn the candle at both ends and live ma’ life”… yeah, but do you really want to suffer at the hands of all these inflammatory diseases, and get taken down a notch? It’s quality of your entire life.
I remember taking nutrition class back in 2004 and our homework was to track the macro-nutrients in my foods (track foods through nutritiondata.com) to make sure make sure my diet consisted of a balance of 20-30% fats (0% trans-fats), 20-30% protein, and 30-40% carbohydrates. Well, now nutritiondata.com has added more than your basic macro-nutrients: now we have glycemic-index scores (anything that spikes your blood sugar too quickly like drinks, juices, and grains/breads/rice) and anti-inflammation scores (processed foods, dairy, and omega-6 rich grainfed and vegetable-oil fed animals are usually inflammatory). And you can add up the inflammation scores and you should end the day with a positive, anti-inflammatory result in the +50 range. Really, I would rather just not pay attention and just get heaping portions of anti-inflammatory foods (a lot of good recommendations for recipes and individual foods in these anti-inflammation books too – check the reviews to find the good books). Hopefully we’ll see these scores listed and even advertised in the grocery store one day.
Now if I could only figure out how to get my Littles on a doggy-specific, anti-inflammatory diet 
