Showing posts with label LDL - reduction. Show all posts
Showing posts with label LDL - reduction. Show all posts

Sunday, 7 April 2013

How to Reduce LDL - Prevention - Heart Disease

How to Reduce LDL - Prevention - Heart Disease

Health Pro Wednesday, 
November 12, 2008
 
In this, the third post on the "Rule of 60," we now turn to ways to reduce LDL cholesterol towards 60 mg/dl.

Of course, the standard reflexive response of most doctors when dealing with LDL cholesterol is to have you "cut the fats" and take a statin cholesterol drug.

How effective is "cutting the fat"?

In most instances, it is a miserable failure. "Cutting the fat" refers to reducing saturated and hydrogenated fats from the diet, a strategy that results in 7-10% reduction in LDL cholesterol. That means if you begin with an LDL cholesterol of, say, 150 mg/dl, you can expect to reduce it to 135 mg/dl. The doctor then usually advises a statin drug.

That simple formula leaves plenty of room for improvement. There are, in fact, a number of useful non-prescription strategies for reducing LDL far more, often sufficient to achieve ambitious drops like the one we use in our heart disease reversal program.

LDL can be reduced by:
  • Non-wheat fibers─Ground flaxseed is by far the best. This combination of protein, fibers, and healthy oils with no digestible carbohydrates can reduce LDL cholesterol 20-30 mg/dl. Another good non-wheat fiber is oat bran, with twice the beta glucan (fiber) content compared to oatmeal. Use it just like flaxseed as a hot cereal, etc. Use it as a hot cereal or added to other foods, such as chilis, yogurt, oatmeal, etc. 2-3 tbsp per day is the desired quantity for both.
  • Raw nuts─Best are the fiber-coated nuts like almonds, walnuts, pecans, and hazelnuts. Raw pistachios (tough to find; try Trader Joe's) are another good choice. Benefits begin at ¼ cup per day or more. Nuts, provided they are raw (and not "honey roasted," "party mix," "beer nuts," mixed nuts roasted in hydrogenated oils, etc.) do not cause weight gain, contrary to popular advice. They can be eaten in unlimited quantities.
  • Elimination of wheat, cornstarch, and sugary snacks─Because over 70% of adults now have small LDL particles triggered by these foods, elimination leads to a dramatic reduction of both small LDL and total LDL. However, this strategy works only if a substantial proportion (>30%) of LDL particles are small. (This requires a test called "lipoprotein analysis.")
  • Flavonoids─These are the brightly-colored components of foods that confer many of the wonderful health properties of vegetables and fruits. The most prominent LDL-reducing effects have been shown for dark chocolate (preferably 70% cocoa or greater) and brewed green tea (brewed only; never instant or pre-mixed bottles). Dark chocolate, 40 grams (approximately 2 inches square) or several cups green tea per day are required for full effect.
  • Vitamin D─Restoration of vitamin D levels to normal can yield reductions in LDL of 10-20 mg/dl.
  • Stanol esters─Stanol esters are available as butter substitute, Benecol®. Adding two tablespoons per day to your diet can reduce LDL cholesterol by about 25 mg/dl. (There is a related additive called "sterol" esters that are being added to many new products such as yogurt, orange juice, and other butter substitutes; however, I have some serious reservations about the safety of sterol esters and therefore do not endorse their use. Perhaps a post for future.)
  • Normal thyroid function is yet another important factor contributing to LDL control. See my post, Correct Heart Disease through Your Thyroid: Learn How for a discussion. Low levels of thyroid dysfunction are very common and often undiagnosed, yet offer another easy, healthy means to reduce LDL, sometimes with dramatic effect. While a prescription thyroid hormone may be required, it is really not a drug, but restoring a hormone level─a lot more preferable to a non-human pharmaceutical agent.
Those are the principle strategies that we use to reduce LDL dramatically. While perhaps not as simple as taking one tablet a day, they work while restoring health in other ways.

See Dr. Davis' previous posts on the "Rule of 60":
Raise HDL Naturally
Reduce Triglycerides Naturally
Why Take Fish Oil If you Take a Statin Drug?

Thursday, 4 April 2013

ApoE and HDL, and heart and cerebrovascular disease: LDL-apheresis therapy

Association of ApoE and HDL-C with cardiovascular and cerebrovascular disease:
potential benefits of LDL-apheresis therapy,
Clinical Lipidology, Future Medicine


June 2009, Vol. 4, No. 3, Pages 311-329 , DOI 10.2217/clp.09.21

Review

Association of ApoE and HDL-C with cardiovascular and cerebrovascular disease: potential benefits of LDL-apheresis therapy

Patrick M Moriarty

ApoE forms a lipid–protein complex with HDL-cholesterols (HDL-C) and remnant lipoproteins and is an important regulator of cholesterol and lipid clearance, transport and distribution. In the CNS, ApoE is strictly bound to HDL.

