Know All 10 Heart Disease Risk Factors? - Alan Watson

Do You & Your Doctor Know All 10 Heart Disease Risk Factors?

 March 7, 2012 by Alan Watson

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Heart disease is the #1 cause of death. About 50 percent of all people who die suddenly from heart disease have low or normal cholesterol. To protect yourself from heart disease, ask your doctor for a complete lipid evaluation. Fast 10-12 hours before blood is drawn (you can drink water). Because Total Cholesterol (TC) and LDL cholesterol are not the most reliable predictors of heart disease, they are not posted in the following chart.

 

QUICK SUMMARY:

Focus on Fasting Glucose, HDL, Triglycerides (TG) and the all important TG:HDL ratio. Keep in mind that before the advent of cholesterol-lowering statin drugs, the normal range for Total Cholesterol (TC) was: 180 mg/dl to 340 mg/dl. Also, it’s important to note that LDL is actually a family of particles. A discussion about LDL subclasses and LDL subclass testing follows in the summary of this article.

 

1. C-reactive protein (CRP) is produced by the liver in response to inflammation in the body. If monitored early enough, elevated CRP can be an early warning of a heart attack several years in advance. Optimum levels are below 1 mg/l. (You will have to request this test with most doctors.)

2. Fasting Glucose (FG) measures fasting blood sugar. Lowest all-cause mortality is associated with fasting glucose in the range of 80-89 mg/dl. According to the clinical experience of Dr. Robert Atkins, the risk of heart disease increases in linear manner as your Fasting Glucose goes over 100 mg/dl. (Specifically ask for this inexpensive test.)

3. Fibrinogen is a protein that in excess promotes blood clots. Elevated fibrinogen = thicker blood. Thicker blood flows less easily through partially blocked arteries. Consistent elevated fibrinogen (over 350 mg/dl) conveys a 250 percent increased risk of heart disease compared to people with fibrinogen levels below 235. (People who have recently suffered a heart attack will have elevated fibrinogen levels.)

4. Homocysteine is normally rapidly cleared from the bloodstream. Elevated homocysteine is a result of B-vitamin deficiencies, particularly folic acid, B-6 and B-12. Elevated homocysteine is associated with increased risk of heart attack, stroke, and all cause mortality. Levels less than 8 mmol/L are associated with longevity. (Again, you may have to request this test.)

5. Lipoprotein(a) has been called the “heart attack cholesterol.” Lipoprotein(a) is a sticky protein that attaches to LDL and accumulates rapidly at the site of arterial lesions or ruptured plaque. Readings of 30 mg/dl or more indicate serious increased risk of heart disease, especially in the presence of elevated fibrinogen (>350). While the Lp(a) level is largely genetically determined, it can be influenced by nutritional factors, such as high blood sugar and trans fatty acid consumption. (This test may not be as important as the rest and is seldom done routinely.)

6. HDL is made in the liver and acts as a cholesterol mop, scavenging loose cholesterol and transporting it back to the liver for recycling. HDL is associated with protection from heart disease. You want as much HDL as possible. HDL of 60 or more is associated with protection for men—70 or more for women.

7. Triglycerides (TG) should be under 100 mg/dl. Triglycerides are blood fats made in the liver from excess energy – especially carbohydrates. Risk is linear—the higher the number, the greater the risk, especially for women. While doctors may insist that a reading up to 150 is okay, Dr. Atkins’ clinical experience suggested otherwise.

8. TG:HDL ratio is the most reliable predictor of heart disease. Calculate your ratio by dividing TG by HDL. As an example, if TG = 80 and HDL = 80, your ratio is 1:1 representing low risk of heart disease. If your TG = 200 and your HDL = 50, your ratio is 4:1 representing serious risk of heart disease.

9. VLDL – Increasingly, Very Low Density Lipoprotein is measured/calculated. VLDL is sent out from the liver to deliver those liver made fats (Triglycerides) – as opposed to a Chylomicron that delivers dietary fat from the gut. Generally, VLDL is one fifth of your triglyceride level, although this is less accurate if your triglyceride level is greater than 400 mg/dl. (Beyond the scope of this article, LDL is the offspring of VLDL – they are closely-related.)

LDL particle size: Small dense Pattern B/Large fluffy Pattern A

An illustration from the Berkeley Heart Labs showing these particles

LDL – low density lipoprotein – is a family of particles. A lot of people with elevated LDL do not develop coronary artery disease, while individuals with low or modest levels often develop serious disease. This can be explained by the LDL particle number and size. Routine cholesterol testing only reveals the amount of LDL; not the quality of LDL.

