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Showing posts with label fibrinogen. Show all posts
Showing posts with label fibrinogen. Show all posts

Wednesday, October 3, 2012

Know All 10 Heart Disease Risk Factors? - Alan Watson

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

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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.

Wednesday, March 14, 2012

Genetic studies lay the foundations for anti-inflammatory drugs to prevent heart disease


Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies

IL6R Genetics Consortium Emerging Risk Factors Collaboration

Summary

Background

Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling.

Methods

In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6.

Findings

The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4—38·2) and of interleukin 6 by 14·6% (10·7—18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9—9·1) and of fibrinogen by 1·0% (0·7—1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8—5·0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes.

Interpretation

Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease.

Funding

British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation.
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View the article here.
See also this article in theheart.org.

Wednesday, September 7, 2011

Latest Study: Cholesterol Theory is Still Rubbish - Anthony Colpo

Latest Study: Cholesterol Theory is Still Rubbish

Anthony Colpo | Wednesday, September 7th, 2011 | Comments Off
Cholesterol-lowering: Probably the biggest wank in the history of medicine.
A soon-to-be published article in the journal Atherosclerosis adds to the vast sum of research contradicting the cholesterol theory of cardiovascular disease.

In this study, researchers tracked 82,380 participants with no known history of cardiovascular disease for an average of eight years (during the period 1994–2004) as part of the Health Survey for England. Mean age of the subjects was 55.4 and the male:female ratio was 45:55.

Given that we’ve been told ad naseum cholesterol causes heart disease, you’d expect blood cholesterol to assert itself as a robust risk factor for heart disease in such a large study. With 82,380 participants followed for almost a decade, and with 806 and 1346 subsequent deaths from stroke and IHD deaths, respectively, cholesterol had every opportunity to leave its allegedly deadly mark.
But it didn’t.

Total cholesterol levels didn’t make a whit of difference to coronary heart disease risk, and were in fact associated with a lower risk of stroke[1].

Oops. Bet this study won’t be getting the extravagant media coverage given to all those shonky Big Pharma-sponsored statin studies that are prematurely ended whilst the “miracle” drug is still showing a piddling but “statistically significant” advantage…

So what factors were associated with increased stroke and heart attack risk?
Only age, smoking, systolic BP, diabetes and physical activity were predictive of stroke, while age, male gender (get those iron levels checked fellas…), smoking, systolic blood pressure, HDL cholesterol, diabetes, BMI, physical activity, CRP, and fibrinogen were predictive of coronary heart disease.

Bottom line: Don’t smoke, do some regular exercise, avoid high blood sugar levels, keep a healthy weight, and keep your serum ferritin between 30-75 (depending on your activity levels). And give cholesterol-phobia a good swift kick in its fraudulent backside.

References
1. Hamer M, et al. Comparison of risk factors for fatal stroke and ischemic heart disease: A prospective follow up of the health survey for England. Atherosclerosis (2011), doi:10.1016/j.atherosclerosis.2011.08.016