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"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"

The Diet-Heart Hypothesis: Subdividing Lipoproteins Two posts ago, we made the rounds of the commonly measured blood lipids (total cholesterol, LDL, HDL, triglycerides) and how they associate with cardiac risk. It's important to keep in mind that many things associate with cardiac risk, not just blood lipids. For example, men with low serum vitamin D are at a 2.4-fold greater risk of heart attack than men with higher D levels. That alone is roughly equivalent to the predictive power of the blood lipids you get measured at the doctor's office. Coronary calcium scans (a measure of blood vessel calcification) also associate with cardiac risk better than the most commonly measured blood lipids. Lipoproteins Can be Subdivided into Several Subcategories In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source): The plasma lipoprotein profile accompanying a preponderance of small, dense LDL particles (specifically LDL-III) is associated with up to a threefold increase in the susceptibility of developing [coronary artery disease]. This has been demonstrated in case-control studies of myocardial infarction and angiographically documented coronary disease. Krauss found that small, dense LDL (sdLDL) doesn't travel alone: it typically comes along with low HDL and high triglycerides*. He called this combination of factors "lipoprotein pattern B"; its opposite is "lipoprotein pattern A": large, buoyant LDL, high HDL and low triglycerides. Incidentally, low HDL and high triglycerides are hallmarks of the metabolic syndrome, the quintessential modern metabolic disorder. Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. J Clin Invest. 2009 May;119(5):1322-34. Epub 2009 Apr 20. PMID: 19381015 doi: 10.1172/JCI37385. Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

In response to the Heart Scan Blog post, Post-Traumatic Grain Disorder, Anne commented: While on the American Heart Association diet my lipids peaked in 2003. I even tried the Ornish diet for a short time, but found it impossible. Total Cholesterol: 201 Triglycerides: 263 HDL: 62 LDL: 86 After I stopped eating gluten (I am very sensitive), my lipid panel improved slightly. This past year I started eating to keep my blood sugar under control by eliminating sugars and other grains. Now this is my most recent lab: Total Cholesterol: 162 Triglycerides: 80 HDL: 71 LDL: 75

Studies done with laboratory rats suggest that supplementation of their diet with lipoic acid had a significant effect in lowering triglycerides.

Coconut oil is one of the few saturated fats that doesn't come from animals, but like other saturated fats can raise cholesterol levels and, therefore, should play only a very limited role, if any, in your diet. In the past, it was widely used in movie popcorn, candy bars and commercial baked goods but was phased out of many of them because of consumer opposition to unhealthy tropical oils. Now coconut oil is being promoted as a weight loss aid; it is also touted in a book by a naturopathic doctor. The rationale goes something like this: as a source of medium-chain triglycerides (MCT), coconut oil isn't stored in the body as fat as readily as oils composed of long-chain triglycerides (LCT). Some research from McGill University in Canada suggests that this is true; MCTs also boost metabolism and satiety, and therefore may promote weight loss when they replace LCTs in the diet. Because they are so easily digested, MCTs are given in hospitals to provide nourishment for critically ill people who have trouble digesting fat. The benefits of coconut oil in the diet, if any, are likely to be minimal, and until we have more and better evidence about coconut oil's effect of metabolism and potential role in promoting weight loss, I do not recommend using it.

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ScienceDaily (Mar. 4, 2009) - Any diet will do? Not if you want to lose fat instead of muscle. Not if you want to lower your triglyceride levels so you'll be less likely to develop diabetes and heart disease. Not if you want to avoid cravings that tempt you to cheat on your diet. And not if you want to keep the weight off long-term. "Our latest study shows you have a better chance of achieving all these goals if you follow a diet that is moderately high in protein," said Donald Layman, a University of Illinois professor emeritus of nutrition. The research was published in the March Journal of Nutrition.

