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In many situations, an excess of LDL, the "bad" cholesterol will overpower HDL, the "good" one. This causes your cells to become filled with fatty wastes that create a serious risk for your heart. Pectin, a natural substance found in the cell walls of certain fruits can help you obtain a good balance between the "good" and the" bad" cholesterol.

Metabolic effects of conjugated linoleic acid in humans: the Swedish experience. Riserus U, Smedman A, Basu S, Vessby B. Am J Clin Nutr. 2004 Jun;79(6 Suppl):1146S-1148S. PMID: 15159248 CONCLUSIONS CLA and specifically the isolated isomers are interesting model fatty acids for studies of the effects of (structural differences of) unsaturated fatty acids in humans. Today, there is no clear indication for human use of CLA concentrates. The possible importance of the small reduction of body fat after supplementation with the commercially available CLA products, without evidence of an associated improvement in the metabolic profile, has to be weighed against the apparent reduction of HDL cholesterol and an increased lipid peroxidation. The possible health consequences of prolonged treatment periods are at present unknown. Human supplementation with high doses of the trans-10,cis-12 CLA isomer should be avoided while awaiting further information on possible effects and side effects. However, it cannot be excluded that future studies could point to clinical applications, eg, as a result of antitumorigenic properties or as a tool to prevent weight gain. This possibility certainly requires more research to increase the understanding of the mechanisms behind the effects of CLA and specific CLA isomers on a molecular level. More controlled studies in defined populations are needed, as are controlled studies for comparisons of the effects of different and well-defined (mixtures of) isomers and human studies of longer duration to secure long-term effects and safety.

If wheat is so bad, what about all the other grains? First of all, I demonize wheat because of its top-of-the-list role in triggering: --Appetite--Wheat increases hunger dramatically --Insulin --Blood sugar--Wheat is worse than table sugar in triggering a rapid, large rise in blood sugar --Triglycerides --Small LDL particles--the number one cause for heart disease in the U.S. --Reduced HDL --Diabetes --Autoimmune diseases--Most notably celiac disease and thyroiditis. Most other "healthy, whole grains" aren't quite as bad. It's a matter of degree.

Ordovas JM. The quest for cardiovascular health in the genomic era: nutrigenetics and plasma lipoproteins. Proc Nutr Soc. 2004 Feb;63(1):145-52. Review. PMID: 15070444 [PubMed - indexed for MEDLINE]

Ordovas JM. Genetic interactions with diet influence the risk of cardiovascular disease. Am J Clin Nutr. 2006 Feb;83(2):443S-446S. Review. PMID: 16470010 [PubMed - indexed for MEDLINE]

Plasma 25-hydroxyvitamin d is associated with markers of the insulin resistant phenotype in nondiabetic adults. Liu E, Meigs JB, Pittas AG, McKeown NM, Economos CD, Booth SL, Jacques PF. J Nutr. 2009 Feb;139(2):329-34. Epub 2008 Dec 23. PMID: 19106328 doi:10.3945/jn.108.093831 After adjusting for age and sex, plasma 25(OH)D was positively associated with ISI(0,120), plasma adiponectin, and HDL cholesterol and inversely associated with plasma triacylglycerol, but these associations were no longer significant after further adjustment for BMI, waist circumference, and current smoking status. 25(OH)D and 2-h post-OGTT glucose were not associated. Among adults without diabetes, vitamin D status was inversely associated with surrogate fasting measures of insulin resistance. These results suggest that vitamin D status may be an important determinant for type 2 diabetes mellitus.

Heart scan scores starting dropping not just 2%, or 8% . . . but 24%, 30%, 50% and more. We also began to see a larger proportion of people achieving these larger successes. Why? I attribute the surge in success to the addition of vitamin D. With vitamin D added to the mix of strategies in Track Your Plaque, HDL cholesterols went up much higher, LDL dropped further, blood sugars dropped, blood pressures dropped. People felt better, had more energy, gained more clarity in thought. And heart scan scores dropped more readily.

"Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides. In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease. Why? Carbohydrates increase small LDL via a multistep process: First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL) Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL. Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL"

A diet rich in coconut oil reduces diurnal postprandial variations in circulating tissue plasminogen activator antigen and fasting lipoprotein (a) compared with a diet rich in unsaturated fat in women. Müller H, Lindman AS, Blomfeldt A, Seljeflot I, Pedersen JI. J Nutr. 2003 Nov;133(11):3422-7. PMID: 14608053 In conclusion, our results indicate that a coconut oil-based diet (HSAFA-diet) lowers postprandial t-PA antigen concentration, and this may favorably affect the fibrinolytic system and the Lp(a) concentration compared with the HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy seem to have a beneficial influence on Lp(a) levels. The connection between Lp(a) and atherosclerosis is not entirely understood. Different studies have provided strong evidence that Lp(a) level is an independent risk factor for developing coronary artery disease in men (47,48), but the question of causality continues to be debated. Recent data suggest that Lp(a) might be atherogenic (49), in particular when combined with other risk factors. High levels of Lp(a) combined with other risk factors such as the ratio of plasma total/HDL cholesterol have been shown to increase the risk for coronary heart diseases (50). It has also been reported that when substantial LDL cholesterol reductions were obtained in men with coronary heart disease, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening (51). In conclusion, the present results show that the HSAFA-diet lowered postprandial t-PA antigen and thus potentially improved fibrinolysis compared with the HUFA-diet. Diets with either high or low levels of saturated fatty acids from coconut oil beneficially decrease Lp(a) compared with a HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy may be of importance if the goal is to decrease Lp(a).