Unlike ApoE2 or ApoE3, the ApoE4 isoform is associated with both coronary artery disease and Alzheimer’s disease. 

HDL-C levels may possess a U-shaped association with vascular diseases and HDL-C size might reflect an alteration in function.

Inflammation plays a key role in coronary artery disease and Alzheimer’s disease.

Elevated inflammatory markers such as C-reactive protein and serum amyloid A are associated with both diseases. Serum amyloid A, similar to ApoE, binds to HDL-C and may alter the lipoproteins size and function.

Familial hypercholesterolemia (FH) is a genetic disorder resulting in elevated plasma levels of LDL-cholesterol (LDL-C), xanthomas and premature coronary artery disease. FH patient’s plasma contains decreased levels of HDL-C with increased levels of ApoE4 and ApoE-bound HDL.

LDL-apheresis therapy lowers LDL-C and is designated for FH patients resistant to pharmacotherapy.

LDL-apheresis also lowers inflammatory HDL-C, ApoE4, and a host of inflammatory markers such as C-reactive protein and serum amyloid A. LDL-apheresis, adjunct to reducing cholesterol, may provide additional benefit to patients with cardiovascular and cerebrovascular diseases.

Full Text PDF (2053 KB) PDF Plus (2177 KB)

Wednesday, 3 April 2013

Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) - Lipids Online

Lipids Online - Educational Resources in Atherosclerosis. Also covers coronary heart disease, hdl cholesterol, ldl cholesterol, free CME credit, continuing medical education, online CME course, medical CME conference

Introduction

Although the clinical benefit of lipid-lowering statin therapy on progression of coronary artery disease (CAD) has been established in multiple placebo-controlled trials using quantitative coronary angiography (QCA), little information has been available on the comparative benefit of different treatment regimens on CAD progression. In the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, the effects of intensive lipid lowering with atorvastatin 80 mg were compared with the effects of moderate lipid lowering with pravastatin 40 mg in 654 patients with angiographically demonstrated CAD and low-density lipoprotein cholesterol (LDL-C) between 125 mg/dL and 210 mg/dL. The primary endpoint was percent change in atheroma volume as assessed by intravascular ultrasound at 18-month follow-up.





Key Points

LDL-C was reduced from a mean baseline of 150 mg/dL to 79 mg/dL with atorvastatin 80 mg/d (46% reduction) and 110 mg/dL with pravastatin 40 mg/d (25% reduction). The atorvastatin group also had significantly greater reductions in triglycerides (20% vs. 7% in the pravastatin group) and apolipoprotein (apo) B-100 (39% reduction vs. 22% in the pravastatin group); high-density lipoprotein cholesterol (HDL-C) was increased by 2.9% and 5.6% in the respective treatment groups, but the difference was not statistically significant. C-reactive protein (CRP) was reduced by 36% with atorvastatin 80 mg and 5% with pravastatin 40 mg. Analysis of the primary endpoint showed significantly less atherosclerotic progression with atorvastatin; progression did not occur in the atorvastatin group (–0.4% change in atheroma volume, p=.98), whereas progression was observed in the pravastatin group (2.7% increase in atheroma volume, p=.001). Significant benefit was also seen for secondary endpoints, including change in total atheroma volume and change in percent atheroma volume.





Implications and Clinical Relevance

Previous randomized trials have used QCA to demonstrate that statin therapy significantly slowed the progression of atherosclerosis compared with placebo. These trials also showed that statin therapy increased the frequency of "regression" of lesions, as defined by increase in minimum lumen diameter or improvement in percent diameter stenosis. However, in previous trials using QCA, if one looks at the average change in all lesions with statin monotherapy, there was continued progression of atherosclerosis. Previous meta-analyses had suggested that LDL-C levels achieved may need to be far below 100 mg/dL to stop progression of CAD.

This is the first large randomized trial of two statin therapies using a new technology, intravascular ultrasound, and demonstrated that more intensive lipid-modifying therapy with atorvastatin 80 mg, which achieved a mean LDL-C of 79 mg/dL, stopped the progression of coronary atherosclerosis, whereas the pravastatin 40 mg group, with a mean LDL-C of 110 mg/dL, continued to have CAD progression. Although the absolute differences were small, endpoints were significantly different by predefined analysis after a treatment period of 18 months, which is a shorter duration than used in almost all QCA trials.

The major clinical implication of the study is that more intensive lipid-modifying therapy achieving an LDL-C level well below 100 mg/dL (on average, <80 mg/dL) was superior to less intensive therapy, i.e., "lower is better." In addition, this trial validates the use of intracoronary ultrasound to detect treatment effects on coronary atherosclerosis between two active therapies over a relatively short period of time. Additional research is needed to understand the relation between progression of CAD as detected by IVUS and development of clinical events.