We now know (my doctor didn’t) that there are different subclasses of LDL (and HDL). Under an electron microscope, some LDL particles appear large and fluffy; others small and dense. The big, fluffy particles are benign, while the small dense particles are strongly associated with increased risk of heart disease.

In excess, small dense LDL is toxic to the artery lining (the endothelium), and much more likely to enter the vessel wall – become oxidized – and trigger atherosclerosis. It’s becoming consensus medical opinion that only oxidized LDL can enter the macrophages in the lining of the arteries and contribute to plaque buildup.

HOW DO YOU KNOW WHAT LDL YOU HAVE? Certain clinical factors predict the presence of small dense LDL. These markers include HDL below 40 in men; below 50 in women – and Triglycerides (TG) higher than 120 mg/dl. Diabetes or pre-diabetes also predicts small dense LDL (Pattern B).

To determine LDL particle size, ask your doctor for a VAP (Vertical Auto Profile) test, which separates lipoprotein particles using a high speed centrifuge. The VAP test measures the basic information provided by a routine cholesterol test, but also identifies lipoprotein subclasses, LDL and HDL. (Go to http://thevaptest.com for more information.)

There are other tests as well. The NMR LipoProfile analyzes the number and size of lipoprotein particles by measuring their magnetic properties (http://theparticletest.com). Also Berkeley HeartLab’s LDL Segmented Gradient Gel Electrophoresis test measures all seven subclasses of LDL. (http://bhlinc.com).

If you don’t have insurance and can pay for just one test, get your fasting blood sugar checked. Any number over 100 – over 95 according to the late Dr. Atkins – is an early warning of diabetes, metabolic syndrome, and heart disease. If you have insurance or can afford a complete lipid panel, consider additional testing to determine the size and number of LDL particles. “A stitch in time saves nine.”
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Why Statins Do More Harm Than Good - Stephanie Seneff

Why Statins Do More Harm Than Good

by Stephanie Seneff
Senior Research Scientist at MIT (Massachusetts Institute of Technology)

Americans have been well trained over the past few decades to avoid dietary fat and cholesterol and to stay out of the sun. Their conscientious implementation of this misguided advice has led to an epidemic in obesity and heart disease, along with a host of other debilitating conditions like arthritis and Alzheimer's disease.

Cholesterol is to animals as chlorophyll is to plants. Cholesterol, absent from plants, is what gives animals mobility and a nervous system. It is therefore not surprising that statin drug side effects mainly impact muscles and the nervous system.

The heart, as a muscle, is not exempt from statin toxicity. This is why the incidence of heart failure has steadily risen in step with the widespread adoption of statin therapy, now displacing cardiovascular disease as the number one killer. In this article I am going to take you on a whirlwind tour of the 60,000 foot view of my understanding of the principle causes of the current health crisis in America.
My extensive research has caused me to hypothesize a remarkable feat that the human body can perform in the presence of sunlight, which is to extract sulfur from hydrogen sulfide in the air and convert it to sulfate, taking advantage of the sun's energy to catalyze the reaction.

This process takes place in the skin upon sun exposure, and also in the endothelial cells lining blood vessels, and in the red blood cells, platelets, and mast cells in the blood. This feat is performed by a very interesting molecule called "endothelial nitric oxide synthase,'' a misnomer, since its main responsibility is to synthesize sulfate rather than nitric oxide.

The sulfate so produced plays a huge role in cardiovascular health, both by preventing blood clots and by keeping pathogenic microbes (bacteria and viruses) at bay. But it also plays another role that is just as important, which is to give cholesterol (as well as vitamin D and other sterols) a free ride through the blood stream.

Vitamin D3 (a highly touted nutrient) is synthesized in the skin from cholesterol (a highly demonized nutrient) and its chemical structure is almost identical to that of cholesterol. By attaching to cholesterol or vitamin D3, sulfate makes the molecule water soluble, and this means that it no longer has to travel packaged up inside an LDL particle. LDL, as you probably know, is the so-called "bad'' cholesterol, which will cause doctors to prescribe statins if the level is too high.

A great way to lower LDL levels is to get adequate sun exposure. It's not going to work to take a vitamin D supplement: you have to go outside and soak up the sun, because supplements are never sulfated and vitamin D is not cholesterol. Raw cow's milk is the only dietary source I know of that actually supplies sulfated vitamin D3, but even that is still not cholesterol sulfate.