"Coconut oil is extracted from the kernel or meat of matured coconut harvested from the coconut palm (Cocos nucifera). Throughout the tropical world it has provided the primary source of fat in the diets of millions of people for generations. It has various applications in food, medicine, and industry. What makes coconut oil different from most other dietary oils is the basic building blocks or fatty acids making up the oil. Coconut oil is composed predominately of a special group of fat molecules known as medium chain fatty acids (MCFA). The majority of fats in the human diet are composed almost entirely of long chain fatty acids (LCFA). The primary difference between MCFA and LCFA is the size of the molecule, or more precisely, the length of the carbon chain that makes up the backbone of the fatty acid. MCFA have a chain length of 6 to 12 carbons. LCFA contain 14 or more carbon Historically, many populations within the tropics have used coconut medicinally as a treatment for a wide variety of ailments.[8] A study into the effects of a "diet rich in.." medium-chain fatty acids (such as in coconut oil and butter) concluded that "MCFAs in the form of MCTs significantly increased plasma triacylglycerol and LDL-cholesterol concentrations and the ratio of LDL to HDL cholesterol and thereby resulted in a less beneficial lipid profile overall."[9] Further, research done by nutritionist Mary Enig has found that non-hydrogenated coconut oil (i.e. extra-virgin) consumed in moderate amounts "is at worst neutral with respect to atherogenicity of fats and oils and, in fact, is likely to be a beneficial oil for prevention and treatment of some heart disease."[10] The lack of negative effects of a diet rich in coconut oil on cardiovascular health is born out in studies of Polynesian populations who consume as much as 65% of their calories in the form of coconut oil and yet, have almost no incidence of heart disease and normal blood lipid profiles.[11]

"Tuesday, December 15, 2009 Overweight, hungry, diabetic, and fat-free Let me tell you about my low-fat experience from 20 years ago. At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.) I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted. I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try. I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course! After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs: HDL 28 mg/dl Triglycerides 336 mg/dl Blood sugar 151 mg/dl (fasting) I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week. "

You may have heard that oat bran lowers LDL cholesterol, but do you know how much oats you need to eat to really lower it? Anyhow, if you have high cholesterol and you are not eating oats, you may want to start eating them right away. Read this article because you are going to be surprised at the amount needed to lower LDL, the bad guy and to increase HDL, the good one.

"Orlando, FL - Adding extended-release niacin (Niaspan, Abbott) to statin therapy results in a significant regression of atherosclerosis as measured by carotid intima-media thickness (IMT), whereas the addition of ezetimibe (Zetia, Merck/Schering-Plough) to statin therapy did not, according to an eagerly anticipated study "

"New research study published in a peer-reviewed publication Nutrition indicates that selenium may be linked to higher cholesterol readings in those who supplement. This one may push it over the edge for me on taking selenium supplements . . . Scientists at the University of Warwick Medical School said consuming too much selenium can have adverse effects. While it has strong antioxidant properties, and the above-mentioned perception that it can reduce cancer risks, there is now an apparently legitimate concern that higher quantities of selenium found in some supplements may be a bad thing. The scientists reached this conclusion after examining the relationship between plasma selenium concentrations (levels of selenium in the blood) with blood lipids (fats in the blood). A cross-sectional study of the1042 participants in the 2000-2001 National Diet and Nutrition Survey (United Kingdom) revealed that among those with higher plasma selenium (more than 1.20 µmol/L) there was an increase in the average total cholesterol level of 8 per cent (0.39 mmol/L (i.e. 15.1 mg/dL). Researchers also found a 10 per cent increase in non-HDL cholesterol levels, which is the bad cholesterol most closely linked to heart disease."

Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations in older adults with low macular pigment taking cholesterol-lowering statins. Vishwanathan R, Goodrow-Kotyla EF, Wooten BR, Wilson TA, Nicolosi RJ. Am J Clin Nutr. 2009 Nov;90(5):1272-9. Epub 2009 Sep 16. PMID: 19759170 Conclusions: Consumption of 4 egg yolks/d, and possibly of 2 egg yolks/d, for 5 wk benefited macular health in older adults with low MPOD. Serum HDL cholesterol increased without an increase in LDL cholesterol in this study population, most of whom were taking cholesterol-lowering statins.

Acai Berry Extracts are present in fatty acids omegas that can help in reducing the level of HDL and LDL cholesterols. They have high concentration of antioxidants that can help in combating the premature aging. Acai Berry is a source of certain flavonoids such as anthocyanins. Acai Berry has ORAC value, which is higher than any other edible berry.

Can including wheat in your diet create hell on earth? Was The Inferno nothing more than Danté's prediction for the state of the U.S. diet circa 2009? I'm kidding on The Inferno allusion, but the American diet nonetheless sure does create an inferno of unhealthy phenomena.

What causes coronary heart disease or coronary atherosclerotic plaque, this thing that we track with heart scans? Well, here are a few little-publicized facts about heart disease that you are unlikely to hear from your When's-the-next-stent? cardiologist or the What is there besides statins? primary care doctor. (Since everybody knows that smoking is a modifiable risk for heart disease that can be readily identified, let's focus on the blood tests that reveal heart disease causes.)

Fernandez ML, West KL. Mechanisms by which dietary fatty acids modulate plasma lipids. J Nutr. 2005 Sep;135(9):2075-8. Review. PMID: 16140878 [PubMed - indexed for MEDLINE]