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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Read the complete article here.

Ask Your Doctor for a Complete Lipid Evaluation - Watson

Ask Your Doctor for a Complete Lipid Evaluation Sent Saturday, March 10, 2012

Diet Heart News, volume 2, number 3

Ask Your Doctor for a Complete Lipid Evaluation

Heart disease is the #1 cause of death. About 50 percent of 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 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 Size 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, request the inexpensive fasting glucose test. 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. Remember, "A stitch in time saves nine." ============================================================= Read the full article here.

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk Sent Wednesday, November 23, 2011

Diet Heart News, volume 1, number 8

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk Since the early 1950s, mainstream researchers have been seeking the cause of atherosclerosis and heart disease spearheaded early on by University of Minnesota professor and American Heart Association board member Ancel Keys. The result - the 50 year old Diet Heart or Cholesterol Hypothesis: If you eat too much food containing cholesterol and/or saturated fat, the level of cholesterol in your blood will rise. The excess cholesterol will be deposited in artery walls, causing them to thicken and narrow. In time, this will block blood supply to the heart or brain causing a heart attack or stroke. According to this still unproven but enduring hypothesis, high blood cholesterol is caused by an atherogenic diet high in cholesterol and saturated fat - found mainly in animal products such as red meat, whole milk, eggs, butter - and the tropical saturates coconut and palm. In this scenario, high blood cholesterol is the main cause of atherosclerosis and heart disease. The medical and nutrition communities and various government agencies have been behind Diet Heart ever since. If animal fat and high blood cholesterol are the chief villains, then cholesterol-lowering diets and cholesterol-lowering drugs would appear to be wise choices. But 50 years later - after a lengthy test of time - the incidence of heart disease has not gone down as promised, and researchers like science writer Gary Taubes have uncovered a great deal of their evidence that is unsupportable, contradictory, and hopelessly wrong. A look at the recent five year UCLA/AHA Study The UCLA research team used an American Heart Association database that included 541 hospitals across the country. The database provided detailed information on 136,905 patients hospitalized for cardiovascular disease whose lipid levels upon hospital admission were documented. The results after five years: 75 percent of patients hospitalized for a heart attack had LDL cholesterol below 130 mg/dl - in the so called safe range. Even more astounding, 50 percent of patients had LDL below 100 mg/dL - considered optimal. (21 percent of the patients were taking a statin cholesterol-lowering drug.) Now don't you think that the UCLA researchers would have concluded that there was no association between elevated LDL and risk of heart attacks? After all, this was a five year study of heart attacks suffered by 136,905 patients in an American Heart Association database that included records from 541 hospitals. Yes - this should have been the nail in the coffin for the Diet Heart or Cholesterol Hypothesis, but not according to study director Dr. Gregg C. Fanarow, Professor of Cardiovascular Medicine and Science, David Geffen School of Medicine, UCLA, who concluded: "Almost 75 percent of heart attack patients fell within recommended targets for LDL cholesterol, demonstrating that the current guidelines may not be low enough to cut heart attack risk... " May not be low enough! Low cholesterol is already associated with depression and death by accidents, cancer and violence. According to the American Heart Association's journal Circulation, 1992; 86:3, the all cause death rate increases when total cholesterol drops below 180. Isn't there sufficient evidence now to conclude that elevated LDL and total cholesterol are not the cause of heart attacks and that the cholesterol hypothesis should be discarded along with official low fat diets and cholesterol-lowering drugs? Don't hold your breath! UK cardiologist Dr. Malcolm Kendrick: "I have come to realize that there is, literally, no evidence that can dent the cholesterol hypothesis... The effect of this study on the cardiovascular research community was....as you would expect...nothing at all, a deafening silence..." Dr. Fonarow disclosed that he has conducted research for GlaxoSmithKline and Pfizer and serves as a consultant and has received honorarium from the following drug companies: Abbott, AstraZeneca, GlaxoSmithKline, Merck, Pfizer and Schering Plough. Dr. H. Bryan Brewer, a physician-scientist at the National Heart, Lung and Blood Institute, failed to disclose his ties to AstraZeneca. Brewer had previously written a glowing report in a medical journal about Crestorwithout disclosing that he is a paid consultant and had presided over a company-sponsored symposium." He and the others forgot! Earlier in 2004, the doctors in the National Cholesterol Education Program (NCEP) who wrote the current cholesterol guidelines and, in effect, control cardiology, failed to disclose that six of the nine authors had direct financial ties to the makers of statin drugs, including: Pfizer's Lipitor, Bristol-Myers Squibb's Pravachol, Merck's Lovastatin, and AstraZeneca's Crestor. The new more stringent cholesterol-lowering guidelines boosted statinsales from $15 billion in 2004 to over $23 billion in 2005. And now the UCLA study provides more proof that lowering cholesterol with drugs or diet will not reduce cardiovascular disease or the risk of heart attack. But as Winston Churchill said: "Men occasionally stumble over the truth, but most of them pick themselves up and hurry off as if nothing had happened." [especially if there is money to be made]. ================================================================= Read the complete article here.