Because most Americans have inadequate cholesterol in their skin and grossly inadequate amounts of sun exposure, they suffer from a huge deficiency in cholesterol and sulfate supply to the tissues. Not surprisingly, most impacted are the muscles and nervous system.

Because the heart muscle is indispensible, the body has developed a back-up strategy to give it special treatment, which is to synthesize cholesterol sulfate from LDL and homocysteine in the fatty deposits (plaque) that build up in arteries supplying the heart. The macrophages in the plaque extract cholesterol from damaged small dense LDL particles, and export it to HDL-A1. The platelets in the plaque will only accept cholesterol from HDL-A1, which they then convert to cholesterol sulfate.

They obtain the sulfate through yet another process which requires energy and oxidizing agents, extracting the sulfur from homocysteine. With insufficient homocysteine, the sulfur will most likely be extracted from cartilage, which gets its strength from extensive disulfide bonds. This, in my view, is the main cause of arthritis -- depletion of sulfur from the cartilage in the joints. So now you have both cardiovascular disease and arthritis as a consequence of a low-fat diet and aggressive sun avoidance.

Statin drugs dramatically lower LDL levels by interfering with cholesterol synthesis, and this wreaks havoc on the liver, the main back-up supplier of cholesterol to the tissues when cholesterol intake and cholesterol sulfate production are down. With the American diet, the liver has another huge task, which is to convert fructose to fat.

The fat cannot be stored or shipped (via LDL) if there is insufficient cholesterol. As a consequence, the liver abandons this task, and the fructose builds up in the blood, causing extensive glycation damage to blood proteins. One of the impacted proteins is the apoB in LDL, which interferes with LDL's ability to deliver its goods to the tissues, including cholesterol, fats, vitamins A, D, E, and K, and antioxidants. So LDL levels fall sharply with statins, and so does the bioavailability of all these nutrients.

Muscle cells come to the rescue, heroically, by extracting excess fructose from the blood and converting it to lactate, using anaerobic metabolism. They have to switch over to anaerobic metabolism anyway, because coenzyme Q10, another casualty of statin therapy, is in low supply. Coenzyme Q10 is crucial for aerobic metabolism.

Lactate is a great fuel for the heart and liver, but the problem is that the muscle cells get wrecked in the process, due to massive overdoses of fructose, in the context of inadequate cholesterol, which would have offered some protection. This is a principle contributor to the excessive muscle pain and weakness associated with statins. Eventually, the muscles can't do it any more, and you're now on the verge towards heart failure.

People on long-term statin therapy start to notice that their hair is receding faster, they're developing cataracts, they can't hear as well as they used to, they keep forgetting things, they can't open the pickle jar any more, and perhaps they'll need rotator cuff surgery soon, as their shoulders are so sore. They think it's just because they're growing old, but these are all side effects that my research, together with my students at MIT, has uncovered, by comparing statin drug side effects with side effects associated with other drugs in age-matched reviews.

Even more alarming are the rare but debilitating and even life-threatening side effects we've detected, such as ALS and Parkinson's disease, heart and liver failure, neuropathy and severe muscle damage. A 17-year study on the elderly confirmed what I already suspected: low serum cholesterol is associated with increased frailty, accelerated mental decline, and early death. (Ref 1.)

Statins are not the answer for anyone seeking to avoid cardiovascular disease. The answer, instead, is to modify the diet to include foods that are rich in cholesterol and saturated fat, to avoid empty carbohydrates, especially high fructose corn syrup, to eat foods that are good sources of sulfur, and, most especially, to spend plenty of time outdoors in the sun.

Stephanie Seneff is a Senior Research Scientist at MIT's Computer Science and Artificial Intelligence Laboratory.
She has a Batchelor's degree from MIT in biology with a minor in food and nutrition, and a PhD in Electrical Engineering and Computer Science, also from MIT. Her website at MIT: people.csail.mit.edu/seneff
Her blog: stephanie-on-health.blogspot.com

Ref 1. http://www.ncbi.nlm.nih.gov/pubmed/21254906

September 2011
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Please visit Spacedoc.com to read this and other related and very credible articles.

Homocysteine By Dr. Kilmer McCully, M.D.

Second in a series by Dr Kilmer McCully, M.D. at the SpaceDoc web site, this two part article covers his research into the relation between homocysteine and arteriosclerosis. Read it here.

Kilmer McCully, M.D. on Cholesterol

Spacedoc.net is running a two part series of articles by Dr Kilmer McCully on the topic of Cholesterol. Lots of insight there. Please read part 1 and part 2.



Dr McCully has written a book titled "The Homocysteine Revolution", And one titled "The Heart Revolution".