Conclusions: Compared with a low-fat diet, a low-carbohydrate diet program had better participant retention and greater weight loss. During active weight loss, serum triglyceride levels decreased more and high-density lipoprotein cholesterol level increased more with the low-carbohydrate diet than with the low-fat diet. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. Ann Intern Med. 2004 May 18;140(10):769-77. PMID: 15148063

This week sees the publication of yet another study showing the superiority of the low-carbohydrate diet as compared to the low-fat diet. This study, published in the prestigious American Journal of Clinical Nutrition, demonstrates that subjects following the low-carb diet experience a decrease in triglyceride levels and an increase in HDL-cholesterol (HDL) levels; and that these changes are accompanied by a minor increase in LDL-cholesterol (LDL), which prompts the authors to issue a caveat. Yes, although just about all the parameters that lipophobes worry about improved with the low-carb diet, the small increase in LDL has caused great concern and has prompted the authors to gravely announce that this small increase is troublesome and should be monitored closely in anyone who may be at risk for heart disease. Since most people who go on low-carb diets do so to deal with obesity issues, and since obesity is a risk factor for heart disease, it would appear that this small increase in LDL often seen in those following a low-carb diet could put these dieters at risk. Does it? We'll see.

Coconut kernel protein modifies the effect of coconut oil on serum lipids. Padmakumaran Nair KG, Rajamohan T, Kurup PA. Plant Foods Hum Nutr. 1999;53(2):133-44. PMID: 10472790 DOI: 10.1023/A:1008078103299 Feeding coconut kernel along with coconut oil in human volunteers has been found to reduce serum total and LDL cholesterol when compared to feeding coconut oil alone. This effect of the kernel was also observed in rats. Since many plant proteins have been reported to exert a cholesterol lowering effect, a study was carried out on the effect of isolated kernel protein in rats. Feeding kernel protein resulted in lower levels of cholesterol, phospholipids and triglycerides in the serum and most tissues when compared to casein fed animals. Rats fed kernel protein had (1) increased hepatic degradation of cholesterol to bile acids, (2) increased hepatic cholesterol biosynthesis, and (3) decreased esterification of free cholesterol. In the intestine, however, cholesterogenesis was decreased. The kernel protein also caused decreased lipogenesis in the liver and intestine. This beneficial effect of the kernel protein is attributed to its very low lysine/arginine ratio 2.13% lysine and 24.5% arginine....

Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins. Kong W, Wei J, Abidi P, Lin M, Inaba S, Li C, Wang Y, Wang Z, Si S, Pan H, Wang S, Wu J, Wang Y, Li Z, Liu J, Jiang JD. Nat Med. 2004 Dec;10(12):1344-51. Epub 2004 Nov 7. PMID: 15531889 doi:10.1038/nm1135 We identify berberine (BBR), a compound isolated from a Chinese herb, as a new cholesterol-lowering drug. Oral administration of BBR in 32 hypercholesterolemic patients for 3 months reduced serum cholesterol by 29%, triglycerides by 35% and LDL-cholesterol by 25%. Treatment of hyperlipidemic hamsters with BBR reduced serum cholesterol by 40% and LDL-cholesterol by 42%, with a 3.5-fold increase in hepatic LDLR mRNA and a 2.6-fold increase in hepatic LDLR protein. Using human hepatoma cells, we show that BBR upregulates LDLR expression independent of sterol regulatory element binding proteins, but dependent on ERK activation. BBR elevates LDLR expression through a post-transcriptional mechanism that stabilizes the mRNA. Using a heterologous system with luciferase as a reporter, we further identify the 5' proximal section of the LDLR mRNA 3' untranslated region responsible for the regulatory effect of BBR. These findings show BBR as a new hypolipidemic drug with a mechanism of action different from that of statin drugs.

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.