Illustrated History of Heart Disease - Alan Watson

Illustrated History of Heart Disease 1825-2015

August 19, 2012 by Alan Watson  Diet Heart News         

1825 French lawyer and gourmand Brillant-Savarin publishes The Physiology of Taste, in which he says he has identified the cure for obesity: “More or less rigid abstinence from everything that is starchy or floury.”
1830 Sugar consumption in the US: 15 pounds per capita (much of it molasses). Today: 150 pounds per capita (much of it high fructose corn syrup).
1863 William Banting published Letter On Corpulence, Addressed to the Public. Banting had lost 85 pounds on a high fat, carbohydrate-restricted diet. The British Medical Journal and Lancet reported that Banting’s diet could be dangerous: “We advise Mr Banting, and everyone of his kind, not to meddle with medical literature again, but be content to mind his own business.”
1880-1910 U.S. population doubled from 37 to 75 million. One out of three people lived on a farm – and ate from the farm. The U.S. population today is over 300 million and about 1 percent live on a farm.
1906 Upton Sinclair’s novel The Jungle exposed unsanitary and inhumane conditions in Chicago area slaughterhouses. Reported meat sales fell 50 percent and took years to recover. As is true today, the highest quality safest meat to eat was grown on the small mixed farms that dotted much of the American landscape.
1910 Lifetime risk of type II diabetes: 1 in 30. The lifetime risk today is 1 in 3 according to the Center for Disease Control (CDC) in Atlanta.
1910 Butter consumption = 18 pounds per capita. When we were using high quality butter lavishly, mortality from heart disease was below 10 percent. (Infections killed a majority of people; a high percentage of infants and women of child-bearing age died during the birthing process.) Today as we consume our “Country Croak,” the mortality from heart disease is 40 to 45 percent. Both Dr. Andrew Weil and the late Dr. Robert C. Atkins agree: “Eat butter; not margarine, regardless of the claims the manufacturer is making for it!”
1910 Lard, the rendered fat from pigs raised outdoors, was the #1 cooking fat – enjoying 70 percent of the market. Lard was the best source of Vitamin D and a good source of palmitoleic acid, a monounsaturated anti-microbial fatty acid that kills bacteria and viruses. Today highly processed soybean oil has 70 percent of the market; zero vitamin D. Now the same experts who told us not to eat lard are telling us we are deficient in Vitamin D!
1911 Proctor & Gamble introduce Crisco, first shortening made from hydrogenated vegetable fat. P & G bought the patent for hydrogenation from an English company that was attempting to make candles out of the artificially hardened fat. When rural electrification wiped out the candle market, P & G saved the day by providing the world with Crisco, a cheap alternative to lard. Crisco featured a much longer shelf life and, over decades, gave unsuspecting Americans hundreds of millions of pounds of trans fatty acids.
1918 The electrocardiogram was introduced helping to launch cardiology.
1920 Sugar consumption in the US reaches 100 pounds per capita – and climbing.
1921 The hormone insulin is discovered.
1924 Four cardiologists found the American Heart Association (AHA).
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Read the complete article here. Much more at DietHeartNews.com.