What is C-reactive protein (CRP)? It is a blood-borne protein that originates in the liver and serves as an index of the body's inflammatory state. It is triggered by yet another inflammatory signal molecule, interleukin-6. What triggers this cascade of inflammatory markers? Any inflammatory stimulus, such as being overweight, lack of exercise, vitamin D deficiency, viral illness no matter how trivial, any inflammatory disease like arthritis, small LDL, high triglycerides, poor diet rich in processed foods, resistance to insulin, any injury, incipient diabetes, hidden cancer, lack of education (no kidding), etc.

Dietary cholesterol from eggs increases plasma HDL cholesterol in overweight men consuming a carbohydrate-restricted diet. Mutungi G, Ratliff J, Puglisi M, Torres-Gonzalez M, Vaishnav U, Leite JO, Quann E, Volek JS, Fernandez ML. J Nutr. 2008 Feb;138(2):272-6. PMID: 18203890 Carbohydrate-restricted diets (CRD) significantly decrease body weight and independently improve plasma triglycerides (TG) and HDL cholesterol (HDL-C) . [..] Eighteen subjects were classified as having the metabolic syndrome (MetS) at the beginning of the study, whereas 3 subjects had that classification at the end. These results suggest that including eggs in a CRD results in increased HDL-C while decreasing the risk factors associated with MetS.

Berberine inhibits adipogenesis in high-fat diet-induced obesity mice. Hu Y, Davies GE. Fitoterapia. 2009 Oct 25. [Epub ahead of print] PMID: 19861153 doi:10.1016/j.fitote.2009.10.010 Our previous studies illustrated that berberine inhibited adipogenesis in murine-derived 3T3-L1 preadipocytes and human white preadipocytes. In this study, the effects of berberine on the adipogenesis of high-fat diet-induced obesity (FD) or normal diet (ND) mice and possible transcriptional impact are investigated. The results demonstrated that in FD mice, berberine reduced mouse weight gain and food intake and serum glucose, triglyceride, and total cholesterol levels accompanied with a down-regulation of PPARgamma expression and an up-regulation of GATA-3 expression. Berberine had no adverse effects on ND mice. These encouraging findings suggest that berberine has excellent pharmacological potential to prevent obesity.

"(NaturalNews) A research team from the University of Washington (UW) recently published a study in Physiology & Behavior revealing that moderate consumption of fructose- and high fructose corn syrup-sweetened beverages leads to significant alterations of lipid metabolization in the liver. Conducted on rats, the study also noted marked increases in both cholesterol and triglyceride levels in rats that fed on fructose-sweetened beverages. Fructose is a monosaccharide sugar that is found in various fruits. It is a simple sugar that is often promoted as being a healthy "fruit" sugar, however the reality is that fructose is just one component of the complex sugar composition that occurs naturally in fruit. Most granulated fructose available today, called crystalline fructose, is derived from fructose-enriched corn syrup. Similarly, high fructose corn syrup is a fructose-enriched form of highly-processed corn syrup that is commonly found in soda, ketchup, candy, dressings, and many other processed foods. The biggest concern about fructose is the fact that, unlike sucrose, it passes undigested through the small intestine where it enters the portal vein and heads directly to the liver. "

"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. "

"5' AMP-activated protein kinase or AMPK or 5' adenosine monophosphate-activated protein kinase is an enzyme that plays a role in cellular energy homeostasis. It consists of three proteins (subunits) that together make a functional enzyme, conserved from yeast to humans. It is expressed in a number of tissues, including the liver, brain, and skeletal muscle. The net effect of AMPK activation is stimulation of hepatic fatty acid oxidation and ketogenesis, inhibition of cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibition of adipocyte lipolysis and lipogenesis, stimulation of skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulation of insulin secretion by pancreatic beta-cells.[1] It should not be confused with cyclic AMP-activated protein kinase (protein kinase A), which, although being of similar nature, may have opposite effects.[2]"

"The Japan eicosapentaenoic acid (EPA) Lipid Intervention Study (JELIS) is a clinical trial that all Track Your Plaquers should know about. This enormous trial followed a simple design: Japanese men, between 40-75 years, and Japanese postmenopausal women aged